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Updated: Jul 10, 2026

Discovery of Driver Genes in Colorectal HT29-derived Cancer Stem-Like Tumorspheres
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Identification of prostate cancer modifier pathways using parental strain expression mapping.

Qing Xu1, Pradip K Majumder, Kenneth Ross

  • 1Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, MA 02115.

Proceedings of the National Academy of Sciences of the United States of America
|November 6, 2007
PubMed
Summary

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This study identifies the glycolysis pathway as a key genetic modifier influencing cancer risk. Findings in mice and human prostate cancer data suggest its role in modulating proliferation and recurrence.

Area of Science:

  • Genetics
  • Cancer Biology
  • Systems Biology

Background:

  • Inherited genetic factors significantly influence cancer susceptibility.
  • Beyond Mendelian cancer genes, individual susceptibility is poorly understood.
  • Germ-line modifiers controlling cancer risk require identification.

Purpose of the Study:

  • To develop a method for identifying germ-line modifier genes and pathways.
  • To investigate modifiers of AKT1-induced proliferation in mice.
  • To explore the relevance of identified pathways in human prostate cancer.

Main Methods:

  • Developed parental strain expression mapping using inbred mice.
  • Utilized genome-wide mRNA expression analysis.
  • Analyzed human prostate cancer expression datasets.

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Published on: July 22, 2020

Main Results:

  • Identified multiple candidate germ-line modifier pathways.
  • The glycolysis pathway emerged as a negative modulator of AKT1-induced proliferation.
  • In human prostate cancer, enriched glycolysis in normal tissue correlated with decreased recurrence.

Conclusions:

  • Parental strain expression mapping is effective for identifying germ-line modifiers.
  • The glycolysis pathway may be a crucial regulator of cancer susceptibility and progression.
  • These findings have implications for understanding and potentially targeting cancer risk in humans.