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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]
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.
A mutation to only one tumor suppressor gene would not cause cancer either, due to the presence of many "backup" genes that duplicate its functions. It is only when enough proto-oncogenes have mutated into oncogenes, and enough tumor suppressor genes deactivated or damaged, that the signals for cell growth overwhelm the signals to regulate it ...
Some substances cause cancer primarily through their physical, rather than chemical, effects on cells. [32] A prominent example of this is prolonged exposure to asbestos, naturally occurring mineral fibers which are a major cause of mesothelioma, which is a cancer of the serous membrane, usually the serous membrane surrounding the lungs. [32]
A tumor suppressor gene (TSG), or anti-oncogene, is a gene that regulates a cell during cell division and replication. [1] If the cell grows uncontrollably, it will result in cancer . When a tumor suppressor gene is mutated, it results in a loss or reduction in its function.
Ulceration can cause bleeding that can lead to symptoms such as coughing up blood (lung cancer), anemia or rectal bleeding (colon cancer), blood in the urine (bladder cancer), or abnormal vaginal bleeding (endometrial or cervical cancer). Although localized pain may occur in advanced cancer, the initial tumor is usually painless.
Under this model, cancer arises as the result of a single, isolated event, rather than the slow accumulation of multiple mutations. [4] The exact function of some tumor suppressor genes is not currently known (e.g. MEN1, WT1), [5] but based on these genes following the Knudson "two-hit" hypothesis, they are strongly presumed to be suppressor genes.
Research has shown that this restoration can lead to regression of certain cancer cells without damaging other cells in the process. The ways by which tumor regression occurs depends mainly on the tumor type. For example, restoration of endogenous p53 function in lymphomas may induce apoptosis, while cell growth may be reduced to normal levels ...