TP53


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TP53

 (tē′pē′fĭf′tē-thrē′)
n.
See p53.

[t(umor) p(rotein) 53; see p53.]
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Conclusion: In Pakistani women the association of TP53 gene codon 72 arginine/proline polymorphism was present.
The 26 patients in this study who carried the high-risk TP53 variants were also almost four times more likely than other pediatric ALL patients to die of their disease or related complications.
In particular, close to 0% of lower-grade IGs overall have mixed molecular features with respect to IDH mutation, 1p/19q codeletion, and TP53 mutation, and these molecular features are superior to histopathology in predicting patient outcome.
Our lab at the University of Utah studies the broken DNA damage response in people with Li-Fraumeni Syndrome who are missing their TP53 genes and have a very high rate of cancer.
Doctors at Dana-Farber are now working on new strategies to overcome the challenges posed by TP53 mutations in MDS.
Droplet digital PCR (ddPCR) was used to validate TP53, PIK3CA, and estrogen receptor 1 (ESR1) mutations as described previously (8).
Conclusions: Dioscin inhibited tumor growth via inducing apoptosis, which was accompanied by altered expression of apoptotic pathway proteins, such as TP53, BAX, BCL2 and CASP3.
BAK1, Bcl-xL, CASPASE3, and TP53 are known regulators of apoptosis, and are related to the intrinsic mitochondrial apoptosis pathway.
miR-145 participates with TP53 in a death-promoting regulatory loop and targets estrogen receptor-alpha in human breast cancer cells.
P53 is a tumor suppressor protein, encoded by the TP53 gene (OMIM 191170), to control cell proliferation [2].
Tumor-suppressive gene TP53 mutation frequently occurs in patients with HCC [14, 15]; 50% of HCC patients living in areas exposed to aflatoxin have tumor suppressor gene P53 (R249S) point mutation, which means amino acid at 249 site AGG changes to AGT [16].
It is approved in Europe for the treatment of adult patients with relapsed or refractory mantle cell lymphoma, or adult patients with chronic lymphocytic leukaemia who have received at least one prior therapy, or in first line patients with CLL in the presence of 17p deletion or TP53 mutation in patients unsuitable for chemo-immunotherapy.