THURSDAY, Jan. 24 (HealthDay News) -- Researchers say they have zeroed in on a biomarker that could detect colorectal cancer in its earliest stages in a simpler, less invasive and more accurate way than existing blood tests.

The marker, called colon cancer-specific antigen-2 (CCSA-2), could also differentiate between early- and late-stage disease, the researchers added.

The study was one of several concerning colon cancer being presented at the annual Gastrointestinal Cancers Symposium being held Jan. 25 to 27 in Orlando, Fla.

A second study found that patients who are uninsured or who have coverage with Medicaid tend to be diagnosed with colorectal cancer at a later stage than individuals with private insurance or Medicare. This is the first nationwide survey to confirm similar findings from smaller polls.

And a third study is a step on the road to so-called personalized medicine. "This study assesses the benefit of treatment with a monoclonal antibody for colorectal cancer patients based on their tumor's molecular signature," Dr. Nicholas Petrelli, an official with the symposium, said during a Wednesday teleconference on the findings.

According to the American Cancer Society, colorectal cancer is the third most common cancer among American men and women. Some 150,000 new cases are diagnosed each year in the United States.

Regular screening can catch the disease while it is still curable. Colon cancer can also be prevented if polyps and adenomas are found and removed before they become malignant.

There are already blood tests for colorectal cancer, but they result in false-positives in 60 percent to 90 percent of cases, depending on the test, said the authors of the first study.

The researchers, from Johns Hopkins University and the University of Pittsburgh, looked at 135 blood samples from individuals who had undergone colonoscopies. They were compared with samples from individuals with other types of cancer or with benign diseases.

Only about 20 percent of results were false positives, while only 9 percent of cancers went undetected.

There was also a correlation between the level of CCSA-2 in the blood and the size of the growth. The highest levels of CCSA-2 indicated the presence of actual cancer. The study was funded by Onconome, which has licensed the patent for the test from the University of Pittsburgh researchers.

The second study, conducted by the American Cancer Society, found that patients without health insurance were almost two times more likely and Medicaid patients 40 percent more likely to be diagnosed with stage II colon cancer rather than stage I disease, compared to those with Medicare or private insurance.

And again, uninsured patients were twice as likely while Medicaid patients were 50 percent more likely to be diagnosed with stage III or IV colon cancer than patients in the other insurance categories. The results held steady no matter where the cancer was found.

Minorities, females, older patients, those who lived in areas with low-income and low-education levels and those who were treated at non-research teaching hospitals were more likely to be diagnosed with advanced cancer.

"Improved access to screening and medical care in these populations may be able to reduce these disparities," said study author Dr. Michael Halpern, strategic director of health services research at the American Cancer Society.

And the third study confirmed that only patients who have a normal form of the KRAS gene in their tumors will benefit from the monoclonal antibody Vectibix (panitumumab). Mutations are found in 30 percent to 50 percent of colorectal cancer patients. The study was funded by Amgen, which makes the drug.

More information

Visit People Living With Cancer   for more on colorectal cancer.

TUESDAY, Jan. 22 (HealthDay News) -- Drinking alcohol doesn't seem to boost a woman's risk of ovarian cancer, while caffeine may help protect against the disease, a new study found.

In the same study, smoking cigarettes wasn't linked with an increase in the most common types of ovarian cancer but was associated with an increase in a rare subtype of the disease.

It's too soon to recommend drinking caffeine to lower ovarian cancer risk, said study senior author Shelley S. Tworoger, an assistant professor of medicine and epidemiology at Harvard Medical School and the Harvard School of Public Health.

"The results do need to be confirmed in other studies," Tworoger said. The lack of risk for alcohol and smoking has been found in other research, she added.

For the study, Tworoger and her colleagues looked at data from questionnaires in the Nurses' Health Study, which includes 121,701 U.S. female registered nurses. The study began in 1976, with women then aged 30 to 35 completing questionnaires, then replying every two years to update the data.

Tworoger's team looked at the association between smoking and ovarian cancer risk among 110,454 of the women, and the association between alcohol and caffeine and ovarian cancer risk among 80,253 women, all followed from 1976 to 2004. For the smoking analysis, the researchers found 737 confirmed cases of epithelial ovarian cancer, the most common type of ovarian cancer. For the diet analysis, they found 507 women with epithelial ovarian cancer.

No association was apparent for drinking alcohol and ovarian cancer, or for smoking, with one exception. "It [smoking] does appear to increase the incidence of a rare type, mucinous ovarian tumors," she said, a subtype of epithelial ovarian cancer.

However, the researchers found an "inverse trend" for total caffeine intake and caffeinated coffee consumption and ovarian cancer, but the individual risk reductions didn't reach statistical significance.

The association for caffeine was strongest if the women had never used either birth control pills or hormones after menopause, Tworoger said. Why caffeine may be protective isn't certain, she said, but its consumption may lower estrogen levels, at least in postmenopausal women.

The study findings are published in the March 1 issue of Cancer.

Sherry Salway Black, executive director of the Ovarian Cancer National Alliance and an ovarian cancer survivor, agreed it's too early to recommend caffeine as a risk-lowering strategy.

Tworoger said her team plans to further study the caffeine-ovarian cancer link.

For now, she advised: "Always talk to your doctor before you make any huge lifestyle changes." And keep the risks in perspective, she added. "Because ovarian cancer is relatively rare, women should talk to their doctor first about the risk of getting ovarian cancer."

