The American Cancer Society this week launched a major new cancer research effort that aims to enroll 500,000 people.
According to the society, the study may be the "last best chance" to do large-scale research in the United States on genetic, lifestyle and environmental factors that cause and prevent cancer.
The Cancer Prevention Study 3 (CPS-3) will seek a geographically and ethnically diverse group of women and men, aged 30 to 65, who have never been diagnosed with cancer. The participants will be tracked for 20 or more years.
"There are no U.S. studies on the horizon positioned to take advantage of rapidly developing new knowledge and technologies over the coming decades, except CPS-3," study leader Eugenia E. Calle, managing director of analytic epidemiology at the American Cancer Society, said in a prepared statement.
"This type of study involves hundreds of thousands of people, with diverse backgrounds, followed for many years, with collection of biological specimens and assessments of dietary, lifestyle and environmental exposures. It also requires active follow-up to discover if and when study participants develop cancer," Calle said.
She noted that large studies of up to a million people are being conducted in a number of countries in Europe and Asia. Many countries are able to conduct such large studies because they have national health-care systems that record information about patients' visits.
"Another important factor is that people in other countries are often willing to be enrolled in a study, historically a serious challenge in the U.S.," Calle said.
Enrollment in CPS-3 will take place at 64 of the 4,800 Relay for Life cancer research fundraising events taking place across the United States in 2007, and will continue at certain Relay for Life events through 2011.
Data collected during CPS-3 will build on information collected from a series of American Cancer Society studies dating back to the 1950s.
Sunday, April 29, 2007
U.S. Cancer Group Launches Major Study
Why Alcohol Consumption Increases Breast Cancer Risk, New Animal Study
Alcohol (EtOH) consumption -- even moderate -- is a well-established risk factor for breast cancer in women. A recent study showed that 60 percent of female breast cancers worldwide were attributable to alcohol consumption. Nevertheless, the mechanisms of alcohol-induced breast cancer are poorly understood.
The definitive biological effects and molecular mechanisms of EtOH on progression and malignancy of breast cancer have not been investigated using a mammalian breast cancer model that mimics the human disease. Scientists have suggested that the possible mechanisms involved include the agitation of estrogen metabolism and response; cell mutation by the EtOH metabolite acetaldehyde; oxidative damage; and one-carbon metabolism pathways through reduced folic acid.
Methodology
To date, there has not been an animal model that faithfully mimics the human disease with respect to characteristics of breast cancer, immunocompetence, and physiologically relevant EtOH intake. The researchers addressed and overcame the obstacles and developed a novel mouse breast cancer model. The model mimics human breast cancer disease in which the estrogen receptor-positive breast adenocarcinoma cells were subcutaneously injected near the pad of the fourth mammary gland of female immunocompetant mice (C57BL/6). The six-week-old female mice were fed with moderate EtOH (one percent in drinking water) for four weeks, the equivalent of two drinks per day in humans. The control mice received regular drinking water only.
In the second week of the experiment, mouse breast cancer cells (5x105 E0771) were injected at cite referenced above. At the end of the experiment, the tumors were isolated to measure tumor size, examine intratumoral microvessel (IM) density via CD 31 immunohistochemistry staining, and assessing VEGF protein levels via ELISA. These steps were taken to determine the effects of EtOH intake in physiologically relevant doses on tumor growth and angiogenesis in mouse breast cancer.
Former Croatia PM Racan dies of cancer
Croatia's former prime minister Ivica Racan, who allowed first free elections in 1990 and later set the country on the road towards European Union membership, died of cancer on Sunday.
Racan died in hospital at the age of 63, his Social Democratic Party (SDP) said in a statement, after kidney cancer discovered in February spread to his brain.
Obesity-breast Cancer Link May Be Due To Fat Tissue-derived Hormone Leptin
Leptin, an adipocyte-derived hormone, is best known for its efforts to send messages to the body that no more food is needed, a process that may go awry in many people with obesity. But it also is involved in many other processes, from reproduction and lactation to cell differentiation and proliferation. Leptin is activated by signals from the leptin receptor ObR, and it is this partnership that has previously been found to be involved in the development of breast cancer. It was recently reported, for example, that leptin was detected in 86.4 percent of primary breast tumors and that its expression was highly correlated with ObR.
In previous studies in Dr. Ando's laboratory, leptin was demonstrated to play a significant role in promoting breast cancer in obese women by increasing the amount of estrogen (estradiol) in breast tissue. In the current study, the researchers found that leptin also upregulated or increases the production of E-cadherin, an intercellular adhesion molecule generally viewed as a tumor suppressor. The researchers grafted human breast cancer tissue in "nude" mice (genetically bred to be unable to reject tumors and therefore a frequently used animal in cancer research) and also in a three dimensional tissue culture which closely mimics biological features of tumors. The results were the same in both. Combined exposure to leptin and estradiol increased tumor size, sometimes doubling it, and these changes correlated with an increase in E-cadherin.
Dr. Ando and his colleagues believe from their data that it is reasonable to suggest that the tumor suppressor E-cadherin may serve as a tumor enhancer when exposed to leptin and estradiol, that its ability to help cells aggregate then enhances the transformation of normal cells to cancerous cones, stimulating the growth of tumor mass.
When the researchers used an E-cadherin antibody or a calcium-chelating agent to block E-cadherin function in the present of estradiol, this enhanced cell growth stopped.
This work is part of an on-going research project concerning inhibition of the effects of leptin and estradiol on breast cancer. It was supported in part by an award from the Associazione Italiana per la Ricerca sul Cancro (AIRC). Dr. Ando's presentation on Sunday, April 29 is part of the scientific program of the American Society of Investigative Pathology.
Bile Duct Obstruction Is Correlated WIth Ductal Cancer, Study Shows
Perhaps even more important, the cancers metastized outside the liver (as they frequently do in human patients with advanced bile duct cancer) only in the animals with bile duct obstruction.
Virginia Commonwealth University scientist Dr. Alphonse Sirica presented the findings at Experimental Biology 2007 in Washington, DC. His presentation, on April 29, is part of the scientific program of the American Society for Investigative Pathology.
The bile ducts are tubes that carry bile (a liquid secreted by the liver that contains cholesterol, bile salts, and waste products) from the liver to the gallbladder and small intestine. Bile duct obstruction has long been known to be present in both malignant and nonmalignant liver disease (jaundice, for example), but before the study by Dr. Sirica and his colleagues the direct effect of such obstruction on bile duct cancer cell growth and aggressiveness had not been previously investigated.
These new findings are highly significant for two reasons, says Dr. Sirica.
First, they establish an important correlation between bile duct obstruction and bile duct cancer, suggesting growth regulatory mechanisms that could be highly significant in the progression of the cancer and that could become good molecular targets for drug therapy.
Second, they establish a unique preclinical model of how bile duct cancer in liver progresses that can be used to rapidly test and evaluate novel molecular treatment strategies.
Such strategies are badly needed for this understudied cancer, adds Dr. Sirica. The incidence and mortality of cholangiocarcinoma, the primary cancer of the bile ducts, is increasing worldwide. Some 3,500 new cases are now diagnosed annually in the United States. Survival rates remain dismally low because most patients have advanced disease at the time of diagnosis and thus are poor candidates for the current best treatment, surgical resection. Although there are some known risk factors for the disease (such as primary sclerosing cholangitis), the cause of most cases remain unknown and the cellular and molecular changes that accompany the disease have not been well understood.
This study is part of ongoing work in Dr. Sirica's laboratory aimed at identifying altered growth factor signaling pathways in cholangiocarcinoma that may be exploited as potential molecular targets for therapy. Dr. Sirica's co-authors for the Experimental Biology 2007 presentation are Dr. Zichen Zhang, Dr. Toru Asano, Dr. Xue-Ning Shen, Deanna J. Ward and Dr. Arvind Mahatme. Support for the work came from the National Cancer Institute, National Institutes of Health.
Fat tissue-derived hormone leptin increases e-cadherin expression, obesity-breast cancer link noted
Being obese increases the risk of breast cancer in post-menopausal women, shortens the time between return of the disease and lowers overall survival rates. Italian researchers speaking at Experimental Biology 2007 in Washington, DC, now report evidence on how leptin, a hormone found in fat cells, significantly influences breast cancer development and progression in mice. This new understanding, says Dr. Sebastiano Ando, establishes a new mechanism for the link between obesity and breast cancer and suggests new targets for drugs that could intervene in that mechanism.
Dr. Ando’s presentation on Sunday, April 29 is part of the scientific program of the American Society of Investigative Pathology.
Leptin, an adipocyte-derived hormone, is best known for its efforts to send messages to the body that no more food is needed, a process that may go awry in many people with obesity. But it also is involved in many other processes, from reproduction and lactation to cell differentiation and proliferation. Leptin is activated by signals from the leptin receptor ObR, and it is this partnership that has previously been found to be involved in the development of breast cancer. It was recently reported, for example, that leptin was detected in 86.4 percent of primary breast tumors and that its expression was highly correlated with ObR.
In previous studies in Dr. Ando’s laboratory, leptin was demonstrated to play a significant role in promoting breast cancer in obese women by increasing the amount of estrogen (estradiol) in breast tissue. In the current study, the researchers found that leptin also upregulated or increases the production of E-cadherin, an intercellular adhesion molecule generally viewed as a tumor suppressor. The researchers grafted human breast cancer tissue in “nude” mice (genetically bred to be unable to reject tumors and therefore a frequently used animal in cancer research) and also in a three dimensional tissue culture which closely mimics biological features of tumors. The results were the same in both. Combined exposure to leptin and estradiol increased tumor size, sometimes doubling it, and these changes correlated with an increase in E-cadherin.
Dr. Ando and his colleagues believe from their data that it is reasonable to suggest that the tumor suppressor E-cadherin may serve as a tumor enhancer when exposed to leptin and estradiol, that its ability to help cells aggregate then enhances the transformation of normal cells to cancerous cones, stimulating the growth of tumor mass.
When the researchers used an E-cadherin antibody or a calcium-chelating agent to block E-cadherin function in the present of estradiol, this enhanced cell growth stopped.
