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Other highlights in the April 3 issue of JNCI

TIG1 Identified as Tumor Suppressor Gene for Prostate Cancer
A new study has identified tazarotene-induced gene 1 (TIG1) as a possible tumor suppressor gene for prostate cancer, and experimental results suggest that decreased expression of the gene may play a role in the progression of prostate cancer.

Chun Jing, Youqiang Ke, Ph.D., and colleagues at the University of Liverpool, United Kingdom, compared genes expressed in malignant prostate cancer cells with those expressed in normal cells of the same tissue to identify oncogenes and tumor suppressor genes. TIG1, a retinoic acid receptor-responsive gene, was expressed in normal prostate tissue and in all 51 benign prostatic hyperplastic tissue samples but in only four of 51 malignant prostate tissue samples.

After inserting TIG1 into a highly malignant prostate cancer cell line, the authors showed that both the invasiveness and the ability of the cells to produce tumors were reduced. The authors conclude that TIG1 may be a tumor suppressor gene whose diminished expression may be involved in the malignant progression of prostate cancer. Their results appear in the April 3 issue of the Journal of the National Cancer Institute.

Marker for Progression of Colon Cancer Identified
Researchers have used gene expression profiles to identify a marker of colon cancer progression through a method called sample pooling. The results appear in the April 3 issue of the Journal of the National Cancer Institute.

Common changes in a gene expression profile can signal tumor progression. However, detecting such changes through gene expression profiling alone is an extremely complex task.

Deepak Agrawal, Timothy J. Yeatman, M.D., of the H. Lee Moffitt Cancer Center, Tampa, and colleagues investigated the feasibility of sample pooling in combination with a novel analysis algorithm to identify markers. RNA from 60 human colon tumors of multiple stages were po
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Contact: Linda Wang
jncinews@oup-usa.org
301-841-1287
Journal of the National Cancer Institute
2-Apr-2002


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