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42. Oncogenes, protooncogenes, oncoproteins. Growth factor and growth factor receptor oncogenes (RET, KIT, PDGFR). Overexpression of normal growth factor receptors (ERBB1, ERBB2). Organ examples.: Difference between revisions

42. Oncogenes, protooncogenes, oncoproteins. Growth factor and growth factor receptor oncogenes (RET, KIT, PDGFR). Overexpression of normal growth factor receptors (ERBB1, ERBB2). Organ examples. (view source)

Revision as of 22:17, 7 May 2022

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(Created page with "''I recommend starting with the relevant medical biochemistry topic (27 - 28) before getting into this''. All cancers start with some genetic damage. This genetic damage is always ''nonlethal'', meaning that the damage isn’t big enough to actually kill the cell, however it is definitely big enough to cause some serious damage. The process where cancer develops is called ''carcinogenesis''. Nonlethal genetic damage causes mutations and can be due to many factors. Comm...")
 
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Loss (of function) of the guardian genes don’t directly cause cells to start proliferating like crazy, however a cell without a guardian accumulates mutations in proto-oncogenes and other tumor suppressors more easily.
Loss (of function) of the guardian genes don’t directly cause cells to start proliferating like crazy, however a cell without a guardian accumulates mutations in proto-oncogenes and other tumor suppressors more easily.
 
[[File:Model of transition from normal epithelium to colorectal carcinoma.png|thumb|This figure illustrated the model of how normal epithelium becomes colorectal carcinoma. It illustrates how not just one mutation, but many are needed for the formation of cancer.]]
Genes that regulate apoptosis or DNA repair don’t transform the cell directly either, but, like guardian genes, can be a factor in accelerating the accumulation of other mutations.
Genes that regulate apoptosis or DNA repair don’t transform the cell directly either, but, like guardian genes, can be a factor in accelerating the accumulation of other mutations.