Friday, April 27, 2007
Woman pleads in cancer fraud
A former Elmhurst woman who defrauded neighbors and local civic groups of meals, clothing and more than $43,000 by falsely claiming she had cancer—even cutting her hair short—pleaded guilty Friday and was sentenced to 6 months in the DuPage County Jail.
Josette Hamilton, 34, a mother of three, collected the funds from hundreds of individuals, created a Web site seeking donations, set up a bank account and was preparing to sell raffle tickets at a fundraiser she was planning. She was charged with theft by deception and operating a fraudulent scheme.
Hamilton was also ordered to repay $43,256 and serve 2½ years probation.
Beginning in 2005, Hamilton told people she had non-Hodgkins lymphoma and needed several costly operations. She claimed she was on the edge of financial ruin because of debilitating treatments.
"You took advantage of hard-working, caring people," said DuPage Judge George Bakalis. "You took advantage of their kind-hearted nature. I can only hope people won't be halted from making such contributions to really needy people in the future."
Hamilton must make restitution to a long list of donors supplied by the Elmhurst Police Department.
Assistant State's Atty. Demetri Demopoulos said besides cash, people donated food, clothes, did her laundry, picked up her children at local schools. Helping to raise money were many business and civic groups, several Elmhurst churches and teachers and staff at the school her children attended, he said.
Hamilton never looked Friday at several of those she defrauded, but she wiped away tears as she was taken by a deputy to the County Jail. She had been free on $50,000 bail since her January 2006 arrest.
Demopoulos said that "most of the people will get their cash back because Elmhurst Detective Steven Weatherford quickly froze her bank accounts containing more than $34,000 in cash. Many of the individual cash donations were for $300, he said.
"We hope we will always have a big heart, but now we know never give cash," said Jena Medema, a member of the Elmhurst Junior Women's Club. "To think, I left my own family on Christmas to pick up her children's Christmas stockings."
Resident Donna Stubbs said at one point Hamilton cut her hair short and wore a bandanna as if she were receiving cancer treatment. But Demopoulos said Hamilton was examined by a physician in February 2006 and no cancer was found.
Hamilton, who had been convicted of passing a bad check in 1998, faced a potential maximum sentence of up to 10 years in prison. Elmhurst police, who believe the scheme went on for about five months, began to investigate after several people grew suspicious and contacted them.
Her children are living with relatives.
Non-aspirin NSAIDs may reduce lung cancer risk
The long-term use of non-aspirin anti-inflammatory painkillers, or NSAIDs, appears to slightly reduce the risk of a person developing lung cancer, according to research published in the International Journal of Cancer.
"Regular use of aspirin or other NSAIDs reduces the risk of colorectal cancer and might reduce the risk of additional gastrointestinal cancers as well," Dr. Sonia Hernandez-Diaz, of Harvard School of Public Health, Boston, and colleagues write. "The effect of NSAIDs on the development and progression of other types of cancer remains controversial."
Because of its high prevalence, the researchers examined whether lung cancer risk is influenced by the use of aspirin or other specific NSAIDs.
Analyses centered on 4,336 lung cancer patients and 10,000 healthy controls. At 13 to 24 months before diagnosis, aspirin was prescribed to 22.1 percent of the lung cancer patients and 17.3 percent of controls. Another 21.6 percent and 21.5 percent of cases and controls, respectively, were prescribed non-aspirin NSAIDs at least 13 months before the first lung cancer was diagnosed.
Compared with non-use, use of non-aspirin NSAIDs was associated with a 24 percent reduced relative risk of lung cancer. The inverse association between non-aspirin NSAIDs and lung cancer was more evident in men than women. It was also more apparent for smokers than for non-smokers.
There was no apparent protective effect of aspirin on lung cancer risk, even for long-term use and higher doses.
Several mechanisms have been proposed to explain the chemo-preventive effects of NSAIDs, including enhancement of the immune system and a reduction in inflammation.
SOURCE: International Journal of Cancer, April 2007.
Woman faked cancer for cash, police say
A woman pretended to have liver cancer and took in about $20,000 from fundraisers to pay for her fictitious treatments, authorities said.
Jean Anne Allen, 36, was arraigned Thursday after state police said they found no evidence she was being treated for the disease.
"She duped a lot of people," said state police Sgt. Lisa Gee-Cram.
Friends and co-workers held a spaghetti-supper fundraiser for Allen last year after she said she needed help paying for chemotherapy to treat a recurrence of liver cancer.
Her lawyer, Kenneth Hotchkiss, did not immediately return a message seeking comment Friday.
Allen, of Norvell Township, faces up to five years in prison if convicted of fraud.
She was freed on $10,000 bond and a May 8 hearing was set.
Better Prostate Cancer Test May Be Near
A test that focuses on a blood protein produced by prostate cancer cells may improve disease diagnosis, researchers report.
Levels of this protein, called prostate cancer antigen-2 (EPCA-2), appear to give a more accurate picture of cancer present in the body, experts say.
"We've been able to show that blood levels of it are low in normal individuals and high in prostate cancer, and that it distinguishes between cancers that are confined to the prostate and those that have spread outside the gland," explained study lead researcher Dr. Robert H. Getzenberg, professor of urology and director of research at Johns Hopkins University's James Buchanan Brady Urological Institute, in Baltimore.
His team published its findings in the May issue of Urology.
Prostate cancer is the most common malignancy in American men. There will be some 218,890 new cases in the United States this year and 27,050 deaths linked to the disease, the American Cancer Society estimates. Prostate cancer is highly curable if caught early, however.
In the new study, Getzenberg's team measured blood levels of EPCA-2 in 330 men. Some of the men had an enlarged but non-cancerous prostate gland, some had prostate cancer but displayed normal PSA levels, some had prostate cancer that had spread beyond the gland, and some had other cancers or medical conditions.
A specific level of ECPA-2 identified 90 percent of the men with cancer confined to the prostate and 98 percent of those in whom it had spread outside the gland. The test was negative in 97 percent of the men without prostate cancer, the researchers said.
That's an improvement on the standard PSA test, which provides only a rough guide in many such cases. For example, a high blood level of PSA can sometimes indicate prostate cancer, but often a biopsy reveals no such malignancy.
Conversely, a low PSA level does not necessarily mean that a man is free of prostate cancer, the researchers said.
"If this test works out, we can avoid a lot of unnecessary biopsies," Getzenberg said. About 1.3 million men in the United States will have biopsies this year to find only 200,000 cancers, he noted.
"Clearly, we need further validation," Getzenberg added. "We are doing good-sized validation studies, and we are also testing the ability of the marker to identify aggressive forms of the disease."
Spotting especially life-threatening prostate tumors is "the holy grail" of diagnosis, he said. Current PSA testing cannot distinguish between cancers that will grow so slowly that they pose no danger to life and those that require quick action. The hope is that the ECPA-2 test will identify men whose slow-growing cancers make them candidates for "watchful waiting" rather than immediate surgery or other treatment.
The Hopkins team, working with researchers from the University of Pittsburgh, has licensed the test to a company, Onconome Inc. The ECPA-2 screen is a simple antibody test requiring "no special kind of technology or equipment," Getzenberg noted.
"We have already met with the Food and Drug Administration and understand the kind of trial we need to do [for approval]," he said. "We want to get the necessary papers out over the next six to nine months." That means that the test might be available in the next 18 months, the researcher said.
The Hopkins team is now working with tissue samples from three other medical centers, "trying to broaden the types of samples we have," Getzenberg added.
"In general, it does look very promising," Dr. Durado Brooks, director of prostate and colorectal cancers at the American Cancer Society, said of the ECPA-2 test. But much more work must be done, he added.
"It does seem to have very high sensitivity and specificity for prostate cancer," Brooks said. "The challenge is taking it out of this isolated and rigorous setting and seeing how it performs in other laboratories and also in much larger screening-type populations."
If the test does prove to be accurate in larger populations, it could be "very useful" in prostate cancer diagnosis, Brooks said. But the real hope that it could single out those cases requiring immediate treatment from those that could be left for watchful waiting has yet to be proved, he said.
Experimental Test Detects Prostate Cancer, Tells Whether It Is Spreading
An experimental blood test for prostate cancer seems to work better than the current PSA test -- and can tell whether the cancer is spreading.
The new test looks for a protein called EPCA-2 -- or early prostate cancer antigen 2. Unlike the PSA (prostate-specific antigen) protein on which the current PSA test is based, this protein isn't found in normal prostate cells. Instead, EPCA-2 occurs in relatively large amounts only in prostate cancer cells.
The test is being developed by Robert H. Getzenberg, PhD, director of urology research at Johns Hopkins University's Brady Urological Institute. Getzenberg began the work while still at the University of Pittsburgh; the test has been licensed to the Seattle biotech firm Onconome Inc.
"We wanted to find something that really identified people with prostate cancer and not people with enlarged or infected prostates," Getzenberg tells WebMD. "This is as close to cancer specific as we could find. We found it is very unique. It is 97% specific, meaning that if you test positive there's only a 3% chance you don't have prostate cancer."
Getzenberg has a financial interest in the test. But experts who do not stand to gain from the test agree that it has enormous potential.
Otis Brawley, MD, chief of the solid tumor service at Emory University's Winship Cancer Institute, calls the test "important" and predicts it will be widely used.
Charles A. Coltman Jr., MD, associate chairman for cancer control and prevention at San Antonio's Southwest Oncology Group, calls the findings "striking" and "remarkable," although he warns that the test has been tried out on only a small number of patients.
Ganesh Palapattu, MD, assistant professor of urology at the University of Rochester, agrees that more studies must be done. But he tells WebMD that the test is a big step toward the "Holy Grail of prostate cancer detection: not so much identifying men with prostate cancer, but identifying men with prostate cancer who have aggressive disease."
"This not only helps tell whether you have prostate cancer, but what kind of prostate cancer you have," Getzenberg says.
Getzenberg and colleagues report early studies of the EPCA-2 test in the April issue of the journal Urology.
EPCA-2 Test Beats PSA
Nobody is entirely happy with the current PSA test for prostate cancer. A man without prostate cancer can have high PSA levels. A man with advanced prostate cancer may have very low PSA levels.
