The publication detail shows the title, authors (with indicators showing other profiled authors), information on the publishing organization, abstract and a link to the article in PubMed. This abstract is what is used to create the fingerprint of the publication. If any grants are referenced by the publication, they will be listed here as well.
Homozygous deletion of the MTAP gene in invasive adenocarcinoma of the pancreas and in periampullary cancer: a potential new target for therapy.
Steven R Hustinx; Ralph H Hruban; Lorenzo M Leoni; Christine Iacobuzio-Donahue; John L Cameron; Charles J Yeo; Priscilla N Brown; Pedram Argani; Raheela Ashfaq; Noriyoshi Fukushima; et al. (Profiled Authors: John Cameron; Chris Iacobuzio-Donahue; Ralph Hruban; Scott Kern; Michael Goggins; Anirban Maitra; Pedram Argani)
Pathology, The Johns Hopkins Medical Institutions, Baltimore, Maryland 21205, USA.
Cancer biology & therapy 2005;4(1):83-6.
Methylthioadenosine phosphorylase (MTAP) plays an important role in the salvage pathway for the synthesis of adenosine. Novel chemotherapeutic strategies exploiting the selective loss of MTAP function in cancers have been proposed. The MTAP gene, on chromosome 9p21, is frequently included within homozygous deletions of the p16INK4A/ CDKN2A gene. Biallelic deletions of the p16INK4A/CDKN2A gene are found in 40% of pancreatic cancers, suggesting that the MTAP gene may be frequently inactivated in pancreatic cancer and that selected patients with pancreatic cancer may benefit from therapies targeting this loss. We immunolabeled six xenografted pancreatic cancers with known MTAP and p16INK4A/CDKN2A gene status and found that immunolabeling mirrored gene status. Loss of expression of both MTAP and p16 was observed only in those pancreatic cancers with homozygous deletions that encompassed both the MTAP and p16INK4A/CDKN2A genes. We then immunolabeled a series of 320 microarrayed infiltrating pancreatic adenocarcinomas, 35 biliary adenocarcinomas, 54 ampullary cancers, and 35 noninvasive intraductal papillary mucinous neoplasms. Immunolabeling for MTAP was lost in 91 of the 300 (30%) evaluable pancreatic cancers, 9 of 54 (17%) ampullary cancers, 4 of 33 (12%) biliary cancers, and in 1 of 35 (3%) IPMNs. All neoplasms with loss of MTAP labeling also demonstrated loss of p16 labeling. These results suggest that MTAP expression is lost in approximately 30% of infiltrating pancreatic cancers and in a lower percentage of other periampullary neoplasms, that this loss is the result of homozygous deletions encompassing both the MTAP and p16INK4A/CDKN2A genes. Thus, pancreatic cancer is a promising cancer type in which to explore novel chemotherapeutic strategies to exploit the selective loss of MTAP function.
This section shows information related to the publication - computed using the fingerprint of the publication - including related publications, related experts and related grants with fingerprints representing significant amounts of overlap between their fingerprint and this publication. The red dots indicate whether those experts or terms appear within the publication, thereby showing potential and actual connections.
Steven R Hustinx; Lorenzo M Leoni; Charles J Yeo; Priscilla N Brown; Michael Goggins; Scott E Kern; Ralph H Hruban; Anirban MaitraModern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc 2005;18(7):959-63.
Eric L Powell; Lorenzo M Leoni; Marcia I Canto; Arlene A Forastiere; Christine A Iocobuzio-Donahue; Jean S Wang; Anirban Maitra; Elizabeth MontgomeryThe American journal of surgical pathology 2005;29(11):1497-504.
H M Ceha; M J Clement; M M Polak; G J Offerhaus; R J SlebosPancreas 1998;17(1):85-8.
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