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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)).
A proto-oncogene is a normal gene that could become an oncogene due to mutations or increased expression. Proto-oncogenes code for proteins that help to regulate the cell growth and differentiation. Proto-oncogenes are often involved in signal transduction and execution of mitogenic signals, usually through their protein products.
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 ...
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]
The National Toxicology Program of the U.S. Department of Health and Human Services is mandated to produce a biennial Report on Carcinogens. [37] As of August 2024, the latest edition was the 15th report (2021). [38] It classifies carcinogens into two groups: Known to be a human carcinogen; Reasonably anticipated to be a human carcinogen
Scientist Otto Warburg, whose research activities led to the formulation of the Warburg hypothesis for explaining the root cause of cancer.. The Warburg hypothesis (/ ˈ v ɑːr b ʊər ɡ /), sometimes known as the Warburg theory of cancer, postulates that the driver of carcinogenesis (cancer formation) is insufficient cellular respiration caused by insult (damage) to mitochondria. [1]
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.
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] Chlamydophila psittaci: Ocular/adnexal lymphoma (forms of eye cancer). [2] Clostridium ssp Colon cancer. [2] Cutibacterium acnes: Bladder and prostate cancer. [2]