Getzenberg's team tried out the EPCA-2 test on blood samples from several different groups of people. Some were known to have early prostate cancer or late prostate cancer, and some had other kinds of cancer. Some had enlarged prostates, but not cancer. Some were women, who have no prostate gland. And some were healthy men with normal PSA levels.
Both in terms of detecting cancer when it was actually there (sensitivity), and in terms of not detecting cancer when it wasn't actually there (specificity), the EPCA-2 test beat the PSA test.
More importantly, it beat the PSA test in predicting whether prostate cancer already had spread outside the prostate gland. When that has happened, standard treatments for prostate cancer -- radical prostatectomy (surgery to remove the prostate) and brachytherapy (tiny radioactive seeds implanted in the prostate) -- fail to cure.
"I predict that within the next year, this test is going to be widely used to find the guy who has prostate cancer and who, if he got radical prostatectomy, would relapse very quickly," Brawley tells WebMD. "It is going to say to this guy, 'Skip the unnecessary surgery and get pelvic radiation and hormone treatment now.'"
Getzenberg says it will be at least two years before the test is "out on the street" with FDA approval. All of the experts who spoke to WebMD agree that large-scale screening tests will be needed before it's known exactly how well the test works.
"What we really need to know is how this test behaves in all comers -- when we don't already know whether the men being tested have prostate cancer," Palapattu says. "It would also be important to identify men with high risk of prostate cancer vs. low risk of prostate cancer, and to test men after prostate surgery to see whether it can predict cancer recurrence."
When -- and if -- the EPCA-2 test is approved, men will still need better prostate cancer tests.
"At least a third, maybe two-thirds of guys with localized disease have cancer that will never leave the prostate and never bother them," Brawley says. "This new test is not going to help those guys who get treated for prostate cancer but shouldn't. I hope there will be help for these men soon."
Scientists Spot Mechanism Behind Lung Cancer Drug Resistance
Scientists have discovered a key means by which some lung cancer tumors become resistant to drugs such as Iressa and Tarceva.
The finding could lead to better combination drug treatments, the researchers report.
"We wanted to find out why tumors become resistant to certain drugs," explained senior researcher Dr. Pasi A. Janne, an assistant professor of medicine at Harvard Medical School. "While patients respond to drugs like Iressa and Tarceva, the majority of patients become resistant to them. The cancers figure out a way to grow in the presence of these drugs."
His team reported its findings in the April 26 online edition of Science.
Doctors often resort to drugs such as Iressa (gefitinib) and Tarceva (erlotinib) to treat advanced non-small-cell lung cancer. These agents work by blocking epidermal growth factor receptor (EGFR), a molecule lying on the surface of cancer cells.
Tumors that respond to these EGFR inhibitors shrink rapidly and dramatically, but in time they can become resistant and start growing again.
In about half of the cases, a mutation in the EGFR gene interferes with the ability of the drug to bind to the receptor. Once this happens, these drugs cease to work.
However, in many other cases the cause of resistance remains unknown.
Investigating that issue, Janne's team experimented with lung cancer cells resistant to Iressa.
They found that a mutation in a second gene can also cause the drug to stop working. "We identified a single mutation in another gene that occurred in the drug-resistant cells," Janne said. "This is the MET oncogene. And we have a specific drug that targets this gene."
Analysis of samples from patients whose tumors became resistant after initially responding to Iressa showed that the MET mutation was present in samples from four of 18 patients.
"When we treated the resistant cells with a MET inhibitor, it completely restored the effectiveness of Iressa," Janne said. "We found the same MET mutation in about 20 percent of lung cancer patients."
This is a wholly new mechanism for lung cancer drug resistance, Janne said, and it is also "a mechanism that we can target with a specific drug. This is a potentially new and important therapy for these individuals." he said. According to Janne, similar mechanisms may also be at work in other cancers.
The Harvard group is working on ways to combine treatment with currently available EGFR inhibitors and MET inhibitors that are currently in clinical trials. They also want to study more drug-resistant samples, to get a better idea of how often this resistance mechanism occurs.
One expert views the finding as another indication of cancer's complexity.
"This shows the complexity of treating a rapidly changing tumor type," said Michael Melner, a scientific program director at the American Cancer Society. "The mutation of the MET gene is only one explanation out of many for the resistance of the tumors."
Drug combinations appear more and more necessary for treating many cancers, Melner added. "This is another study that points to things being more complex than we think they are. Clearly, combinations of drugs are going to be necessary to treat multiple cancer types. And this is just another indication of that," he said.
Cervical Cancer and HPV: What Women and Girls Should Know
Nearly two decades ago, experts discovered a relationship between infection with HPV (human papillomavirus) and cervical cancer. Since then, these experts have learned much more about cervical cancer and HPV.
Here, what every woman and girl should know about HPV and cervical cancer.
About HPV Virus
There are more than 100 types of HPV. About 30 or so types can cause genital infections. Some can cause genital warts; other types can cause cervical or other genital cancers. (The other 70 or so HPV types can cause infections and warts elsewhere on the body, such as on the hands.)
Most sexually active women and men will contract HPV at some time in their lifetime. Most will never even know it. Usually, this virus does not cause any symptoms and doesn't cause disease. Often, the body can clear HPV infection on its own within two years or less.
Some types of HPV, typically HPV 6 and HPV 11, cause genital warts. The warts are rarely associated with cervical cancers. They are considered "low-risk" HPV.
HPV and Cancer
Certain HPV types are classified as "high-risk" because they lead to abnormal cell changes and can cause genital cancers: cervical cancer as well as cancer of the vulva, anus, and penis. In fact, researchers say that virtually all cervical cancers – more than 99% -- are caused by these high-risk HPV viruses. The most common of the high-risk strains of HPV are types 16 and 18, which cause about 70% of all cervical cancers.
If the body clears the infection, the cervical cells return to normal. But if the body doesn't clear the infection, the cells in the cervix can continue to change abnormally. This can lead to precancerous changes or cervical cancer.
Rates of Cervical Cancer
Actual cervical cancer is rare in the U.S. because most women get Pap tests and have abnormal cells removed before they turn into cancer. In 2006, about 10,000 women in the U.S. found out they had cervical cancer and 4,000 women died from cervical cancer.
HPV Transmission
HPV types associated with genital infections are transmitted sexually, primarily through skin-to-skin contact during sexual activity. HPV can also be transmitted through oral sex. The chance of getting HPV rises with certain risk factors:
Symptoms of High-Risk HPV Infection and Tests
When infection with high-risk HPV types occurs, there usually are no symptoms. Often, the first clue is a Pap test result that is abnormal. In a Pap test, the doctor takes a swab of cervical cells and has them analyzed in a laboratory. If the Pap test results are unclear, the doctor may order a HPV test to check the DNA type of the virus. This analysis can identify 13 of the high-risk HPV types associated with cervical cancer. It does not identify cancer. But it tells the woman and her doctor if she has a type of HPV capable of causing cancer.
Treatment of HPV Infection
A positive HPV test may not mean a woman needs treatment, at least not immediately. Having a positive test puts a woman in the "high-risk" class, alerting the doctor that she is at higher risk for cervical tissue changes and may need close evaluation.
To watch for further tissue changes, the doctor may order frequent Pap tests. Or the doctor may perform a colposcopy, in which a lighted magnifying device is used to closely examine cervical tissues.
Researchers have discovered that high-risk HPV viruses produce certain proteins. These proteins interfere with the cell functions that limit excessive cell growth.
If abnormal cervical tissue changes progress, treatment may be needed. Among the options are surgery, laser treatment, and freezing.
Pregnant women, or women considering pregnancy, should consult closely with their doctor. The risk of passing HPV on to the baby is very low. But HPV treatments can affect pregnancy, so doctors may want to delay treatment until after childbirth.
Prevention of HPV Transmission
There’s only one sure way to eliminate any chance of HPV transmission: Avoid all genital contact with another person. To reduce risk, it’s best to have a mutually monogamous sexual relationship with an uninfected partner. But keep in mind: Many people don’t know if they’re infected. Using condoms can help prevent HPV transmission but are not foolproof. The virus can be transmitted to genital areas not covered by the condom.
A vaccine, Gardasil, was approved for use in 2006 for use in girls and women aged 9 to 26. Eventually, it may be approved for use in boys, too. Another vaccine, Cervarix, may be approved by the FDA in 2007. Over time, widespread vaccination will help prevent transmission of the HPV types covered by the vaccines.
The Gardasil HPV vaccine protects against several high-risk strains of HPV, including HPV types 16 and 18, which account for 70% of cervical cancers. It also protects against HPV 6 and 11, which account for about 90% of genital warts. Cervarix, if approved, would protect against HPV types 16, 81, 31, and 45 – all of which can cause cervical cancer.
A Promising New Screen for Prostate Cancer
The prostate-specific antigen (PSA) test, used to screen for prostate cancer, is imperfect. It often flags conditions that turn out to be benign, resulting in unnecessary biopsies for more than a million men every year, and it misses other cases of cancer entirely. So the search is on for a better way to find the disease and avoid needless bother and pain for those who don't have it.
Researchers at the Johns Hopkins University School of Medicine think they have a promising candidate. In the April issue of Urology, they report that they've found another marker in the blood, a protein called EPCA-2, which in a preliminary study did a far better job than the PSA at pointing to real cancers and ignoring noncancers. It also predicted whether a man's cancer was confined to the prostate gland or had spread beyond it, a key piece of information in deciding how to treat it. While there have been other potential improvements over the PSA, "only a handful have shown this type of results," says Robert Uzzo, a urologic oncologist at the Fox Chase Cancer Center in Philadelphia who wasn't involved with the study.
Robert Getzenberg, director of urology research at the Brady Urological Institute at Hopkins and lead author, cautions that it will take more extensive trials to nail down whether EPCA-2 might someday become a screening test that either complements or replaces the PSA test. In this study of 385 men, the test was negative in 97 percent of those who didn't have cancer, which means only 3 percent of men got false positive results. (Meantime, PSA test results cause 1.6 million men to have biopsies every year, only 20 percent of whom actually have cancer.) It was also adept at distinguishing between cancer and enlarged prostate: Seventy-seven percent of men with the benign condition had a negative EPCA-2 test. And it didn't miss many cancers either–about 10 percent of cancers limited to the prostate and 2 percent of those that had spread outside the gland. It also picked out 78 percent of the cancers in men who had normal PSA results but nonetheless had prostate cancer.
