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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)).
Otto Warburg postulated this change in metabolism is the fundamental cause of cancer, [8] a claim now known as the Warburg hypothesis. Today, mutations in oncogenes and tumor suppressor genes are thought to be responsible for malignant transformation, and the Warburg effect is considered to be a result of these mutations rather than a cause. [9 ...
Cancer stem cell arises by clonal evolution as a result of selection for the cell with the highest fitness in the neoplasm. This way, the heterogeneous nature of neoplasm can be explained by two processes – clonal evolution, or the hierarchical differentiation of cells, regulated by cancer stem cells. [ 87 ]
Generally, it is believed that the cancer arises, or a pre-existing cancer is encouraged, during the process of repairing the trauma, rather than the cancer being caused directly by the trauma. [83] However, repeated injuries to the same tissues might promote excessive cell proliferation, which could then increase the odds of a cancerous mutation.
Increased DNA damage tends to cause increased errors during DNA synthesis, leading to mutations that can give rise to cancer. If hypermethylation of a DNA repair gene is an early step in carcinogenesis, then it may also occur in the normal-appearing tissues surrounding the cancer from which the cancer arose (the field defect). See the table below.
Although a DNA repair deficiency can predispose a cell lineage to develop cancer, increased (rather than decreased) expression of a repair capability may also emerge in the progression of cancer cell lineages, and this capability may be clinically important as reviewed by Lingg et al. [9] For instance, the DNA repair gene DMC1 encodes a protein ...
An increase in the amount of a certain protein (protein concentration), caused by an increase of protein expression (through misregulation) an increase of protein (mRNA) stability, prolonging its existence and thus its activity in the cell; gene duplication (one type of chromosome abnormality), resulting in an increased amount of protein in the ...
During this time, necessary mitotic proteins are produced and the cell is once more subjected to regulatory mechanisms to ensure proper status for entry into the proliferative Mitotic (M) phase. Multiple mechanistic checkpoints are involved in this transition from G2 to M, with a common uniting factor of cyclin-Cdk activity.