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Tumor Suppressor Genes


A tumor suppressor gene or antioncogene, is a gene which protects a cell from one step on the path to cancer. When this gene cause mutation to cause a loss or reduction in its function, the cell can growth to cancer, typically in combination with other genetic changes. The loss of these genes may be even more important than proto-oncogene/oncogene activation for the formation of many kinds of human cancer cells. Tumor suppressor genes can be grouped into categories including caretaker genes, gatekeeper genes, and landscaper genes; the classification schemes are evolving as medicine advances, learning from fields including molecular biology, genetics, and epigenetics.

Functions
Tumor-suppressor genes, the proteins they code for, either have a reducing or repressive effect on the regulation of the cell cycle or promote apoptosis, and sometimes do both. The functions of tumor-suppressor proteins fall into several categories including the following:
1. Repression of genes which are essential for the continuing of the cell cycle. If these genes are not expressed, the cell cycle does not continue, effectively inhibiting cell division.
2. Coupling the cell cycle to DNA damage. As long as there is damaged DNA in the cell, it should not divide. The cell cycle can continue, when the damage is repaired. 3. If the damage cannot be repaired, the cell should initiate apoptosis (programmed cell death) to remove the threat it poses for the greater good of the organism.
4. Some proteins involved in cell adhesion prevent tumor cells from dispersing, block loss of contact inhibition, and inhibit metastasis. These proteins are called as metastasis suppressors.
5. DNA repair proteins are usually classified as tumor suppressors as well, as mutations in their genes increase the risk of cancer, for example mutations in HNPCC, MEN1 and BRCA. Furthermore, increased mutation rate from decreased DNA repair leads to increased inactivation of other tumor suppressors and activation of oncogenes.

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This page was last updated on November 22, 2024

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