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Also in the Sept. 9 JNCI
Date:9/9/2008

Bias Correction of Familial Risk Estimates Increases Estimated Melanoma Risk But Not Risk of Other Common Cancers

The relative risk of familial melanoma increases substantially when researchers account for a known potential bias in a large cohort study. The relative risk of familial lung, breast, prostate, and colorectal cancer do not change substantially with the correction.

Researchers have used the Swedish Cancer Registry and the Swedish MultiGenerational Register to estimate the relative risk of cancers for individuals who have an affected first-degree relative. However, Kamila Czene, Ph.D., of the Karolinksa Institute and colleagues recently determined that such database analyses may underestimate the risk because cancers that occur before the start of registration are not included.

In the current study, Czene and colleagues adjusted for the bias by using data from a simulated population and applying that information to the Swedish cohort.

The relative risk of familial melanoma increased from 2.68 to 3.18 following the adjustment for the bias. The impact was even greater when an affected parent was diagnosed at a young age, increasing the relative risk to 4.07. The relative risks for colorectal, lung, breast, and prostate cancer remained close to 2.

"The lack of bias for most of these cancers is due to the relatively low familial riskand/or relatively low incidence in the population, combined with a reasonably high sensitivity of the observed family history," the authors write. "Because sensitivity depends on age at onset, it is not surprising that the lowest sensitivity was observed for melanoma, a cancer with relatively young age at onset."

Contact: Kamila Czene, Kamila.Czene@ki.se, 0046-8-524-86144


Experts Call for Renewed Efforts in Gastroenteropancreatic Neuroendocrine Tumors

During a September 2007 summit on neuroendocrine and carcinoid tumor, clinicians and researchers presented the current standards of care and identified key areas that require investigation and development.

Over the last 30 years, the incidence of these tumors has steadily increased in the United States, but there have been no substantial improvements in survival during that same time period.

At a National Cancer Institute-sponsored meeting, basic science and clinical researchers identified specific areas in the field that need to be addressed, which are summarized in a commentary by Irvin M. Modlin, M.D., Ph.D., D.Sc., of Yale University in New Haven, Conn., and colleagues. Those issues include increased public and physician education, identification of molecular markers for diagnosis and disease monitoring during therapy, standardization of pathology classifications, creation of regional centers of excellence, and improved in vitro and animal models of disease.

"The group of experts at the meeting considered that the increasing incidence and prevalence of neuroendocrine disease in the United States was of considerable concern, particularly in light of the lack of evidence of improvement of outcome and the lack of any tangible evidence of the development of demonstrably effective novel therapies," the authors write.

Contact: Irvin Modlin, imodlin@optonline.net, (203) 397-0440


Confirmation of Association with Chromosome 15 Locus and Familial Lung Cancer

Two single-nucleotide polymorphism (SNP) variants on the short arm of chromosome 15 appear to be associated with familial lung cancer.

Several research groups recently reported an association between the 15q24-25.1 locus and sporadic lung cancer risk.

To confirm that association with familial lung cancer, Ming You, M.D., Ph.D., of Washington University in St. Louis and colleagues performed a genome-wide association study using SNPs on 194 case patients with familial lung cancer and 219 cancer-free individuals.

You and colleagues found a strong association between the 15q24-25.1 locus and familial lung cancer. Two SNP variants were associated with the risk of lung cancer, although the identity of a causal gene was not identified.

"Determination of a likely single candidate gene and further delineation of whether variants affect lung cancer directly or indirectly or both are warranted," the authors conclude.

Contact: Gwen Ericson, ericsong@wustl.edu, (314) 286-0141


Also in the September 9 JNCI:


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

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