Tumor Suppressor Protein p53
"Tumor Suppressor Protein p53" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus,
MeSH (Medical Subject Headings). Descriptors are arranged in a hierarchical structure,
which enables searching at various levels of specificity.
Nuclear phosphoprotein encoded by the p53 gene (GENES, P53) whose normal function is to control CELL PROLIFERATION and APOPTOSIS. A mutant or absent p53 protein has been found in LEUKEMIA; OSTEOSARCOMA; LUNG CANCER; and COLORECTAL CANCER.
Descriptor ID |
D016159
|
MeSH Number(s) |
D12.776.157.687.650 D12.776.260.820 D12.776.624.776.775 D12.776.660.720.650 D12.776.744.845
|
Concept/Terms |
Tumor Suppressor Protein p53- Tumor Suppressor Protein p53
- p53 Antigen
- TP53 Protein
- TRP53 Protein
- p53 Tumor Suppressor Protein
- pp53 Phosphoprotein
- Phosphoprotein, pp53
- Cellular Tumor Antigen p53
- Oncoprotein p53
|
Below are MeSH descriptors whose meaning is more general than "Tumor Suppressor Protein p53".
Below are MeSH descriptors whose meaning is more specific than "Tumor Suppressor Protein p53".
This graph shows the total number of publications written about "Tumor Suppressor Protein p53" by people in this website by year, and whether "Tumor Suppressor Protein p53" was a major or minor topic of these publications.
To see the data from this visualization as text,
click here.
Year | Major Topic | Minor Topic | Total |
---|
1994 | 1 | 1 | 2 |
1995 | 1 | 0 | 1 |
1997 | 0 | 1 | 1 |
1999 | 1 | 3 | 4 |
2001 | 0 | 1 | 1 |
2002 | 0 | 1 | 1 |
2003 | 1 | 1 | 2 |
2004 | 0 | 2 | 2 |
2005 | 1 | 0 | 1 |
2006 | 2 | 4 | 6 |
2007 | 1 | 0 | 1 |
2008 | 3 | 3 | 6 |
2009 | 1 | 4 | 5 |
2010 | 1 | 3 | 4 |
2011 | 0 | 1 | 1 |
2012 | 2 | 3 | 5 |
2013 | 4 | 2 | 6 |
2014 | 1 | 2 | 3 |
2015 | 2 | 3 | 5 |
2016 | 0 | 2 | 2 |
2017 | 0 | 2 | 2 |
2018 | 0 | 1 | 1 |
2019 | 1 | 1 | 2 |
2020 | 3 | 2 | 5 |
2021 | 1 | 1 | 2 |
2022 | 0 | 2 | 2 |
2023 | 1 | 1 | 2 |
2024 | 2 | 1 | 3 |
To return to the timeline,
click here.
Below are the most recent publications written about "Tumor Suppressor Protein p53" by people in Profiles.
-
ENGOT-EN20/GOG-3083/XPORT-EC-042 - A phase III, randomized, placebo-controlled, double-blind, multicenter trial of selinexor in maintenance therapy after systemic therapy for patients with p53 wild-type, advanced, or recurrent endometrial carcinoma: rationale, methods, and trial design. Int J Gynecol Cancer. 2024 Aug 05; 34(8):1283-1289.
-
Proteomics Analysis of Interactions between Drug-Resistant and Drug-Sensitive Cancer Cells: Comparative Studies of Monoculture and Coculture Cell Systems. J Proteome Res. 2024 Jul 05; 23(7):2608-2618.
-
Long-term follow-up of efficacy and safety of selinexor maintenance treatment in patients with TP53wt advanced or recurrent endometrial cancer: A subgroup analysis of the ENGOT-EN5/GOG-3055/SIENDO study. Gynecol Oncol. 2024 06; 185:202-211.
-
CopA3 treatment suppressed multidrug resistivity in HCT-116 cell line by p53-induced degradation of hypoxia-inducible factor 1a. Life Sci. 2023 Sep 15; 329:121933.
-
CopA3 peptide inhibits MDM2-p53 complex stability in colorectal cancers and activates p53 mediated cell death machinery. Life Sci. 2023 Apr 01; 318:121476.
-
Rhabdomyolysis-induced acute kidney injury and concomitant apoptosis induction via ROS-mediated ER stress is efficaciously counteracted by epigallocatechin gallate. J Nutr Biochem. 2022 Dec; 110:109134.
-
HPV51-associated Leiomyosarcoma: A Novel Class of TP53/RB1-Wildtype Tumor With Predilection for the Female Lower Reproductive Tract. Am J Surg Pathol. 2022 06 01; 46(6):729-741.
-
Genomic landscape of gliosarcoma: distinguishing features and targetable alterations. Sci Rep. 2021 09 09; 11(1):18009.
-
Mutated p53 portends improvement in outcomes when bevacizumab is combined with chemotherapy in advanced/recurrent endometrial cancer: An NRG Oncology study. Gynecol Oncol. 2021 04; 161(1):113-121.
-
The transcriptional cofactor Jab1/Cops5 is crucial for BMP-mediated mouse chondrocyte differentiation by repressing p53 activity. J Cell Physiol. 2021 08; 236(8):5686-5697.