NDLI: A cluster of cooperating tumor-suppressor gene candidates in chromosomal deletions

Content Provider	PubMed Central
Author	Xue, Wen Thomas, Kitzing Roessler, Stephanie Zuber, Johannes Alexander, Krasnitz Schultz, Nikolaus Revill, Kate Susann, Weissmueller Rappaport, Amy R. Simon, Janelle Zhang, Jack Luo, Weijun Hicks, James Zender, Lars Wang, Xin Wei Powers, Scott Wigler, Michael Lowe, Scott W.
Abstract	The large chromosomal deletions frequently observed in cancer genomes are often thought to arise as a “two-hit” mechanism in the process of tumor-suppressor gene (TSG) inactivation. Using a murine model system of hepatocellular carcinoma (HCC) and in vivo RNAi, we test an alternative hypothesis, that such deletions can arise from selective pressure to attenuate the activity of multiple genes. By targeting the mouse orthologs of genes frequently deleted on human 8p22 and adjacent regions, which are lost in approximately half of several other major epithelial cancers, we provide evidence suggesting that multiple genes on chromosome 8p can cooperatively inhibit tumorigenesis in mice, and that their cosuppression can synergistically promote tumor growth. In addition, in human HCC patients, the combined down-regulation of functionally validated 8p TSGs is associated with poor survival, in contrast to the down-regulation of any individual gene. Our data imply that large cancer-associated deletions can produce phenotypes distinct from those arising through loss of a single TSG, and as such should be considered and studied as distinct mutational events.
Related Links	http://dx.doi.org/10.1073/pnas.1206062109
Ending Page	8217
Page Count	6
Starting Page	8212
File Format	PDF
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	21
Volume Number	109
Language	English
Publisher	National Academy of Sciences
Publisher Date	2012-05-22
Access Restriction	Open
Rights Holder	National Academy of Sciences
Subject Keyword	General Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in

A cluster of cooperating tumor-suppressor gene candidates in chromosomal deletions.

Localization of a putative tumor suppressor gene by using homozygous deletions in melanomas.

STOP gene Phactr4 is a tumor suppressor

Concomitant deletions of tumor suppressor genes MEN1 and AIP are essential for the pathogenesis of the brown fat tumor hibernoma

ANX7, a candidate tumor suppressor gene for prostate cancer

DBC2, a candidate for a tumor suppressor gene involved in breast cancer

PRDM1 is a tumor suppressor gene in natural killer cell malignancies

Rare chromosomal deletions and duplications increase risk of schizophrenia

RBSP3 (HYA22) is a tumor suppressor gene implicated in major epithelial malignancies

A cluster of cooperating tumor-suppressor gene candidates in chromosomal deletions

Similar Documents

A cluster of cooperating tumor-suppressor gene candidates in chromosomal deletions.

Localization of a putative tumor suppressor gene by using homozygous deletions in melanomas.

STOP gene Phactr4 is a tumor suppressor

Concomitant deletions of tumor suppressor genes MEN1 and AIP are essential for the pathogenesis of the brown fat tumor hibernoma

ANX7, a candidate tumor suppressor gene for prostate cancer

DBC2, a candidate for a tumor suppressor gene involved in breast cancer

PRDM1 is a tumor suppressor gene in natural killer cell malignancies

Rare chromosomal deletions and duplications increase risk of schizophrenia

RBSP3 (HYA22) is a tumor suppressor gene implicated in major epithelial malignancies

A cluster of cooperating tumor-suppressor gene candidates in chromosomal deletions