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Related Experiment Videos

Putting the rap on Akt.

James E Thompson1, Craig B Thompson

  • 1University of Pennsylvania, Abramson Family Cancer Research Institute, 421 Curie Blvd, Room 450 BRB II/III, Philadelphia, PA 19104-6160, USA.

Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology
|October 16, 2004
PubMed
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The protein kinase Akt, crucial in many cancers, promotes tumor growth and resistance to cell death. Targeting Akt activation pathways offers a promising strategy for novel cancer therapies.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • The protein kinase Akt is frequently activated in diverse cancers, contributing to apoptosis resistance.
  • This activation is controlled by the interplay between the PI3-K oncogene and the PTEN tumor suppressor.
  • Aberrant Akt activation is linked to oncogenic mutations like HER-2/neu amplification and BCR/ABL fusion.

Purpose of the Study:

  • To review the mechanisms controlling Akt activation in cancer.
  • To elucidate the antiapoptotic functions of activated Akt.
  • To discuss therapeutic strategies targeting the Akt pathway.

Main Methods:

  • Review of existing literature on Akt signaling in cancer.
  • Analysis of molecular mechanisms underlying Akt activation and function.

Related Experiment Videos

  • Discussion of therapeutic implications of targeting Akt.

    • Main Results:

    • Activated Akt confers resistance to apoptosis via inhibition of Bad, downregulation of death receptors, and enhanced glycolysis.
    • Increased glycolysis, a hallmark of malignancy, aids in cancer diagnosis and staging.
    • Specific oncogenic mutations drive Akt activation, essential for their transforming activity.

    Conclusions:

    • Akt signaling is a critical mediator of cancer development and survival.
    • Understanding Akt regulation provides insights into therapeutic vulnerabilities.
    • Rapamycin and analogs show promise as antineoplastic agents, particularly in Akt-activated tumors.