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MYC Deregulation in Primary Human Cancers

Manpreet Kalkat1,2, Jason De Melo3, Katherine Ashley Hickman4,5

  • 1Department of Medical Biophysics, University of Toronto, Toronto, ON M5G 1L7, Canada. manpreet.kalkat@mail.utoronto.ca.

Genes
|June 8, 2017
PubMed

Insights

MYC is a master regulator frequently deregulated in cancer, driving disease initiation and progression. Understanding MYC deregulation reveals new therapeutic targets for cancer treatment.

Area of Science:

  • Oncology
  • Molecular Biology
  • Gene Regulation

Background:

  • MYC is a crucial transcription factor regulating cell cycle, metabolism, and ribosome biogenesis.
  • MYC activity is frequently deregulated in various cancers, contributing to tumorigenesis.
  • Constitutive MYC overexpression is a hallmark of many cancers, driven by genetic and signaling alterations.

Purpose of the Study:

  • To summarize the frequency and mechanisms of MYC deregulation across different cancer types.
  • To review established and novel findings on MYC's role in cancer.
  • To identify potential therapeutic vulnerabilities arising from MYC dysregulation.

Main Methods:

  • Literature review and synthesis of existing studies on MYC in cancer.
  • Analysis of genetic abnormalities and signaling pathways leading to MYC overexpression.
  • Examination of MYC's transcriptional network in various malignancies.

Main Results:

  • MYC deregulation occurs through diverse mechanisms including copy number alterations, translocations, and aberrant signaling.
  • Overexpression of MYC is a common driver in numerous cancer types.
  • Understanding these deregulation mechanisms is key to discovering therapeutic strategies.

Conclusions:

  • MYC's central role in cancer pathogenesis is underscored by its frequent deregulation.
  • Targeting MYC or its regulatory pathways presents a promising therapeutic avenue.
  • Further research into MYC deregulation mechanisms can uncover novel anti-cancer strategies.
Keywords:
MYCcancercell signalingderegulationenhancersgene amplificationtranslocation

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