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Why Tumor Genetic Heterogeneity May Require Rethinking Cancer Genesis and Treatment.

Bruce Gottlieb1, Mark Trifiro2, Gerald Batist3

  • 1Lady Davis Institute for Medical Research, Jewish General Hospital, Montreal, Quebec, Canada; Segal Cancer Center, Jewish General Hospital, Montreal, Quebec, Canada; Department of Human Genetics, McGill University, Montreal, Quebec, Canada; Department of Nursing, McGill University, Montreal, Quebec, Canada.

Trends in Cancer
|November 27, 2020
PubMed
Summary
This summary is machine-generated.

Genetic heterogeneity, common in tumors, may arise early in development. A novel hypothesis suggests targeting normal cells within tumors could be a new cancer treatment strategy.

Keywords:
genetic heterogeneity-based selection-centric cancer hypothesisnormal cell selection treatment approachtumor genetic heterogeneity

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Area of Science:

  • Oncology
  • Genetics
  • Developmental Biology

Background:

  • Tumor genetic heterogeneity, the presence of diverse genes within a single tumor, is frequently observed but its functional significance remains unclear.
  • This heterogeneity involves both cancer-associated and normal genes, complicating our understanding of early cancer development.

Purpose of the Study:

  • To propose a novel genetic heterogeneity-based selection-centric hypothesis for cancer development.
  • To explore the early origins of genetic heterogeneity and its role in precancerous states.
  • To suggest a new therapeutic strategy based on normal cell selection within tumors.

Main Methods:

  • The study proposes a hypothesis based on existing literature regarding genetic heterogeneity and DNA repair.
  • It involves a conceptual framework linking early developmental events to cancer initiation.
  • The hypothesis is supported by analogies to metastasis and therapeutic resistance.

Main Results:

  • Genetic heterogeneity may originate from transiently reduced DNA repair efficiency early in development.
  • This process can lead to dormant cancer-associated genes in a small fraction of normal cells.
  • Altered tissue microenvironments can select for these precancerous cells, driving cancer progression.

Conclusions:

  • Cancer development, metastasis, and therapeutic resistance may be driven by selection processes acting on genetically heterogeneous cells.
  • A potential therapeutic approach involves preferentially selecting normal cells within tumors.
  • This normal cell selection strategy may offer a novel avenue for cancer treatment.