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Carcinogenesis: the biology of neoplasia
The transformation of a normal cell into a malignant cell involves a series of mutations in genes, termed oncogenes, that directly contribute to neoplasia when their functions are altered.
Oncogenes normally function in cellular processes such as cell division, apoptosis, and differentiation.
Examples of oncogenes:
Growth factor receptors
Tyrosine kinases play essential roles in transmitting mitogenic signaling pathways.
Genes that regulate the cell division cycle
Genes that regulate programmed cell death programmed
Genes involved in DNA repair
Tumour genesis is a multistep process that requires the accumulation of multiple mutations.
All tumours share a number of attributes that contribute to their malignant phenotype, but the specific molecular events that produce these phenotypes vary greatly among tumor types and individuals.
Carcinogenesis is a multistep process, and the development of fully malignant cancers requires many independent events.
It is known that these steps involve the acquisition of mutations in cancer genes and that genetic instability allows these rare events to accumulate at a rate that ultimately gives rise to aggressive neoplasms.
Although the specific mutations that cause human cancers vary greatly between types of cancers and individuals, the broad consequences of these mutations are abnormal phenotypes that are shared by most cancers.