PTEN , a Putative Protein Tyrosine Phosphatase Gene Mutated in Human Brain, Breast, and Prostate Cancer-Reference-Cited by-同舟云学术

PTEN , a Putative Protein Tyrosine Phosphatase Gene Mutated in Human Brain, Breast, and Prostate Cancer

Published:1997-03-28 Issue:5308 Volume:275 Page:1943-1947
ISSN:0036-8075
Container-title:Science
language:en
Short-container-title:Science

Author:

Li Jing¹,Yen Clifford²,Liaw Danny¹,Podsypanina Katrina¹,Bose Shikha³,Wang Steven I.¹,Puc Janusz¹,Miliaresis Christa¹,Rodgers Linda²,McCombie Richard²,Bigner Sandra H.⁴,Giovanella Beppino C.⁵,Ittmann Michael⁶,Tycko Ben³,Hibshoosh Hanina³,Wigler Michael H.²,Parsons Ramon¹

Affiliation:

1. J. Li, D. Liaw, K. Podsypanina, S. I. Wang, J. Puc, C. Miliaresis, R. Parsons, Department of Pathology and Department of Medicine, College of Physicians & Surgeons, Columbia University, 630 West 168 Street, New York, NY 10032, USA.

2. C. Yen, L. Rodgers, R. McCombie, M. Wigler, Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724, USA.

3. S. Bose, B. Tycko, H. Hibshoosh, Department of Pathology, College of Physicians & Surgeons, Columbia University, New York, NY 10032, USA.

4. S. H. Bigner, Department of Pathology, Duke University Medical Center, Durham, NC 27710, USA.

5. B. Giovanella, Stehlin Foundation for Cancer Research, St. Joseph Hospital, Houston, TX 77003, USA.

6. M. Ittmann, New York VA Medical Center and Department of Pathology, New York University, 423 East 23 Street, New York, NY 10010, USA.

Abstract

Mapping of homozygous deletions on human chromosome 10q23 has led to the isolation of a candidate tumor suppressor gene, PTEN , that appears to be mutated at considerable frequency in human cancers. In preliminary screens, mutations of PTEN were detected in 31% (13/42) of glioblastoma cell lines and xenografts, 100% (4/4) of prostate cancer cell lines, 6% (4/65) of breast cancer cell lines and xenografts, and 17% (3/18) of primary glioblastomas. The predicted PTEN product has a protein tyrosine phosphatase domain and extensive homology to tensin, a protein that interacts with actin filaments at focal adhesions. These homologies suggest that PTEN may suppress tumor cell growth by antagonizing protein tyrosine kinases and may regulate tumor cell invasion and metastasis through interactions at focal adhesions.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

Reference31 articles.

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