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Contact: Liz Savage
jncimedia@oxfordjournals.org
301-841-1287
Journal of the National Cancer Institute

Other highlights in the February 7 JNCI

Study Examines Second Cancer Risk Among Hairy Cell Leukemia Survivors

Survivors of a rare cancer called hairy cell leukemia are at an increased risk of Hodgkin lymphoma, non-Hodgkin lymphoma, and thyroid cancer, and at an increased risk of death from leukemia and lymphoma, according to a new study. However, the absolute risk of those second cancers is small.

Hairy cell leukemia is a malignancy of a type of white blood cell called B lymphocytes. It accounts for about 2 percent of all leukemias. Better treatments have improved the prognosis for this disease, but the treatments may be associated with an increased risk of second cancers. To determine the risk of second cancers and to examine the causes of death among these patients, Michie Hisada, M.D., Sc.D., and colleagues at the National Cancer Institute examined the records for 3,104 patients with hairy cell leukemia who survived for at least two months after diagnosis.

They found that hairy cell leukemia survivors had a 6.6-fold increased risk of Hodgkin lymphoma, a 5-fold increased risk of non-Hodgkin lymphoma, a 3.6-fold increased risk of thyroid cancer, but a decreased risk of lung cancer compared with the general population. Among survivors, there was a lower risk of death from cardiovascular and cerebrovascular diseases than among the general population. "… Extrapolating from our results, among 10,000 hairy cell leukemia patients, a total excess of about 34 cancers—21 non-Hodgkin lymphomas, 2 Hodgkin lymphomas, and 7 solid tumors (including two thyroid cancers)—might be observed per year," the authors write.

"Future studies should address the influence of such factors as changes in treatment regimens, immunologic impairment, natural history, diagnostic misclassification, and tobacco use on risk of second cancers in hairy cell leukemia patients," the authors conclude.

Contact: National Cancer Institute, Media Relations Branch, 301-496-6641, ncipressofficers@mail.nih.gov


New Test May Better Identify Certain Colorectal Cancer Types

A new test may more accurately identify colorectal cancer patients with a specific type of gene mutation. These mutations usually indicate that a patient has an inherited form of the disease or may respond to certain cancer drugs differently.

Some people with colorectal cancer have defects in their so-called DNA mismatch repair genes. Researchers test for these mutations by looking for a gene marker called microsatellite instability, which is caused by those gene defects. These mutations indicate that the cancer is likely an inherited condition called Lynch syndrome. It's important to identify patients with Lynch syndrome because they and their family members are at an increased risk of colorectal and other cancers. Patients with a non-hereditary form of colorectal cancer that shows microsatellite instability tend to have a better prognosis than other cancer patients, but they don't respond to a common cancer drug called 5-fluorouracil.

Rosa M . Xicola, a graduate student at the Germans Trias i Pujol Hospital in Barcelona, and colleagues tested two different methods, a standard method and an experimental method, of identifying patients with microsatellite instability. They found that the experimental method better identified—and more accurately ruled out—patients with defects in DNA mismatch repair genes. Furthermore, their results suggest that an even simpler test could be developed to identify patients with these mutations.

"The improved test could result in more patients being assigned to proper treatment based on their disease profile," the authors conclude.

Contact: Xavier Llor, M.D.. associate professor, University of Illinois at Chicago, 312-996-6651, xllor@uic.edu


Reports of Prognostic Tumor Markers Often Inadequate

Reports of studies of cancer prognostic factors are largely suboptimal, a new study concludes.

Researchers believe that certain characteristics of a tumor, such as the expression of a particular gene, may help doctors predict a patient's prognosis—how they respond to a certain chemotherapy drug or how likely they are to survive their cancer, for example. However, most proposed prognostic markers have not been validated and have not changed clinical practice.

Panayiotis A. Kyzas, M.D., Ph.D., of the University of Ioannina School of Medicine, Ioannina, Greece, and colleagues decided to examine the quality of reports of studies of cancer prognostic factors and see whether certain aspects of report quality were associated with particular conclusions about a tumor marker. Among 331 studies identified from 20 meta-analyses of cancer prognostic markers, the researchers didn't find any association between study quality and reported outcome. However, they did find several shortcomings: An important statistical test called a power calculation was rarely reported, most studies were too small to reveal modest effects of a particular tumor marker, many studies did not state that the analysis was blinded, and only a small percentage of studies were prospective.

"Our analysis indicates that the reporting of important quality in formation in cancer prognostic studies is often suboptimal," the authors write. "Given the potential clinical importance of this prognostic information, efforts to improve the design and reporting of these studies are warranted."

Contact: John Ioannidis, M.D., professor and chair, University of Ioannina School of Medicine, Ioannina, Greece, jioannid@cc.uoi.gr


Growth Factor May Interfere With Normal Blood Cell Production

Patients with so-called clonal myeloid disorders, such as myelofibrosis and some leukemias, often have bone marrow cells that are defective in making new blood cells, a process called hematopoiesis. Defective hematopoiesis may cause severe side effects and even death.

Laboratory studies have found that the bone marrow from patients with clonal myeloid disorders and defective hematopoiesis express abnormally high levels of various growth factors. In a new study, Takayuki Nakayama, M.D, Ph.D., of the National Cancer Institute, and colleagues looked at the role of one of these growth factors, fibroblast growth factor 2 (FGF-2), in mouse and human cells. They found that FGF-2 inhibits a gene that is critical in regulating hematopoiesis. When they injected FGF-2 into mice, they found that the growth factor did indeed disrupt normal hematopoiesis.

"Thus, FGF-2 represents a promising therapeutic target for correction of hematologic abnormalities of clonal myeloid disorders and, potentially, other diseases," the authors conclude.

Contact: National Cancer Institute, Media Relations Branch, 301-496-6641, ncipressofficers@mail.nih.gov

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EMBARGOED FOR RELEASE: 6 FEBRUARY 16:00 EST

Also in the February 7 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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