Intestinal mucositis: the role of the Bcl-2 family, p53 and caspases in chemotherapy-induced damage

Support Care Cancer. 2006 Jul;14(7):713-31. doi: 10.1007/s00520-005-0004-7. Epub 2006 Feb 2.

Abstract

Intestinal mucositis occurs as a consequence of cytotoxic treatment through multiple mechanisms including induction of crypt cell death (apoptosis) and cytostasis. The molecular control of these actions throughout the gastrointestinal tract has yet to be fully elucidated; however, they are known to involve p53, the Bcl-2 family and caspases. This review will provide an overview of current research as well as identify areas where gaps in knowledge exist.

Publication types

  • Review

MeSH terms

  • Animals
  • Antineoplastic Agents / adverse effects*
  • Apoptosis / drug effects
  • Benzothiazoles / pharmacology
  • Caspases / biosynthesis
  • Caspases / drug effects
  • Caspases / metabolism*
  • Cell Proliferation / drug effects
  • Humans
  • Intestinal Mucosa / drug effects*
  • Intestinal Mucosa / metabolism
  • Intestinal Mucosa / pathology
  • Mucositis / chemically induced*
  • Mucositis / metabolism
  • Mucositis / prevention & control
  • Proto-Oncogene Proteins c-bcl-2 / biosynthesis
  • Proto-Oncogene Proteins c-bcl-2 / drug effects
  • Proto-Oncogene Proteins c-bcl-2 / metabolism*
  • Radiation-Protective Agents / pharmacology
  • Stem Cells / drug effects
  • Toluene / analogs & derivatives
  • Toluene / pharmacology
  • Tumor Suppressor Protein p53 / biosynthesis
  • Tumor Suppressor Protein p53 / drug effects
  • Tumor Suppressor Protein p53 / metabolism*

Substances

  • Antineoplastic Agents
  • Benzothiazoles
  • Proto-Oncogene Proteins c-bcl-2
  • Radiation-Protective Agents
  • Tumor Suppressor Protein p53
  • Toluene
  • pifithrin
  • Caspases