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Beyond apoptosis of JNK1 in liver cancer.

Authors
Chen-F; Castranova-V
Source
Cell Cycle 2009 Apr; 8(8):1145-1147
NIOSHTIC No.
20035123
Abstract
Hepatocellular Carcinoma (HCC) is the fourth most common neoplasm and the third leading cause of cancer-related death worldwide. Tremendous effort has been made during the past several years in understanding the molecular mechanisms governing the pathogenesis and progression of HCC. Recent studies indicated that c-Jun N-terminal kinase 1 (JNK1), but not JNK2, played pivotal role in the expression of the key signature genes and the prognostic outcomes of HCC. Accordingly, we believe that targeting JNK1 is not only mechanistically sound but also clinically feasible for the treatment of HCC.
Keywords
Biological-systems; Biological-transport; Biological-monitoring; Cell-biology; Cell-damage; Cell-function; Cell-morphology; Cellular-function; Cellular-reactions; Carcinogenesis; Carcinogenicity; Carcinogens; Carcinomas; Genes; Genetic-factors; Hepatocytes; Hepatotoxicity; Hepatotoxins; Liver-cancer; Liver-cells; Liver-disorders; Toxic-effects; Author Keywords: JNK1; HCC; apotosis; epigenetics
Contact
Fei Chen, CDC, National Institute for Occupational Safety and Health, Pathology and Physiology Research Branch, Health Effects Laboratory Division, Rm. 2015, 1095 Willowdale Road, Morgantown, WV 26505
CODEN
CCEYAS
Publication Date
20090415
Document Type
Journal Article
Email Address
lfd3@cdc.gov
Fiscal Year
2009
NTIS Accession No.
NTIS Price
Issue of Publication
8
ISSN
1538-4101
NIOSH Division
HELD
Priority Area
Manufacturing; Mining
Source Name
Cell Cycle
State
WV
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