"It's certainly interesting, and it seems to be promising in those men whose PSA is in midrange," says Howard Scher, chief of the genitourinary oncology service at the Sidney Kimmel Center for Prostate and Urologic Cancers at Memorial Sloan-Kettering Cancer Center in New York. But the test needs to be validated in men of different age groups, among much larger populations, and in different labs, he says. And this test, like the PSA, can't identify which cancers are likely to grow slowly and cause no harm and which need aggressive treatment. "That's the holy grail in my mind," says Getzenberg (who has financial ties to the test's manufacturer, Onconome Inc.).
A Promising New Screen for Prostate Cancer
The prostate-specific antigen (PSA) test, used to screen for prostate cancer, is imperfect. It often flags conditions that turn out to be benign, resulting in unnecessary biopsies for more than a million men every year, and it misses other cases of cancer entirely. So the search is on for a better way to find the disease and avoid needless bother and pain for those who don't have it.
Researchers at the Johns Hopkins University School of Medicine think they have a promising candidate. In the April issue of Urology, they report that they've found another marker in the blood, a protein called EPCA-2, which in a preliminary study did a far better job than the PSA at pointing to real cancers and ignoring noncancers. It also predicted whether a man's cancer was confined to the prostate gland or had spread beyond it, a key piece of information in deciding how to treat it. While there have been other potential improvements over the PSA, "only a handful have shown this type of results," says Robert Uzzo, a urologic oncologist at the Fox Chase Cancer Center in Philadelphia who wasn't involved with the study.
Robert Getzenberg, director of urology research at the Brady Urological Institute at Hopkins and lead author, cautions that it will take more extensive trials to nail down whether EPCA-2 might someday become a screening test that either complements or replaces the PSA test. In this study of 385 men, the test was negative in 97 percent of those who didn't have cancer, which means only 3 percent of men got false positive results. (Meantime, PSA test results cause 1.6 million men to have biopsies every year, only 20 percent of whom actually have cancer.) It was also adept at distinguishing between cancer and enlarged prostate: Seventy-seven percent of men with the benign condition had a negative EPCA-2 test. And it didn't miss many cancers either–about 10 percent of cancers limited to the prostate and 2 percent of those that had spread outside the gland. It also picked out 78 percent of the cancers in men who had normal PSA results but nonetheless had prostate cancer.
"It's certainly interesting, and it seems to be promising in those men whose PSA is in midrange," says Howard Scher, chief of the genitourinary oncology service at the Sidney Kimmel Center for Prostate and Urologic Cancers at Memorial Sloan-Kettering Cancer Center in New York. But the test needs to be validated in men of different age groups, among much larger populations, and in different labs, he says. And this test, like the PSA, can't identify which cancers are likely to grow slowly and cause no harm and which need aggressive treatment. "That's the holy grail in my mind," says Getzenberg (who has financial ties to the test's manufacturer, Onconome Inc.).
Cancer society seeking cancer-free study subjects
The American Cancer Society is looking for half a million volunteers willing to let researchers watch them for the next 20 years to see whether they get cancer.
The aim is to match similar big studies in Europe and Asia that are looking on a large scale for the environmental and lifestyle factors that cause cancer, the second-leading cause of death in the United States after heart disease.
"This type of study involves hundreds of thousands of people, with diverse backgrounds, followed for many years, with collection of biological specimens and assessments of dietary, lifestyle and environmental exposures," Eugenia Calle, managing director of analytic epidemiology at the American Cancer Society, said in a statement.
"It also requires active follow-up to discover if and when study participants develop cancer."
The group will recruit men and women between the ages of 30 and 65 in whom cancer has never been diagnosed. They will give blood to be tested and answer questionnaires at various times over the next 20 years.
Similar big studies have confirmed the link between cigarette smoking and lung cancer, shown that obesity increases the risk of several cancers, and linked aspirin use to a lower death rate from colon cancer.
They have also found evidence that defied conventional wisdom, such as the Women's Health Initiative study that found hormone replacement therapy actually raises the risk of breast cancer, stroke and heart attack.
Mechanism produces resistance to lung cancer drugs
Researchers have identified a new mechanism that provokes resistance to certain lung cancer drugs, which may exist in other types of cancerous tumors, according to a study published Thursday in the United States.
The international team of scientists, in a report to appear in the April 27 issue of the journal Science and released online in advance, said their findings suggest a treatment strategy for patients with the resistant tumors.
The mechanism was discovered in about 20 percent of patients with tumors that became resistant to Tarceva or Iressa, two commonly used targeted therapy drugs in the United States, said Jeffrey Engelman of Massachusetts General Hospital, the paper's lead author.
The resistance was "caused by the genetic activation of an oncogene that is not the normal target of the drug, which is something that has never been seen before," Engelman said.
Tarceva (eriotinib) and Iressa (gefitinib) are used to treat advanced types of lung cancer, the leading cause of cancer deaths in the United States.
"We also identified a potential new way to treat these resistant tumors with combination therapy directed against both protein targets," said Pasi Jaenne of the Dana-Farber Cancer Institute in Boston, Massachusetts, the study's senior author.
The drugs act by blocking a growth factor receptor, a molecule on the surface of cancer cells.
Scientists Spot Mechanism Behind Lung Cancer Drug Resistance
Scientists have discovered a key means by which some lung cancer tumors become resistant to chemotherapy drugs such as Iressa and Tarceva.
The finding could lead to better combination drug treatments, the researchers report.
"We wanted to find out why tumors become resistant to certain drugs," explained senior researcher Dr. Pasi A. Janne, an assistant professor of medicine at Harvard Medical School. "While patients respond to drugs like Iressa and Tarceva, the majority of patients become resistant to them. The cancers figure out a way to grow in the presence of these drugs."
His team reported its findings in the April 26 online edition of Science.
Doctors often resort to drugs such as Iressa (gefitinib) and Tarceva (erlotinib) to treat advanced non-small-cell lung cancer. These agents work by blocking epidermal growth factor receptor (EGFR), a molecule lying on the surface of cancer cells.
Tumors that respond to these EGFR inhibitors shrink rapidly and dramatically, but in time they can become resistant and start growing again.
In about half of the cases, a mutation in the EGFR gene interferes with the ability of the drug to bind to the receptor. Once this happens, these drugs cease to work.
However, in many other cases the cause of resistance remains unknown.
Investigating that issue, Janne's team experimented with lung cancer cells resistant to Iressa.
They found that a mutation in a second gene can also cause the drug to stop working. "We identified a single mutation in another gene that occurred in the drug-resistant cells," Janne said. "This is the MET oncogene. And we have a specific drug that targets this gene."
Analysis of samples from patients whose tumors became resistant after initially responding to Iressa showed that the MET mutation was present in samples from four of 18 patients.
"When we treated the resistant cells with a MET inhibitor, it completely restored the effectiveness of Iressa," Janne said. "We found the same MET mutation in about 20 percent of lung cancer patients."
This is a wholly new mechanism for lung cancer drug resistance, Janne said, and it is also "a mechanism that we can target with a specific drug. This is a potentially new and important therapy for these individuals." he said. According to Janne, similar mechanisms may also be at work in other cancers.
The Harvard group is working on ways to combine treatment with currently available EGFR inhibitors and MET inhibitors that are currently in clinical trials. They also want to study more drug-resistant samples, to get a better idea of how often this resistance mechanism occurs.
One expert views the finding as another indication of cancer's complexity.
"This shows the complexity of treating a rapidly changing tumor type," said Michael Melner, a scientific program director at the American Cancer Society. "The mutation of the MET gene is only one explanation out of many for the resistance of the tumors."
Drug combinations appear more and more necessary for treating many cancers, Melner added. "This is another study that points to things being more complex than we think they are. Clearly, combinations of drugs are going to be necessary to treat multiple cancer types. And this is just another indication of that," he said.
Black cohosh may cut breast cancer risk
A new study provides preliminary evidence that an herbal medicine used to help women cope with menopausal symptoms may reduce breast cancer risk.
However, much more research is needed before the herb, black cohosh, can be recommended to prevent the disease, Dr. Timothy R. Rebbeck of the University of Pennsylvania School of Medicine in Philadelphia and colleagues caution.
Many women use hormone-related supplements such as black cohosh, dong quai, red clover, ginseng and yam to deal with hot flashes and other symptoms of menopause, Rebbeck and his team note in the International Journal of Cancer.
To examine how the use of these herbs might relate to breast cancer risk, the researchers compared 949 women with breast cancer to 1,524 healthy controls.
African-American women were more somewhat likely than European Americans to use the herbs. Women who reported taking black cohosh (5 percent of blacks and 2 percent of whites) were at 61 percent lower risk of breast cancer, the researchers found.
Also, those who took an herbal preparation derived from black cohosh called Remifemin had a 53 percent lower risk of the disease.
Previous studies have shown that black cohosh can block cell growth, Rebbeck and colleagues note. The herb is also an antioxidant, and has been shown to have anti-estrogen effects as well. On the negative side, the herb can have side effects, and animal studies have suggested it may affect breast cancer severity.
"Substantial additional research must be undertaken before it can be established that black cohosh, or some compound found in black cohosh, is a breast cancer chemopreventive agent," the researchers write.
"Furthermore," they stress, "women may wish to seek guidance from their physician before using these compounds."
SOURCE: International Journal of Cancer, April 1, 2007.
Protein could boost prostate cancer screening accuracy
A newly discovered blood protein could change the way men are screened for prostate cancer with a simple-to-use blood test, researchers say.
Led by Dr. Robert H. Getzenberg, professor of urology and director of research at the James Buchanan Brady Urological Institute at the Johns Hopkins University School of Medicine, the study detected an unprecedented 94 percent of men with prostate cancer and correctly identified 97 percent of men who don't have the disease, a far greater accuracy rate for prostate cancer than the current PSA test.
The protein, called Early Prostate Cancer Antigen or EPCA-2 is exclusively licensed to Seattle-based biotechnology company Onconome, Inc., led by CEO and co-founder Ray Cairncross.
