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Line 22: − Universal tumor suppressor associated with many cancer types. Can also be an activating oncogene.+ − The ''TP53'' gene is well-known tumor suppressor gene that has been implicated in many cancer types [1]. The ''TP53'' protein product is involved in regulating the cell cycle pathway and can prevent replication if cell damage has occurred [2]. Deletions, LOH, and loss of function (LOF) mutations have been associated with ''TP53''. These alterations often confer a poor prognosis and chemoresistance.+ − − Put your text here and/or fill in the table Line 73:
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Beth Pitel, MS, ASCP(CG)CM
Beth Pitel, MS, ASCP(CG)CM
Jennelle C, Hodge, PhD
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==Cancer Category/Type==
==Cancer Category/Type==
Nearly universal involvement in diverse cancer types.
==Gene Overview==
==Gene Overview==
The ''TP53'' protein product is involved in regulating the cell cycle pathway and can prevent replication if cell damage has occurred [1, 2]. ''TP53'' has been implicated in many cancer types, and is classically considered the prototypic tumor suppressor gene [3, 4]. Inactivating mutations resulting in loss of p53 function, including deletions, LOH, and loss of function (LOF) alterations often confer a poor prognosis and chemoresistance. Alternatively, gain-of-function mutations promoting the expression and stability of the p53 protein in the nucleus can also lead to oncogenic effects, including genomic instability and excessive cell proliferation [5].
==Common Alteration Types==
==Common Alteration Types==
{| class="wikitable sortable"
{| class="wikitable sortable"
1. Hampp S, et al., (2016). DNA damage tolerance pathway involving DNA polymerase ι and the tumor suppressor p53 regulates DNA replication fork progression. PNAS 113(30): E4311-4319, PMID 27407148.
1. Hampp S, et al., (2016). DNA damage tolerance pathway involving DNA polymerase ι and the tumor suppressor p53 regulates DNA replication fork progression. PNAS 113(30): E4311-4319, PMID 27407148.
2. Wang M, et al., (2018). Characterizing genomic differences of human cancer stratified by the TP53 mutation status. Mol Genet Genomics doi: 10.1007/s00438-018-1416-7 [Epub ahead of print], PMID 29330617.
2. Levine AJ. (1997). p53, the cellular gatekeeper for growth and division. Cell 88(3):323-231, PMID 9039259.
3. Wang M, et al., (2018). Characterizing genomic differences of human cancer stratified by the TP53 mutation status. Mol Genet Genomics doi: 10.1007/s00438-018-1416-7 [Epub ahead of print], PMID 29330617.
4. Kato S, et al., (2003). Understanding the function-structure and function-mutation relationships of p53 tumor suppressor protein by high-resolution missense mutation analysis. Proc Natl Acad Sci U S A 100(14):8424-8429, PMID 12826609.
5. Olivier M, et al., (2009). Recent advances in p53 research: an interdisciplinary perspective. Cancer Gene Ther 16(1):1-12, PMID 18802452.
== Notes ==
== Notes ==