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Updated: May 5, 2026

Deficient Pms2, ERCC1, Ku86, CcOI in Field Defects During Progression to Colon Cancer
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APCの喪失によって引き起こされる結腸腺腫の発症と進行の2段階モデル

Reid A Phelps1, Stephanie Chidester, Somaye Dehghanizadeh

  • 1Huntsman Cancer Institute, University of Utah, Salt Lake City, UT 84112, USA.

Cell
|May 20, 2009
PubMed
まとめ

アデノマトス・ポリポシス・コライ (APC) 遺伝子の喪失は,腸内細胞の分化に失敗するが,すぐに腫瘍が成長することはない. C末端結合タンパク質-1 (CtBP1) は初期アデノマ形成を促し,KRASの活性化はがんへの進行を促進する.

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Cancer arises from mutations in the critical genes that allow healthy cells to escape cell cycle regulation and acquire the ability to proliferate indefinitely. Though originating from a single mutation event in one of the originator cells, cancer progresses when the mutant cell lines continue to gain more and more mutations, and finally, become malignant. For example, chronic myelogenous leukemia (CML) develops initially as a non-lethal increase in white blood cells, which progressively...
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Notch signaling was first discovered in Drosophila melanogaster, where it is involved in cell lineage differentiation. Notch signaling regulates the maintenance and differentiation of intestinal stem cells or ISCs by controlling the expression of atonal homolog 1 or Atoh1. Atoh1 directs cells to differentiate into secretory cells.
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