"The results from the Johns Hopkins University research study demonstrate that the ProstaMark® EPCA-2 test is highly specific and sensitive to prostate cancer and could greatly reduce the number of unnecessary prostate biopsies," Cairncross said in a press release.
For the past 25 years, prostate-specific antigen (PSA) has been the standard in the effort to detect prostate cancer; however, it is not highly specific or sensitive. For example, 80 percent of patients with elevated PSA levels do not have prostate cancer and 15 percent of patients with normal PSA levels do have prostate cancer. Nevertheless, nearly 1.7 million prostate biopsies are performed each year based primarily on results from PSA testing and an estimated 25 million men have had at least one negative biopsy (i.e. no cancer found).
Not only was the EPCA-2 test negative in 97 percent of men who do not have prostate cancer and positive in 94 percent of men with prostate cancer, it also showed that EPCA-2 levels are highest in patients with non-organ confined prostate cancer, which is important because cancer that has spread outside of the prostate is much more deadly.
The company is also working with Johns Hopkins University on an early detection test for colon cancer, and early results indicate that the performance characteristics of the colon cancer test are similar to those achieved in the development of the prostate cancer test.
Onconome will also use its novel, proteomic technologies to assist pharmaceutical companies in developing cancer therapies and to select clinical trial candidates. The company also will collaborate with in-vivo imaging and targeted therapeutics companies to improve treatment.
A Radical Attack On Prostate Cancer
Seattle-based biotech Dendreon is hoping to get U.S. approval for the first cancer drug that would train the body to fight off cancer on its own, with few side effects. But researchers, statisticians and Wall Street analysts are fiercely debating whether there is enough data about this radical new treatment.
Dendreon's (nasdaq: DNDN - news - people ) Provenge is a so-called cancer vaccine. Researchers prefer the term immunotherapy because it would treat, not prevent, cancer. A personalized drug, composed of human immune system cells, is created for each patient; the idea is to give the immune system the tools it needs to fight off the disease.
On Thursday, a panel of experts convened by the Food and Drug Administration will debate whether the drug is ready to be marketed. The FDA often follows the recommendation of such panels, but it doesn't have to. Already, briefing documents have been posted saying that the drug seems very safe--although there is a worry of stroke--and reviewing the arguments about whether or not it is effective at prolonging patients' lives.
Why is there any question at all? When researchers run a clinical study, they define a specific goal. For instance, that drug will extend life over a prespecified time or prevent tumors from growing compared to a placebo. The whole study is designed around this goal. If the trial falls short, its results can only be used to generate new questions, not to draw scientific conclusions.
Provenge has failed in both of its main studies--but it seems to help patients live longer.
The clinical trials tested the drug in a relatively small number of cases, with only 127 men in the main study who showed a benefit. But survival was extended four months for patients with metastatic prostate cancer. Statistical rules aside, Provenge fans say, survival is awfully hard to fake, and desperate metastatic prostate cancer patients who would get Provenge have only one drug, the chemotherapy Taxotere, at their disposal. The Taxotere drug, made by Sanofi-Aventis (nyse: SNY - news - people ), has many unpleasant and dangerous side effects.
The data has convinced some who were skeptical that Provenge may have merit. Philip Kantoff, a urological oncologist at Harvard Medical School and the Dana Farber Cancer Institute, is conducting a big clinical trial that should firmly establish whether and how much Provenge helps patients. He has consulted with Dendreon. For a long time, he was one of Provenge's doubters.
"I thought the concept was too simplistic for belief," Kantoff says. "I didn't think it had a snowball's chance in hell of working."
But the data showing the drug increases survival has made him cautiously optimistic. "I'm still skeptical, but I think there's something going on here," he says. His doubts rest mainly on the fact that results were small. "If this were a much larger study, to me this would be a slam dunk."
Kantoff says that if the drug were approved, he would probably prescribe it. So far Provenge seems mostly to cause flu-like symptoms, but FDA reviewers note there may also be an increased risk of stroke. If the medicine is fairly safe and might be effective, why not offer it to patients?
David Penson, a urologist at USC's Keck School of Medicine, has also gone from being a doubter to an investigator in a Provenge clinical trial and a consultant for Dendreon (he says he has received less than $10,000 in fees). "When they first released their data, they had to massage some data to show a clinical difference," he says. Dendreon's first study showed efficacy only in less-sick patients.
Colleagues convinced Penson to give Provenge a try in clinical trials, and he was impressed. He remembers one patient, a doctor, who went from being wasted and fatigued from his metastatic prostate cancer to being able to play golf again. Patients don't care if a drug meets the original primary endpoint of Dendreon's study, an improvement in X-rays, says Penson. "All they care about is living longer."
This is the argument at the heart of the case for Provenge. Neal Shore, medical director of the Carolina Research Center, says rejecting Provenge now would be "grossly unfair to the patients who have no other options but to enter clinical trials." Shore argues that "a lot of people will end up dying" before bigger clinical trials could show a benefit.
But there are other issues at play. Once a drug is approved, other medicines can get on the market by proving they are better. If an ineffective drug slips through, that could open the door to other less effective medicines. Another worry is that the benefit of Provenge might be real but less robust than it appears.
Because larger issues are at play, this is exactly the kind of situation in which the FDA might go against the decision of an advisory panel. Even if Dendreon has a great day on Thursday, the company won't be home free.
Cancer steps into limelight
In his recent book, When Illness Goes Public: Celebrity Patients and How We Look at Medicine, Barron Lerner describes how the National Enquirer "outed" actor Steve McQueen's diagnosis of terminal cancer in March 1980. McQueen didn't even want his close acquaintances and his children, ages 21 and 19, to know, let alone the public, Lerner writes.
Fast-forward to March 2007, when in a week's time two high-profile cancer patients, Elizabeth Edwards and Tony Snow, outed themselves.
"There's been an evolution in the public disclosure and very public sharing about cancer," says Richard Wender, the American Cancer Society's national volunteer president.
Sure, first ladies Betty Ford and Nancy Reagan were open about their breast cancer diagnoses in 1974 and 1987, respectively, but their cancers were curable.
On the other hand, Edwards, wife of Democratic presidential candidate John Edwards, and White House spokesman Snow have metastatic cancers, cancers that have spread beyond their original site.
Cancers that, like McQueen's, are likely to kill.
"That's something different," says Wender, chairman of family practice medicine at Thomas Jefferson University in Philadelphia. "It's hard to find a lot of examples of that" among high-profile people who have gone public about their cancer, he says.
"I'm not sure we can quite call it a sea change, but it did feel different, what Edwards did," Wender says. He noted her optimism in the face of incurable cancer, saying, in effect, "I'm probably going to die of this disease, but we're not going to change our life plans."
Even Snow, whose colon cancer has spread to his liver, talked about beating the disease.
Lerner calls their attitude "almost defiantly optimistic."
Optimism vs. denial
"I think it's adaptive," says Lerner, an associate professor of medicine and public health at Columbia University. "There's sort of a healthy denial that goes on among people who get a terminal cancer prognosis."
When his patients appear to be in denial, "I'm reluctant to call them on that," Lerner says. "You've got to let people have some optimism."
But, he says, there is a danger that celebrity patients' optimism about serious illness "is potentially giving misinformation."
For example, John Edwards described his wife's metastatic cancer as a chronic disease like diabetes, although some breast cancer experts and, Wender says, probably some patients cringed when they heard that comparison. Diabetics can live for decades with their disease — far longer than most women with breast cancer that has spread to the bone.
"The important message is the course is variable, and there are women who continue to battle breast cancer once it's metastatic for years," he says. "I hope Elizabeth Edwards is enormously successful, but that doesn't mean the next woman will have the same experience."
Edwards' and Snow's cases illustrate that, at least for some patients with metastatic disease, current therapies "have turned cancer from just being a quick fight that you win or lose into a longer battle that has setbacks and skirmishes and triumphs," Wender says.
In his book, Lerner notes that Lance Armstrong "is careful to state that beating cancer is not the same as beating opponents in a bike race." Surviving cancer "was more a matter of blind luck," Lerner quotes from Armstrong's 2001 book, It's Not About the Bike: My Journey Back to Life.
"If (Edwards) does better than average, her story will be told that she was optimistic and that she fought it," Lerner says. "And if she doesn't, she'll be lionized as someone who tried her hardest and had bad luck."
A chance to educate
Whether Edwards will become a celebrity spokeswoman for breast cancer remains to be seen. University of Michigan internist A. Mark Fendrick in 2003 co-authored a paper about the "Couric Effect" — the upswing in colonoscopies after Katie Couric had one on Today in 2000. Her husband, Jay Monahan, died of colon cancer at 42.
"We're hopeful that America's obsession with people in the media can somehow be turned in a way to improve public education and cancer prevention behaviors," Fendrick says.
Edwards has talked about mammograms on the campaign trail. At a campaign event in Davenport, Iowa, this month, an audience member asked whether Edwards had had regular mammograms, The Des Moines Register reported.
When she was diagnosed with a half-dollar-sized tumor in 2004, Edwards, then 55, said she hadn't had a screening mammogram since son Jack, then 4, was born. The cancer society recommends annual mammograms for women 40 and older.
Edwards told the Davenport audience that her cancer might not have spread if it had been detected earlier.
"The trickier thing will be if she gets worse, will she talk about hospice, advanced directives, that sort of thing?" Lerner says. "That would really be entering new ground."
Test shows promise in detecting prostate cancer
Researchers at the Johns Hopkins University School of Medicine are trying to develop a more reliable way to find prostate cancer. While experts say the new test is promising, they say it's too soon to know whether it really works better than older screening methods.
Experts note that the most commonly used screening test today — the PSA, which measures a protein called prostate-specific antigen in the blood — is far from perfect. The PSA doesn't find all cancers. It causes about 1.6 million American men to have needle biopsies each year, 80% of which are negative, says Robert Getzenberg, a Johns Hopkins professor. The American Cancer Society estimated that nearly 219,000 men will be diagnosed with prostate cancer this year and more than 27,000 will die from it.
