The drug temozolomide, which stops tumor growth by preventing DNA replication in the cell, was approved in 2005 for the treatment of glioblastoma, a rapidly fatal type of brain cancer. However, some glioblastomas do not completely respond to this drug because the cancer cells repair DNA damage induced by the drug before the damage forces the cell to die.
Manish Aghi, M.D., Ph.D., of the Massachusetts General Hospital in Boston, and colleagues paired temozolomide with an oncolytic, or cancer killing, genetically engineered form of the herpes simplex virus called G207. They tested both agents together and separately in cancer cells and in mice with gliomas. Their laboratory studies on human cancer cells found that the virus and the drug act synergistically in cancer cells to promote cell death. Mice with brain gliomas treated with both the virus and the drug survived more than twice as long as those treated with either agent alone.
"Glioma treatment with temozolomide and G207, possibly giving temozolomide before inoculating virus during surgery to take advantage of temozolomide-induced DNA repair in residual glioma cells, warrants a clinical trial," the authors conclude.
Contact: Manish Aghi, Massachusetts General Hospital, 617-840-5111, firstname.lastname@example.org
Autoimmune Disorders Associated with Risk of Non-Hodgkin Lymphoma
A new study confirms that certain autoimmune and inflammatory disorders are associated with an increased risk of non-Hodgkin lymphoma (NHL), a type of cancer that occurs in the lymphatic system. The study also examines the association between these disorders and specific subtypes of NHL.
Past studies have consistently found an association between certain autoimmune disorders (such as lupus, rheumatoid arthritis, and Sjögren syndrome) and NHL, but results have been more inconsistent for related disorders (such as inflammatory bowel disorders, psoriasis, and sarcoidosis). To further characterize these associations and to determine if certain disorders are associated with specific subtypes of NHL, Karin Ekström Smedby, M.D., at the Karolinska Institute in Stockholm, Sweden, and colleagues interviewed 3055 NHL patients and 3187 control subjects about their history of autoimmune and inflammatory disorders.
The authors found that rheumatoid arthritis, primary Sjögren syndrome, systemic lupus erythematosus, and celiac disease were associated with an increased risk of developing NHL. Other similar conditions--type I diabetes mellitus, inflammatory bowel disorders, psoriasis, and sarcoidosis--were not associated with increased risk of NHL. Specific disorders were associated with an increased risk of specific NHL subtypes; for example, there was a positive association between rheumatoid arthritis, Sjögren syndrome, lupus, and celiac disease and risk of a subtype of NHL called diffuse large B-cell lymphoma. The authors suggest that their findings may serve as a model understanding the mechanism by which NHL develops in patients without autoimmune or inflammatory conditions.
Contact: Karin Ekström Smedby, Karolinska Institute, 591-2-277-15-80, email@example.com
Study Examines Reliability of Self-Reported Family History of Cancer
Differences in accurately reporting a family history of cancer between cancer patients and control subjects may bias results in some studies of family cancer risk, according to a new study.
Ellen T. Chang, Sc.D., now of the Northern California Cancer Center, and colleagues at the Karolinska Institute in Stockholm, Sweden, compared questionnaire data and registry data on family history of cancer from 1508 lymphoma patients and 1229 control patients. Cancer patients correctly reported verified (true positive) cases of cancer, especially lymphomas and leukemias, in family members more often than those in the control group, but cancer patients also reported unverified (false positive) cases of family cancer slightly more often than control subjects.
The authors write that self-reported data on family cancer history, "are far from perfectly reliable." "Future observational studies," they suggest, "should make any possible effort to validate both positive and negative self-reports of cancer in family members."
Contact: Ellen T. Chang, Northern California Cancer Center, 510-608-5033, firstname.lastname@example.org
Study Examines Association Between Carbonated Soft Drinks and Risk of Esophageal Cancer
Carbonated soft drink consumption may be associated with a decreased risk of esophageal adenocarcinoma, according to a new study.
Consumption of soft drinks has been associated with gastroesophageal reflux, a recognized risk factor for a specific type of esophageal cancer called esophageal adenocarcinoma. Rates of esophageal adenocarcinoma have increased markedly since the mid-1970s, as has the rate of soft drink consumption. Susan T. Mayne, Ph.D., of Yale University School of Medicine and Yale Cancer Center in New Haven, and colleagues studied the association between soft drink consumption and risk of esophageal adenocarcinoma in a population of 1095 cancer patients and 687 control subjects.
The authors found that consumption of carbonated soft drinks or diet soft drinks was associated with an unexpected decreased risk of esophageal cancer, a finding mainly associated with consumption of diet soft drinks. The authors caution that consumers of diet soft drinks may differ from other consumers in that they may engage in other unmeasured healthy behaviors. They conclude that drinkers of carbonated soft drinks are no more at risk for esophageal adenocarcinoma than the general population.
Commentary Highlights Cancer Survivorship Strategies and Recommendations
Cancer survivors now constitute 3.5% of the United States population, but second primary malignancies among this group account for 16% of all cancer incidence. In a commentary, Lois B. Travis, M.D., of the National Cancer Institute (NCI) in Bethesda, and colleagues highlight research priorities identified at a 2004 NCI workshop called "Cancer Survivorship – Genetic Susceptibility and Second Primary Cancers." These priorities include developing a national research infrastructure for studies of cancer survivorship; creating a coordinated system for biospecimen collection; developing new technology, bioinformatics, and biomarkers; designing new epidemiologic methods; and developing evidence-based practice guidelines.
Contact: NCI Press Office, 301-496-6641, NCIPressOfficers@mail.nih.gov
Also in the January 4 JNCI:
Note: The Journal of the National Cancer Institute is published by Oxford University Press and is not affiliated with the National Cancer Institute. Attribution to the Journal of the National Cancer Institute is requested in all news coverage. Visit the Journal online at http://jncicancerspectrum.oxfordjournals.org/.
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