Tumor promotion is a process in carcinogenesis by which various factors permit the descendants of a single initiated cell to survive and expand in number, i.e. to resist apoptosis and to undergo clonal growth.[1] This is a step toward tumor progression.[2][3]
In order for a tumor cell to survive, it must decrease its expression of tumor suppressor genes such as p53, BRCA1, BRCA2, RB1, or the fas receptor.[4][5] A tumor suppressor would trigger an apoptotic pathway in a cancer cell if there were DNA damage, polyploidy, or uncontrolled cell growth.
Simultaneously, tumor cells need to upregulate oncogenes, which promote or cause downstream activation of growth factors and cell survival signals such as RAS,[6] Mitogen-activated protein kinase kinase, VEGF, or Akt.[7]
See also
editReferences
edit- ^ Compton C (2020). "Cancer initiation, promotion, and progression and the acquisition of key behavioral traits.". Cancer: The Enemy from Within. Cham: Springer. pp. 25–48. doi:10.1007/978-3-030-40651-6_2. ISBN 978-3-030-40650-9. S2CID 218945664.
- ^ Rakoff-Nahoum S (December 2006). "Why cancer and inflammation?". The Yale Journal of Biology and Medicine. 79 (3–4): 123–130. PMC 1994795. PMID 17940622.
- ^ "NCI Dictionary of Cancer Terms:Tumor promotion". National Cancer Institute. Retrieved 10 Nov 2012.
- ^ Cooper GM (2000). "Tumor Suppressor Genes". The Cell: A Molecular Approach (2nd ed.). Sinauer Associates.
- ^ "Oncogenes, Tumor Suppressor Genes, and Cancer" (PDF). American Cancer Society.
- ^ Cancer Genes: RAS
- ^ "Oncogenes, Tumor Suppressor Genes, and Cancer" (PDF). American Cancer Society.
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