That's why Getzenberg and other scientists are trying to improve cancer screening by searching for biomarkers — proteins in blood or urine that signal the presence of cancer. One potential new marker is early prostate cancer antigen, or EPCA-2. In a study released today from the April issue of Urology, Getzenberg says doctors may one day use this test to help men with high PSA results avoid unnecessary biopsies.
Using blood samples from 385 people, Getzenberg found that EPCA-2 correctly spotted 94% of prostate cancers. Previous studies have found that the PSA finds only about 80% of cancers. Just as important, he says, the new test produced false alarms in only 3% of patients. The new test was better than the PSA at helping to spot more advanced cancers. The EPCA-2 was 89% accurate in differentiating cancers inside the prostate gland from those that have spread beyond it; the PSA was 63% accurate.
Getzenberg notes that his results are still preliminary. He's collaborating with scientists at other universities to see if these results hold up over time. Scientists have yet to validate any of the dozens of potential new biomarkers found in recent years.
Ian Thompson, chairman of urology at the University of Texas Health Science Center in San Antonio, says he doubts the new test will replace the PSA. Instead, doctors likely will incorporate new biomarkers into a panel of tests that will help men gauge their risk of prostate cancer, says Thompson, who was not involved in the study.
Howard Parnes of the National Cancer Institute, who also was not involved in the Johns Hopkins study, notes that prostate screenings have not yet been shown to save lives. Finding more cancers could actually lead to "overdiagnosis" and "overtreatment," in which men are treated for slow-growing tumors that don't really need to be found. An ideal screening test, he says, would call attention only to lethal cancers.
Johns Hopkins and the University of Pittsburgh own the patent to the EPCA-2 test. They have licensed the test to Seattle-based Onconome Inc. Getzenberg, who has served as a consultant to Onconome, also is entitled to royalties from sales of the test, if it is approved. The study was financed by the NCI and Onconome.
Test improves prostate cancer diagnosis
U.S. researchers say an experimental blood test for prostate cancer may detect more tumors and reduce unnecessary biopsies.
In a study published in the April issue of the journal Urology, Johns Hopkins Hospital researchers said EPCA-2 testing is more accurate than the current PSA test in identifying cancer in the prostate.
The PSA test measures a protein normally produced by the prostate, while EPCA-2 detects a chemical primarily made in cancerous tissue, The Washington Post reported.
Robert H. Getzenberg -- professor of urology and director of research at the James Buchanan Brady Urological Institute at The Johns Hopkins University School of Medicine -- said PSA testing often erroneously highlights non-cancerous conditions and can miss some cases of cancer.
Getzenberg, lead author of the study, said approximately 1.6 million men undergo prostatic biopsies in the United States annually, and roughly 80 percent of them have negative results.
Johns Hopkins Hospital is working with Onconome Inc., a biomedical company based in Seattle, to bring the test to market within the next 18 months.
Wednesday, April 25, 2007
Phil Kessel back with Bruins after cancer battle
I love a good cancer comeback story -- like the story of Phil Kessel and his courageous return to the NHL.
Kessel, 19-year-old Bruins forward and fifth overall draft pick for 2006, was diagnosed with testicular cancer last month. He underwent surgery and has been recovering off the ice until just recently -- when he was recalled to Boston from its farm team in Providence.
It's back to life and back to work for Kessel -- who is winning his match against cancer.
Kessel, a Wisconsin native, was the second Boston athlete this year diagnosed with cancer. Red Sox pitcher Jon Lester was diagnosed in August with lymphoma.
Lottery winner succumbs to cancer
A man who won $1 million in the lottery shortly after finding out he had terminal cancer has died.
Wayne Schenk died Monday at the Veterans Administration Hospital in Syracuse, according to the Baird-Moore Funeral Home. He was 51.
"He is in a better place now. He was starting to suffer, and we didn't want that," friend Nick Pascazi told The Daily Messenger of Canandaigua.
On Jan. 12, Schenk won $1 million playing a $5 scratch-off ticket in the New York State Lottery's High Stakes Blackjack. Five weeks earlier, he had found out that he had less than a year to live because of inoperable lung cancer.
Schenk had tried to get the lottery to give him a lump sum so he could enter a hospital that specialized in treating advanced cancer. His prize pays out in $50,000 annual installments over 20 years.
Lottery officials said they were sympathetic but couldn't break the rules to give him a lump sum. He had received just $34,000 of his win by the time of his death.
In an interview with The Associated Press in January, Schenk said he was trying to take each day in stride.
"I haven't given up, but it's getting right down there where time is of the essence," he said. "There's only one way to go, and that's up. I've already been down."
Schenk was a lifelong smoker whose parents died of lung cancer in the 1990s. He served on a troop ship off Lebanon during a stint in the Army from 1976 to 1980. Last year, he bought a tavern after decades of working odd jobs in construction, in the highway department and at a ski resort.
On April 4, Mr. Schenk married his longtime partner, Joan DeClerck, who was with him when he died. About 15 people attended the small wedding, he said.
Pascazi said Schenk made plans to leave his winnings to Joan.
Racial gap in cancer death linked to social status
Black patients with colon cancer seem to fare just as well as their white counterparts after accounting for differences in socioeconomic status and the treatment received, according to a report in the journal Cancer.
"Few studies have addressed racial disparities in survival for colon cancer by adequately incorporating both treatment and socioeconomic factors, and the findings from those studies have been inconsistent," write Dr. Xianglin L. Du and colleagues from the University of Texas Health Science Center, Houston.
The researchers conducted an analysis of published data to determine the association between socioeconomic status and racial disparities in colon cancer survival. Of 66 articles reviewed, 56 were excluded, leaving 10 studies for the final analysis.
"All 10 studies provided estimates on racial disparities in survival for colon...cancer that adjusted for some measures of socioeconomic status, age and sex," the team found. However, only three studies adjusted for all the key variables -- socioeconomic status, treatment, the presence of other diseases, and the stage of cancer.
A total of 96,494 patients with colon cancer were included in the analysis. After accounting for socioeconomic factors and treatment differences, there was little difference in survival between black and white patients.
Du and colleagues conclude that survival differences are marginal once socioeconomic factors and treatment are taken into account.
"Attempts to modify treatment and socioeconomic factors with the objective of reducing racial disparities in health outcomes may have important clinical and public health implications," they point out.
SOURCE: Cancer, June 1, 2007.
Mouth rinse spots early head and neck cancer
Detecting head and neck cancer early, when the odds of successful treatment are best, may be as simple as gargling with saline and spitting in a cup, according to a study conducted by a Miami, Florida-based research team.
Oral rinsing flushes out a protein called CD44 -- a known biomarker for cancers of the head and neck. It also detects altered DNA related to these tumors. And the combination of these two biomarkers reliably detects head and neck tumors, the research shows.
Dr. Elizabeth J. Franzmann of the University of Miami's Sylvester Comprehensive Cancer Center reported her team's work at the annual American Association for Cancer Research meeting in Los Angeles.
"Cancer of the head and neck is a very debilitating and deadly disease that is often detected in late stages when cure rates are only about 30 percent," Franzmann told Reuters Health. "If we could catch it earlier, we should be able to cure it at least 80 percent of the time but we really need an early detection test."
The CD44 protein is involved in normal cell functions, but in cancer it is over expressed and appears in alternative forms that are also involved in tumor formation. Importantly, the protein and altered form can be found in bodily fluids.
"Initially, we found that if a patient swishes and gargles for 5 seconds each with saline and spits in a cup, we can actually measure the CD44 level; and it turned out that it was high in most of our head and neck cancer patients," Franzmann said.
The potential value of the oral rinse test was confirmed in a subsequent study of 102 head and neck cancer patients and 69 subjects with benign head and neck disease who were smokers and drinkers. "Head and neck cancer is primarily a disease of tobacco and alcohol users, although about 20 percent don't have any such history," Franzmann explained.
In this study, the oral rinse test detected two individuals with symptom-less cancer or precancer and it detected few "false positives" in the comparison group. Overall, "we found CD44 in spit in the head and neck cancer patients 62 percent of the time," Franzmann reported.
"We wondered whether some of the cancers were being missed because the CD44 gene can get turned off later on in the process of tumor formation. This turning off can be detected in the oral rinse."
"Sure enough, we found that in 9 out of 11 head and neck cancers with low CD44, the gene had been turned off," Franzmann said.
Looking at the two markers contained in the oral rinse distinguished head and neck cancer from benign disease almost 90 percent of the time, Franzmann. "And that's pretty good; it's similar to what the PSA test for prostate cancer does."
The mouth rinse test, Franzmann added, is simple enough to be administered at any community health center for individuals at high risk of head and neck cancer.
Teen Raises Money To Help Soldier Battling Cancer
A Jacksonville teenager moved by the story of a young Callahan soldier who is fighting cancer said she had to do something to help, and she did.
After serving two tours of duty in Iraq, where he survived several attacks, U.S. Army Sgt. Casey Watters is at home in Callahan with his family, battling a rare form of cancer that doctors found after he was wounded in Iraq.
Since the diagnosis, Watters and his family have been fighting an uphill battle that's not only physical but also mental and financial.
Rachel Fallin, a 17-year-old from the Arlington area, said she was brought to tears when she first heard Watters' story.
"When I saw his story and started crying, I was like, 'I have to do something,'" Fallin said.
She said she did all she could to raise money for the Army sergeant, and on Monday she met him for the first time.
"I think it's wonderful because she's reaching out to people she doesn't even know, and that's something special to me," said the teen's mother, Christy Fallin.
Fallin said she was amazed at the support she received to help the family in need.
"It's just been great. People have been really supportive and giving to me so I can give to them," she said.
"I just can't say enough. This is awesome. You guys took care of us, and you took initiative by yourself. You don't see that a lot," Watters said to the teen.
The two said Monday's meeting is not going to be the last -- Fallin and Watters said they would stay in contact with each other as long as they could.
Next week, Watters is going to visit Fallin's school and talk with the kids who helped raise the donated money.
Abortion does not raise breast cancer risk
Abortion and miscarriage do not raise the risk of breast cancer, according to a study published Monday by the US National Cancer Institute in the Archives of Internal Medicine.
The 10-year study, performed on a sample of 105,716 US participants, rejects prior studies that suggested a link between prematurely terminated pregnancies and breast cancer.
