Two new studies of colon cancer treatment add to a growing body of knowledge regarding racial disparities in cancer care. The first report found that 11 percent fewer black than white patients received adjuvant chemotherapy after surgery. The second concluded that non-English-speaking patients were less satisfied with their care than English-speaking patients.
The first study, published in the August 17 Journal of the National Cancer Institute (JNCI), examined Medicare records from 5,294 people diagnosed with stage III colon cancer between 1992 and 1996. By studying diagnosis and treatment codes, the researchers found that 70 percent of white patients received adjuvant chemotherapy, compared with 59 percent of black patients. The disparity was highest among patients aged 66 to 70. The authors, from the University of Washington, write that the trend is "worrisome because these 'young' elderly are most likely to derive a survival benefit from chemotherapy."
By integrating Medicare data with information from NCI's Surveillance, Epidemiology, and End Results database, the researchers were able to calculate the impact of many factors, including physician experience, hospital environment, and the sociodemographics of each patient's neighborhood. However, the study "showed no single or simple explanation."
The second report was published online August 22 in the Journal of Clinical Oncology by investigators at the Harvard Medical School, California Cancer Registry, and Northern California Cancer Center. The survey of 1,067 colorectal cancer patients found that non-white and non-English-speaking patients reported significantly more problems with cancer care than white and English-speaking patients. Only 52 percent of non-English speaking patients rated overall quality of cancer care as very good or excellent, compared with 81 percent of English-speaking patients. Much of the dissatisfaction among non-English-speaking patients appeared to stem from concerns about coordination of care among the nurses, physicians, and other health care providers encountered. An accompanying editorial suggests that communication and coordination of care present the greatest opportunity to raise the bar on overall cancer care quality.
A phase II clinical trial has found that some lymphoma patients may have benefited from an experimental cancer vaccine and the novel dose-adjusted EPOCH chemotherapy regimen with the drug rituximab. Although 80 percent of the patients eventually relapsed after the treatments, they lived longer on average than others with mantle cell lymphoma. After nearly 4 years, 89 percent of the patients were alive; typically, half the patients with this disease die within 3 years.
It is not clear whether the vaccine or some combination of the treatments were responsible for the prolonged survival. But the study, which included 26 patients, demonstrates that a vaccine can stimulate the body's T cells to attack the mutant B cells responsible for the lymphoma. This was true despite the fact that rituximab had eradicated the healthy B cells in these patients along with the mutant B cells.
"This study shows that healthy B cells were not necessary for generating a T-cell response, and the role of these cells in generating a T-cell response has not been known in humans," says Dr. Wyndham Wilson of NCI's CCR. He co-led the study along with Dr. Larry Kwak of the University of Texas M. D. Anderson Cancer Center.
The researchers made "personalized" vaccines for each patient based on a unique protein found on the surfaces of a patient's mutant B cells. The results, published in the August 21 Nature Medicine, suggest that additional doses of the vaccine should be administered for longer periods of time to achieve an optimal immune response.
"We're now trying to make the vaccine formulation more potent, and we're also investigating a universal vaccine that might be effective in every lymphoma patient," says Dr. Sattva Neelapu of M.D. Anderson and the first author of the study.
A British cohort study has found that men with Klinefelter syndrome suffer higher rates of lung cancer, breast cancer, and non-Hodgkin's lymphoma. Klinefelter syndrome is a genetic disorder caused by an excess number of X chromosomes in men.
The study examined the medical histories of 3,518 men diagnosed with Klinefelter syndrome and followed each for an average of 15.1 years; the longest follow-up was 44 years. When compared with the general population, the men's overall mortality from cancer was not significantly elevated. However, mortality from lung cancer, breast cancer, and non-Hodgkin's lymphoma was significantly higher (absolute excess risks were 23.7, 9.3, and 12.1, respectively). However, mortality from prostate cancer among the participants was significantly decreased. As found in similar studies, there was a modest association between Klinefelter syndrome and leukemia.
The report, published in the August 17 JNCI, warns that several limitations should be considered when interpreting the data. The vast majority of Klinefelter syndrome cases go undiagnosed, the research team noted, and many were only detected after a diagnosis of breast cancer. Nonetheless, they concluded, the statistically significant differences in risks for certain cancer types "do not appear to be due to bias or confounding."
Scientists have identified a genetic variation in mice that may influence whether a tumor metastasizes to other tissues. The specific variant has not been found in the human version of the gene, called Sipa1, but the researchers have preliminary evidence that the human gene may be associated with some prostate cancers. They are investigating whether Sipa1 may be involved in other types of tumors.
The new research demonstrates that an inherited gene variant - a polymorphism - can have a significant impact on tumor metastasis, according to findings published online September 4 in Nature Genetics. Dr. Kent Hunter of NCI's CCR, who led the study, and his team have published evidence that inherited genetic factors may influence whether tumors are successful in colonizing other parts of the body.
If the findings in mice are borne out in humans, they may have implications for cancer patients. "The research suggests that a person's genetic background may play an important role in whether a tumor will spread," says Dr. Hunter. "And this means in theory you could identify patients at risk for metastases and plan their treatments accordingly."
Most cancer deaths are associated not with primary tumors but with their spread. Dr. Hunter predicts that multiple genes will eventually be found to play a role in the efficiency of tumor metastasis. His team identifies potential factors in mice using a strategy they call "transomics," which includes a combination of research techniques such as gene expression profiling, functional genomics, and proteomics.