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10.1016/j.celrep.2017.02.013

http://scihub22266oqcxt.onion/10.1016/j.celrep.2017.02.013
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suck abstract from ncbi


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pmid28249168
      Cell+Rep 2017 ; 18 (9 ): 2243-2255
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  • Autocrine IGF1 Signaling Mediates Pancreatic Tumor Cell Dormancy in the Absence of Oncogenic Drivers #MMPMID28249168
  • Rajbhandari N ; Lin WC ; Wehde BL ; Triplett AA ; Wagner KU
  • Cell Rep 2017[Feb]; 18 (9 ): 2243-2255 PMID28249168 show ga
  • Mutant KRAS and c-MYC are oncogenic drivers and rational therapeutic targets for the treatment of pancreatic cancer. Although tumor growth and homeostasis are largely dependent on these oncogenes, a few residual cancer cells are able to survive the ablation of mutant KRAS and c-MYC. By performing a genome-wide gene expression analysis of in vivo-derived bulk tumor cells and residual cancer cells lacking the expression of mutant KRAS or c-MYC, we have identified an increase in autocrine IGF1/AKT signaling as a common survival mechanism in dormant cancer cells. The pharmacological inhibition of IGF-1R reduces residual disease burden and cancer recurrence, suggesting that this molecular pathway is crucial for the survival of cancer cells in the absence of the primary oncogenic drivers.
  • |Animals [MESH]
  • |Autocrine Communication/*genetics [MESH]
  • |Carcinogenesis/genetics/pathology [MESH]
  • |Cell Line, Tumor [MESH]
  • |Cell Proliferation/genetics [MESH]
  • |Gene Expression/genetics [MESH]
  • |Genes, myc/genetics [MESH]
  • |Humans [MESH]
  • |Insulin-Like Growth Factor I/*genetics [MESH]
  • |Mice [MESH]
  • |Mice, Inbred C57BL [MESH]
  • |Mice, Knockout [MESH]
  • |Mice, Transgenic [MESH]
  • |Mutation/genetics [MESH]
  • |Neoplasm Recurrence, Local/genetics/pathology [MESH]
  • |Oncogenes/*genetics [MESH]
  • |Pancreas/pathology [MESH]
  • |Pancreatic Neoplasms/*genetics/*pathology [MESH]
  • |Proto-Oncogene Proteins c-akt/genetics [MESH]
  • |Proto-Oncogene Proteins p21(ras)/genetics [MESH]
  • |Receptor, IGF Type 1/genetics [MESH]


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