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The central role of DNA damage and epigenetic defects in DNA repair genes in carcinogenesis. DNA damage is considered to be the primary cause of cancer. [17] More than 60,000 new naturally-occurring instances of DNA damage arise, on average, per human cell, per day, due to endogenous cellular processes (see article DNA damage (naturally occurring)).
From proto-oncogene to oncogene. The proto-oncogene can become an oncogene by a relatively small modification of its original function. There are three basic methods of activation: A mutation within a proto-oncogene, or within a regulatory region (for example the promoter region), can cause a change in the protein structure, causing
The viral promoter or other transcription regulation elements in turn cause overexpression of that proto-oncogene, which in turn induces uncontrolled cellular proliferation. Because viral genome insertion is not specific to proto-oncogenes and the chance of insertion near that proto-oncogene is low, slowly transforming viruses have very long ...
Bacteria involved in causing and treating cancers. Cancer bacteria are bacteria infectious organisms that are known or suspected to cause cancer. [1] While cancer-associated bacteria have long been considered to be opportunistic (i.e., infecting healthy tissues after cancer has already established itself), there is some evidence that bacteria may be directly carcinogenic.
For some of these diseases, cancer is not the primary feature and is a rare consequence. Many of the cancer syndrome cases are caused by mutations in tumor suppressor genes that regulate cell growth. Other common mutations alter the function of DNA repair genes, oncogenes and genes involved in the production of blood vessels. [12]
Species or genera Possibly associated cancers Ref Bacteroides fragilis: Colon cancer. [1] Borrelia burgdorferi: MALT lymphoma. [2] Campylobacter jejuni. Immunoproliferative small intestinal disease (IPSID), which is rare a type of MALT lymphoma. [2] Chlamydia pneumonia: Lung MALT lymphoma. [2] Chlamydia trachomatis Cervical cancer. [2]
Myc is a family of regulator genes and proto-oncogenes that code for transcription factors. The Myc family consists of three related human genes: c-myc , l-myc , and n-myc . c-myc (also sometimes referred to as MYC) was the first gene to be discovered in this family, due to homology with the viral gene v-myc.
It was later found that carcinogenesis (the development of cancer) depended both on the mutation of proto-oncogenes (genes that stimulate cell proliferation) and on the inactivation of tumor suppressor genes, that keep proliferation in check. Knudson's hypothesis refers specifically, however, to the heterozygosity of tumor suppressor genes.