The subjects were nurses aged 29-46 at the start of the study. They answered questions every two years via anonymous questionnaire about their medical history, including whether they had abortions, miscarriages and breast cancer.
"Among this predominantly pre-menopausal population, neither induced nor spontaneous abortion was associated with the incidence of breast cancer," said the study's authors from Brigham and Women's hospital and Harvard Medical School in the northeastern state of Massachusetts.
The data provides "further evidence of a lack of an important overall association between induced or spontaneous abortions and risk of breast cancer."
"We found no association between induced abortion and breast cancer incidence and a suggestion of an inverse association between spontaneous abortion (miscarriage) and breast cancer during 10 years of follow up," the study said.
However, the inverse relationship -- women who had a miscarriage before age 20 showed a reduced risk of breast cancer -- was found in a small sampling of women and "thus, chance has to be considered as a possible explanation."
The conclusions of the study were similar to those of a 2003 panel convened by the National Cancer Institute which found no evidence linking abortion or miscarriage to higher breast cancer rates.
Women who binge drink face increased breast cancer risk
Boffins are warning that women who go on a drinking spree and guzzle the equivalent of roughly two bottles of wine over a weekend more than double their risk developing breast cancer.
The study, of 17,647 nurses, was conducted by researchers at the Centre for Alcohol Research in Denmark. The study was led by Dr Lina Morch.
The researchers found that women, who downed 22-27 drinks a week as compared with those who drank one to three drinks, faced an increased risk of breast cancer.
Women in the study were aged over 44, and most drank a moderate amount of alcohol, with more than a quarter drinking more than the recommended 14 drinks a week.
The boffins noted that each additional drink consumed increased the risk of breast cancer by 2 percent. But this doubled at weekends, which is the time that women usually let their hair down and go on a binge.
While women who consumed excessive drinks on just one day during the week increased their risk of breast cancer by 55 percent, drinking 22-27 drinks over the course of the week was linked to a 130 percent increased risk.
"What our study suggests is that the total amount of alcohol consumed has a detrimental effect on the risk of breast cancer, but also the drinking pattern seems to have an impact on the risk," the BBC quoted Dr Lina Morch, as saying.
"When more drinks are consumed within a limited time frame the concentration of alcohol in the blood peaks, which we suppose is more harmful than when the same amount of alcohol is consumed over longer time periods," she added.
A drink was classed as a bottle of beer or a glass of wine or spirit, which in Denmark is roughly 12g of alcohol.
One in 10 women in the study were week-day binge drinkers, having more than four drinks a day and 13 percent were weekend binge drinkers, defined as more than 10 drinks between Friday and Sunday.
The findings are reported the European Journal of Public Health.
Tuesday, April 24, 2007
Can aspirin prevent cancer? Jury's out
The research could give you whiplash: Aspirin prevents cancer, one study says. Oops, maybe not, says another. Now comes word that aspirin may fend off cancer only if people take much more than is used to fight heart disease, suggesting some of the earlier back-and-forth may have been due to confusion over the right dose.
Even that evidence is circumstantial, offering no end to the competing headlines.
"A general perspective that people have is, 'Why is it so difficult to get a clear answer on a pill that costs a few pennies and is available over-the-counter and taken by millions of people?'" says the
American Cancer Society's Dr. Michael Thun, a coauthor of the newest study.
For decades, scientists have chased the hope that aspirin could be an easy way to prevent certain cancers. The idea: Aspirin fights inflammation, and thus pain, by inhibiting substances known as cyclooxygenase, or COX, enzymes. COX enzymes also are involved in the formation of certain kinds of tumors, such as colorectal, prostate and breast cancers.
Aspirin does something else, as well: It makes blood less likely to form clots, giving it an important role in fighting heart disease. A daily baby aspirin — 81 milligrams — is recommended for people with cardiovascular disease or who are at high risk for it.
In contrast, connecting the cancer dots — showing that reducing COX would in turn reduce tumors — is vexing. And because aspirin can cause stomach ulcers and bleeding, firm proof of an anticancer benefit is a must before any health group will recommend using it for that reason.
The hints of that benefit are tantalizing.
"Aspirin and cancer's not going to go away, and there's great value in figuring out how to use it," says Dr. Phillip Febbo, an oncologist at Duke University Medical Center who is closely following the research.
Aspirin and similar anti-inflammatory drugs reduce the risk of many cancers when tested in animals bred to develop human-like tumors. Evidence in people isn't nearly so clear-cut.
In so-called observational studies, people who say they regularly use aspirin seem at lower risk of colorectal cancer in particular, and also prostate, breast and a few other cancers. However, people who take aspirin on their own may be healthier than the general population and thus at lower risk of cancer anyway.
Some more rigorous trials randomly assigned people at high risk of colon cancer to use aspirin, and found those who did developed fewer precancerous growths called polyps — but stopped short of showing the drug really prevented cancer, Thun explains. More disappointing news came in 2005, when a major study that assigned women to use either a baby aspirin or dummy pills found no effect on a whole list of cancers.
Thun and colleagues at the cancer society wondered if many of those earlier studies used too low a dose of aspirin to have an anticancer effect. So they examined adult-strength aspirin — 325 mg or more — in a study tracking more than 140,000 people.
Taking an adult-strength aspirin daily for at least five years was associated with a 30 percent lower risk of colorectal cancer, a 20 percent lower risk of prostate cancer, and 15 percent less cancer overall, they reported last week in the Journal of the
National Cancer Institute.
That's not proof of aspirin's benefit, either, but it does suggest that clinical trials start looking at higher doses to tease out an answer.
Duke's Febbo says answers also may come from improved testing of the COX enzyme's role in individual tumors. As with other tumor stimulators, there may be subsets of people for whom COX is a big cancer factor, and others where COX, and thus aspirin, won't matter.
Until then, what's the average person to do? Neither the cancer society nor a government committee that sets health guidelines recommends aspirin to prevent cancer, even for those at high risk of colorectal cancer. Consult a doctor first if you're considering it anyway, Thun stresses — aspirin can be dangerous if someone bleeds easily or has certain other conditions.
For now, cancer specialists quote their cardiac colleagues' advice.
"Stick with what's heart-healthy," says Febbo. And stay tuned: "There's a lot of potential for aspirin" and cancer.
CT imaging cost-effective for colorectal cancer
Computed tomography (CT) imaging of the colon may be the most cost-effective option for colorectal cancer screening, according to a report in the online issue of Cancer.
"CT colonography, when properly implemented, is not only a clinically effective screening test, it is also a much safer and more cost-effective approach than subjecting all healthy adults to invasive colonoscopy," Dr. Perry J. Pickhardt told Reuters Health.
Colonoscopy, the most accurate test for colorectal cancer detection currently used, involves insertion of a tube, or "endoscope," through the colon while the patient is sedated. A small camera visualizes any polyps, which are snared and removed for microscopic evaluation.
Pickhardt from the University of Wisconsin Medical School, Madison, and associates used a mathematical model to evaluate the clinical and economic impact of CT colonography compared with two tests currently used for colorectal cancer.
CT colonography, colonoscopy, and flexible sigmoidoscopy -- were all cost-effective compared with no screening, the authors report, each costing less than $10,000 per additional year of life gained. Flexible sigmoidoscopy, a procedure performed in a physician's office, also uses a scope to identify potentially cancerous growths, but doesn't extend as far into the colon as colonoscopy.
CT colonography was the least expensive at $7,138 per year of life gained, the results indicate, followed by flexible sigmoidoscopy at $7,407 and colonoscopy at $9,180 per year of life gained. CT colonography was even less expensive when only polyps larger than 6 millimeters were removed, at $4,361 per year of life gained, the researchers note.
Removal of polyps smaller than 6 millimeters "appears to carry an unjustified burden of costs and complications relative to the minimal gain in clinical efficacy," they add.
"I believe that CT colonography will be a recommended front-line screening option (alongside optical colonoscopy) within the year," Pickhardt said.
"It is critical to remember that no single screening test will appeal to all individuals," he added. "Providing more effective options should improve overall screening compliance for this deadly yet readily preventable disease."
SOURCE: Cancer, April 23, 2007.
'Skypad' cancer unit to be built
A turf-cutting ceremony will mark the start of work on the 10-bed facility at Cardiff's University Hospital of Wales.
The Teenage Cancer Trust, which is behind the plans, said it will enable patients of similar ages to support each other through the same experience.
It said treatment on such a ward can improve survival chances by up to 15%.
Young patients from across Wales will be treated at the futuristic-looking building, which will be built on stilts between the adult and paediatric oncology centre.
It will include computers, TVs and game consoles to keep teenagers occupied during long stays in hospital, as well as facilities to allow relatives to stay close by over night.
The Teenage Cancer Trust (TCT) has specialist teenage units at seven hospitals in England but this is its first in Wales and is expected to be finished and opened in 2008.
An appeal was launched by the charity in 2004 to raise money towards construction costs and will continue until the project is completed.
"We are working to provide better services for Welsh teenagers with cancer, closer to where they live" said Simon Davies, chief executive officer of the Teenage Cancer Trust.
"This is our most ambitious project to date and will be a beacon for future TCT services".
Christian Evelyn, who was diagnosed with acute lymphoblastic leukaemia aged 16, said he would have appreciated thefacility during his treatment as he had been bored during long hospital admissions and never met patients of his age.
The 18-year-old is now in remission and, by coincidence, working for Cowlins, the contractor for the unit in Cardiff.
He said: "I know that this job will be a real eye-opener for my colleagues and one that we will take extra pride in.
"I am so glad we can actually help create this special ward for teenagers to make a very difficult time in their life that little bit easier."
Teenagers with cancer need specific care due to the rarity of the tumours they get and the type of psychological and social problems they face, according to Heidi Traunecker, a consultant paediatric oncologist at the University Hospital of Wales.
She said: "Their lives are changing - they are moving from education to the world of work and they have cancer on top of that.
"It can be a very difficult time for them, but this unit will really make a difference by catering for their specific needs in a purpose built environment."
No Link Between Abortion, Miscarriage and Breast Cancer
either induced abortion nor miscarriage appears to influence breast cancer risk in premenopausal women, a new U.S. study concludes.