Black agreed, adding: "Know the symptoms of ovarian cancer. Know your family history and your risk and talk with your health-care provider." Get advice about what to do, she said, especially if you have a higher-than-average risk.

About 22,430 new cases of ovarian cancer were found in the United States in 2007, according to the American Cancer Society, and about 15,280 women died of the disease that year. Ovarian cancer is the eighth most common cancer in women -- not counting skin cancer -- and it's the fifth-leading cause of cancer death in women.

Symptoms include bloating, pelvic or abdominal pain, urinary frequency and difficulty eating or feeling full quickly.

In another study published this week, caffeine was found to increase the risk of miscarriage. Kaiser Permanente researchers in California looked at 1,063 pregnant members of the HMO and found those who drank 200 milligrams or more of caffeine a day -- about two or more cups of coffee or five 12-ounce sodas -- had twice the miscarriage risk of those who avoided caffeine entirely. Even smaller amounts increased risk, with women drinking less than 200 milligrams of caffeine a day showing more than a 40 percent increased risk of miscarriage, compared to those who took in no caffeine.

The study was published online in the January issue of the American Journal of Obstetrics and Gynecology.

More information

To learn more about ovarian cancer symptoms, visit the Ovarian Cancer National Alliance  .

TUESDAY, Jan. 22 (HealthDay News) -- A drug that prolongs the lives of patients with kidney or liver cancer also increases the risk of developing high blood pressure.

Patients taking Nexavar (sorafenib) need to be carefully monitored and treated, said the authors of a study appearing in the Jan. 22 online issue of Lancet Oncology.

Nexavar is an anti-angiogenesis drug, meaning it fights cancer by cutting off a tumor's blood supply.

It was approved in 2005 to treat advanced kidney cancer and in 2007 to treat the most common form of liver cancer that can't be surgically removed (unresectable hepatocellular carcinoma or HCC).

In clinical testing, Nexavar improved overall survival by 44 percent among people with HCC. Median overall survival was 10.7 months among those treated with the drug, versus 7.9 months among those who took a placebo. This was considered a major inroad against one of the most voracious cancers.

Nexavar is also being assessed to treat small-cell lung cancer, prostate cancer and melanoma.

Earlier trials, however, had shown a 16 percent to 42.6 percent incidence of hypertension in patients taking the drug. If not properly controlled, hypertension can lead to strokes and heart attacks, as well as kidney failure.

For this paper, researchers at the State University of New York Stony Brook conducted a meta-analysis of published clinical trials on Nexavar.

In all, nine studies involving 4,599 patients published between January 2006 and July 2007 were analyzed.

There was a 23.4 percent incidence of all-grade hypertension, and a 5.7 percent incidence of high-grade hypertension.

This is not the first time hypertension has been associated with an angiogenesis inhibitor. Several other drugs in this category, including Avastin (bevacizumab) and Sutent (sunitinib), have also raised blood pressure in patients.

More information

Visit the American Cancer Society   for more on liver cancer.

THURSDAY, Jan. 17 (HealthDay News) -- By studying blood cells in a young pair of twins, scientists say they're gaining new insight into how some children are poised to develop leukemia even before birth.

The researchers report in a new study that both twins -- one who developed leukemia and one who didn't -- shared cells that mutated and became precancerous. In one of the twins, the cancer-ready cells developed enough mutations to sicken the child.

The findings are a "first look at the earliest events in the process that ultimately leads to leukemia," said study co-author Tariq Enver, a professor at John Radcliffe Hospital in Oxford, England.

According to Enver, the next step is to figure out how to use this knowledge to help scientists do a better job of targeting specific leukemia cells with "smart" drugs.

Leukemias can affect both children and adults. An estimated 44,240 cases of the disease were diagnosed in the United States in 2007, according to The Leukemia & Lymphoma Society.

Fortunately, the death rate from leukemia for children has fallen drastically over the past 30 years, although several hundred still die of the disease in the United States each year. The society estimates that 21,790 Americans died of the disease in 2007.

In the new study, published in the Jan. 18 issue of the journal Science, Enver and colleagues in the United Kingdom, Japan and Italy looked at cells in the blood of identical female twins. One developed leukemia at the age of 2, while the other remained healthy.

At issue: Before birth, did the twins share a certain type of cell that became cancerous in one twin but not in the other? The answer, the study found, is yes.

According to Enver, both twins ended up with precancerous cells, which they shared in the uterus by both getting blood from the same placenta. Somehow, further mutations made the precancerous cells become cancerous in the twin who became ill.

Dr. Bart Kamen, chief medical officer of The Leukemia & Lymphoma Society, lauded the study as a "remarkable paper" that provides a new perspective on how leukemia develops. Essentially, he said, the study suggests that the precancerous cells don't always cause cancer but can do so under a specific condition -- that is, if they mutate beyond the initial aberration that made them dangerous in the first place.

As for the implications for treatment, the research suggests that "even if we killed the leukemia by killing the cells that are malignant, this one [cell type] might still be there. Maybe we didn't kill it," Kamen said.

But if scientists can figure out where the precancerous cells are, they can try to destroy them as well, he said.

Evers said the research could allow scientists to figure out which specific cells need to be targeted by drugs and allow doctors to monitor whether a treatment is working properly.

More information:

There's more on leukemia at The Leukemia & Lymphoma Society  .