Clinical Cancer Research CTRC-AACR San Antonio Breast Cancer Symposium Infection and Cancer: Biology, Therapeutics, and Prevention
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cancer Prevention Research
Cancer Prevention Journals Portal Cancer Reviews Online
Annual Meeting Education Book Meeting Abstracts Online

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Dong, S. M.
Right arrow Articles by Sidransky, D.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Dong, S. M.
Right arrow Articles by Sidransky, D.
Clinical Cancer Research Vol. 8, 2939-2941, September 2002
© 2002 American Association for Cancer Research


Molecular Oncology, Markers, Clinical Correlates

Absence of ST7 Gene Alterations in Human Cancer

Seung Myung Dong and David Sidransky1

Department of Otolaryngology-Head and Neck Surgery, Head and Neck Cancer Research Division, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205-2196

The ST7 gene was cloned and mapped to chromosome 7q31.1-q31.2, a region suspected of containing a tumor suppressor gene involved in a variety of human cancers. Subsequent investigation described the presence of ST7 mutations in human cell lines derived from breast tumors and primary colon carcinoma. Introduction of the ST7 cDNA into a prostate cancer-derived cell line abrogated in vivo tumorigenecity in nude mice. To clarify the role of the ST7 gene in cancer, we scrutinized primary head and neck squamous cell carcinomas, invasive ductal carcinomas of the breast, and adenocarcinomas of the colon. Loss of heterozygosity of D7S522/D7S677 was detected in 24% (4 of 17) of head and neck squamous cell carcinomas, 17% (2 of 12) of invasive ductal carcinomas of the breast, and 33% (8 of 24) of adenocarcinomas of the colon, but no somatic mutations were found in any of these specimens. We then searched for mutations in breast cancer cell lines and found a complete wild-type sequence in all, including cell lines previously reported to harbor mutations. We believe that the ST7 gene is not a primary target of inactivation in most human cancers with loss of heterozygosity at 7q31.1-q31.2.




This article has been cited by other articles:


Home page
Clin. Cancer Res.Home page
J. V. Tricoli, M. Schoenfeldt, and B. A. Conley
Detection of Prostate Cancer and Predicting Progression: Current and Future Diagnostic Markers
Clin. Cancer Res., June 15, 2004; 10(12): 3943 - 3953.
[Abstract] [Full Text] [PDF]


Home page
Mol. Interv.Home page
R. Hnasko and M. P. Lisanti
The Biology of Caveolae: Lessons from Caveolin Knockout Mice and Implications for Human Disease
Mol. Interv., December 1, 2003; 3(8): 445 - 464.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cancer Prevention Research
Cancer Prevention Journals Portal Cancer Reviews Online
Annual Meeting Education Book Meeting Abstracts Online
Copyright © 2002 by the American Association for Cancer Research.