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Articles by T Jacks
Total Records ( 2 ) for T Jacks
  K. K Wong , T Jacks and G. Dranoff
 

This perspective on Deng et al. (beginning on p. 424 in this issue of the journal) examines the link between NF-B and lung tumorigenesis. Experiments in genetically engineered mouse models of lung cancers are elucidating protumorigenic roles of NF-B activation in lung cancer pathogenesis. Our growing understanding of the tumor-promoting NF-B downstream effector pathways could lead to the development of novel approaches for lung cancer therapy and chemoprevention. Cancer Prev Res; 3(4); 403–5. ©2010 AACR.

  T. G Oliver , K. L Mercer , L. C Sayles , J. R Burke , D Mendus , K. S Lovejoy , M. H Cheng , A Subramanian , D Mu , S Powers , D Crowley , R. T Bronson , C. A Whittaker , A Bhutkar , S. J Lippard , T Golub , J Thomale , T Jacks and E. A. Sweet Cordero
 

Chemotherapy resistance is a major obstacle in cancer treatment, yet the mechanisms of response to specific therapies have been largely unexplored in vivo. Employing genetic, genomic, and imaging approaches, we examined the dynamics of response to a mainstay chemotherapeutic, cisplatin, in multiple mouse models of human non-small-cell lung cancer (NSCLC). We show that lung tumors initially respond to cisplatin by sensing DNA damage, undergoing cell cycle arrest, and inducing apoptosis—leading to a significant reduction in tumor burden. Importantly, we demonstrate that this response does not depend on the tumor suppressor p53 or its transcriptional target, p21. Prolonged cisplatin treatment promotes the emergence of resistant tumors with enhanced repair capacity that are cross-resistant to platinum analogs, exhibit advanced histopathology, and possess an increased frequency of genomic alterations. Cisplatin-resistant tumors express elevated levels of multiple DNA damage repair and cell cycle arrest-related genes, including p53-inducible protein with a death domain (Pidd). We demonstrate a novel role for PIDD as a regulator of chemotherapy response in human lung tumor cells.

 
 
 
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