"In this cohort study of young women, we found no association between induced abortion and breast cancer incidence and a suggestion of an inverse association between spontaneous abortion (miscarriage) and breast cancer incidence during 10 years of follow-up," says a team from Brigham and Women's Hospital, Harvard Medical School and the Harvard School of Public Health, Boston.
They reported their findings in the April 23 issue of the Archives of Internal Medicine.
The researchers examined data on almost 106,000 women who took part in the Nurses' Health Study II, which began in 1993. The women were ages 29 to 46 at the start of the study.
Among the women, more than 16,000 reported having had an induced abortion at some point in their lives and almost 22,000 reported having had a miscarriage. Between 1993 and 2003, there were 1,458 new cases of breast cancer diagnosed among the women.
They found no link between abortion, miscarriage and breast cancer generally. However, "we observed associations in two subgroups, an association between induced abortion and progesterone receptor-negative breast cancer (cancer that does not respond to the hormone progesterone) and an inverse association between spontaneous abortion before the age of 20 years and breast cancer incidence."
The researchers noted that these secondary analyses were based on small numbers of women, however. "No obvious mechanisms can be provided for these subgroup findings; thus, chance has to be considered as a possible explanation," they wrote.
Abortion doesn't boost breast cancer risk, large study finds
An abortion or a miscarriage does not increase a woman's risk of breast cancer, according to results released Monday from a decade-long study of more than 100,000 women.
The findings are the latest, and perhaps most convincing, in a series of studies that have discredited a concern cited by antiabortion activists to dissuade women from having the procedure.
"It's important for women to have the facts," said Karin B. Michels of Brigham and Women's Hospital in Boston. Michels is lead author of the study.
She said her group's study was "very much in line" with a 2003 expert panel convened by the National Cancer Institute that concluded no evidence supported a link between abortion and breast cancer. The institute funded Michels' study as well.
Karen Malec, president of the Coalition on Abortion/Breast Cancer, took issue with the findings. Her group uses the purported link as an argument against abortion.
"Clearly [the cancer institute] must suspect a link, or else they know that a link really exists," Malec said. "Why else would they continue to pay for these studies?"
Texas, Minnesota and Mississippi require physicians to warn women seeking an abortion about the supposed cancer risk. Several other states considered similar laws but rejected them in light of the 2003 consensus report.
The new results, reported in the Archives of Internal Medicine, are from an arm of the Nurses' Health Study that involved 105,716 women.
Beginning in 1993, Michels and her colleagues biennially questioned the women — who were ages 29 to 46 in 1993 — about abortions, miscarriages and breast cancer.
They found that through 2003, a total of 16,118 had had at least one induced abortion and 21,753 had had at least one spontaneous abortion (miscarriage). The team found 1,458 new cases of breast cancer — an incidence that was the same among women who had had an abortion (induced or spontaneous) and those who had not.
The design of the study, Michels said, was much more reliable than previous studies, which started with women who'd had breast cancer and asked them if they had undergone an abortion. Such studies introduce "recall bias," she said, because women with breast cancer are more likely to acknowledge an abortion, thinking it might be related to their condition.
"There will always be some underreporting of abortion [among healthy women] because it is such a sensitive issue," she said.
Malec criticized the design of the study, which allowed reports of abortions that had occurred through 2003. Malec said that would tend to "dilute" cancer links because cancer in those women would not have had time to develop. "That's like asking, 'If you smoke cigarettes today, would you develop lung cancer tomorrow?' " she said.
Michels said 90% of the abortions and miscarriages reported in the study occurred before 1993.
Melanoma in kids differs from the adult cancer
The demographics, site of appearance, and outcome of children and teenagers with melanoma differ from the features seen in young adults, according to study findings published in the Journal of Clinical Oncology.
The results suggest melanoma may be biologically different in children and adolescents.
"Melanoma is uncommon in teenagers and rare in younger children," Dr. Julie R. Lange, of Johns Hopkins Medicine, Baltimore, Maryland, and colleagues write. However, differences in this cancer between children and adults are not well understood.
Using the National Cancer Data Base, the researchers compared melanoma cases of children and teenagers who were between 1 and 19 years old with those for patients between 20 and 24 years.
Among the 3,158 children and teenagers, 96.3 percent had melanoma of the skin, the most common site; 3.0 percent had melanoma of the eye; and 0.7 percent had an unknown primary site. Skin melanoma was more common in girls (55 percent) than in boys, and in subjects older than 10 years (90.5 percent).
The authors detected a relationship between the demographics, the site of skin melanomas and age. Younger patients were significantly more likely to be male and nonwhite, to have primary tumors of the head and neck, and to have regional or distant cancer spread.
The patients were followed-up for an average of 59 months. An association was observed between poorer survival and more extensive disease progression and younger age. "Females had significantly better overall survival than males, except in patients aged 1 to 9 years," the investigators found.
Patients between 20 and 24 years with thinner melanomas had significantly better survival rates (96.8 percent) than patients with thicker tumors (82.4 percent)," Lange's team reports. However, within the younger group, survival rates were not significantly different between the thinner and thicker tumors.
The lack of prognostic value of tumor thickness in the young group suggests biologic differences, even more than does the demographic differences compared to the older patients, Dr. Lange and colleagues point out. "More research in the molecular genetics of pediatric melanoma is needed," they conclude.
SOURCE: Journal of Clinical Oncology, April 2007.
Monday, April 23, 2007
Asia's Cancer Rate May Pose Threat to Economic Growth
Asia's cancer rate may jump by almost 60 percent to 7.1 million new cases a year by 2020, straining the region's ill-prepared health systems, said Richard Horton, editor of the British medical journal Lancet.
Aging populations, tobacco use and increasing rates of obesity are fueling the incidence of deadly tumors in Asian patients too poor to afford the most advanced treatments including Herceptin and Avastin, sold by Roche Holding AG, the drugmaker based in Basel, Switzerland, Horton said April 21 at an international cancer meeting in Singapore.
Asia's prevalence of cancer deaths may climb 45 percent to 163 per 100,000 people by 2030 from about 112 per 100,000 in 2005, according to the World Health Organization. At that rate it would overtake the Americas, where cancer-related mortalities are expected to rise to 156 per 100,000 from 136 over the same period. Europe, which has the highest prevalence at 215 per 100,000, may increase about 9 percent to 234 per 100,000.
``There really is going to be an incredible pandemic of cancer like we've not seen -- we couldn't have imagined it -- over the next 20 years,'' Horton said in an interview in Singapore, where he spoke at the Lancet Asia Medical Forum. ``We barely have the health systems to handle infectious diseases, so how on earth are we going to deal with this?''
Cancer already kills more people worldwide than AIDS, tuberculosis and malaria combined. Spending to prevent and treat chronic diseases such as cancer and diabetes may slow the expansion of China and India, the world's two fastest-growing major economies, researchers said at the meeting in Singapore.
`A Fortune'
``It is going to cost them a fortune in terms of health care expenditure,'' Horton said, adding that it will ``eliminate a huge number of people from the labor market. We think AIDS is a disaster to the world now. You have seen nothing yet.''
It costs close to $50,000 in Great Britain to treat a breast cancer patient using Herceptin, which generated $3.2 billion in sales last year for Roche and its partner South San Francisco, California-based Genentech Inc. In comparison, per capita government expenditure on health was $4 in Bangladesh, $7 in India, $11 in Indonesia and $22 in China in 2003, according to data compiled by the WHO.
Asia accounted for about half the 7 million cancer deaths worldwide in 2002, with 23 percent in China alone, D. Maxwell Parkin, a visiting research fellow at the University of Oxford's clinical trial service unit, told the two-day forum.
Health Insurance
``Historically in developing countries, people died before they could get cancer,'' said You-Lin Qiao, a professor of cancer epidemiology at the Chinese Academy of Medical Sciences in Beijing. ``Now they are living longer, we're seeing more cancer'' and degenerative diseases of the brain, he said.
The majority of China's rural dwellers don't have health insurance, Qiao said in an interview. The cost of treatment, therefore, is borne by the entire family.
Attacks on China's medical personnel almost doubled last year to 9.83 million cases, with 5,519 staff injured, causing 200 million yuan ($26 million) in costs, the official Xinhua News Agency reported last week, citing Vice Minister of Health Chen Xiaohong.
The violence reflects the growing frustration in China over a health system struggling to provide affordable medical care, said Tony Mok, professor of clinical oncology in Hong Kong's Prince of Wales Hospital, who consults in the southern Chinese city of Guangzhou.
Doctor Shortage
``The doctor treats the patient,'' Mok said. ``The family thinks it is going to work. They get all their money, sell their cow, sell their house, and then the patient dies. They get very angry.''
About 1.1 million doctors and nurses are urgently needed in Southeast Asia alone, where shortages of health-care workers exist in six of the region's 11 countries, according to the WHO's 2006 World Health Report. Developing countries make up 85 percent of the world's population, but have a third of the world's radiotherapy machines, which are used to treat cancer.
``If nothing happens, there will be a disaster,'' said Franco Cavalli, president of the Geneva-based International Union Against Cancer. ``For the time being, governments don't realize, or do not want to realize, that this is a bomb which is going to explode.''
Developing nations in Asia have little access to anti- cancer drugs now, with the U.S., Europe and Japan absorbing 95 percent of the global supply, Cavalli said.
`Westernization' of Diets
Lung cancer, Asia's biggest cancer-killer and driven by tobacco-smoking, may increase 42 percent to almost 1 million deaths a year between 2005 and 2015, the Geneva-based agency reports. Stomach cancer, the second-biggest type of the disease in Asia, may grow 25 percent to 1.2 million deaths a year over the same period, the WHO says.
Still the ``Westernization'' of Asian diets, including rising consumption of alcohol and red meat, is causing higher rates of breast, colon and rectum cancer, Oxford's Parkin said.
Pursuing sophisticated drugs and technologies for treating cancer patients ``is incredibly high-cost and probably beyond the bounds of most countries'' in Asia, the Lancet's Horton said. Instead, priority should be given to a campaign to stop smoking, increase exercise and consumption of fruit and vegetables, prevent obesity and reduce salt.
``These seem simple things, but they would eradicate a vast proportion of the potential cancer burden,'' he said.
