ReviewCold Spring Harbor perspectives in medicine2016
Genetic Modifiers of the p53 Pathway.
Review in Cold Spring Harbor perspectives in medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
45 citing papers in PubMed, 66 citations in OpenAlex.
- The role of BMI1 in assessing endometrial receptivity and its clinical implications.Frontiers in medicine · 2026Article
- Genetic Variations inCancers · 2025Article
- Genetic variability profiling of the p53 signaling pathway in chronic lymphocytic leukemia. Individual and combined analysis of TP53, MDM2 and NQO1 gene variants.Annals of hematology · 2024Article
- Article
- Article
- The African-centric P47S Variant ofCancer research communications · 2023Article
- Review
- Association of TP53 gene polymorphisms with the risk of acute lymphoblastic leukemia in Moroccan children.Molecular biology reports · 2022Article
- Targeted Next-Generation Sequencing of Thymic Epithelial Tumours Revealed Pathogenic Variants inCancers · 2022Article
- Association of TP53 and CDKN2A Mutation Profile with Tumor Mutation Burden in Head and Neck Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2022Article
- The Role of the CREB Protein Family Members and the Related Transcription Factors in Radioresistance Mechanisms.Life (Basel, Switzerland) · 2021Review
- miR-138-5p induces aggressive traits by targeting Trp53 expression in murine melanoma cells, and correlates with poor prognosis of melanoma patients.Neoplasia (New York, N.Y.) · 2021Article
- Mechanisms of TP53 Pathway Inactivation in Embryonic and Somatic Cells-Relevance for Understanding (Germ Cell) Tumorigenesis.International journal of molecular sciences · 2021Review
- Associations ofJournal of clinical medicine · 2021Article
- Cancer and Tumour Suppressor p53 Encounters at the Juncture of Sex Disparity.Frontiers in genetics · 2021Review
- MiR-3614-5p Is a Potential Novel Biomarker for Colorectal Cancer.Frontiers in genetics · 2021Article
- Long noncoding RNA MEG3 blocks telomerase activity in human liver cancer stem cells epigenetically.Stem cell research & therapy · 2020Article
- Survival of Lung Cancer Patients Dependent on the LOH Status forInternational journal of molecular sciences · 2020Article
- Evaluation ofReports of biochemistry & molecular biology · 2020Article
- BMP9 mediates the anticancer activity of evodiamine through HIF‑1α/p53 in human colon cancer cells.Oncology reports · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The tumor suppressor gene TP53 is the most frequently mutated gene in human cancer; this gene is subject to inactivation by mutation or deletion in >50% of sporadic cancers. Genes that encode proteins that regulate p53 function, such as MDM2, MDM4, and CDKN2A (p14(ARF)) are also frequently altered in tumors, and it is generally believed that the p53 pathway is likely to be inactivated by mutation in close to 100% of human tumors. Unlike most other cancer-relevant signaling pathways, some of the genes in the p53 pathway contain functionally significant single nucleotide polymorphisms (SNPs) that alter the amplitude of signaling by this protein. These variants, thus, have the potential to impact cancer risk, progression, and the efficacy of radiation and chemotherapy. In addition, the p53 pathway plays a role in other biological processes, including metabolism and reproductive fitness, so these variants have the potential to modify other diseases as well. Here we have chosen five polymorphisms in three genes in the p53 pathway for review, two in TP53, two in MDM2, and one in MDM4. These five variants were selected based on the quality and reproducibility of functional data associated with them, as well as the convincingness of epidemiological data in support of their association with disease. We also highlight two other polymorphisms that may affect p53 signaling, but for which functional or association data are still forthcoming (KITLG and ANRIL). Finally, we touch on three questions regarding genetic modifiers of the p53 pathway: Why did these variants arise? Were they under selection pressure? And, is there compelling evidence to support genotyping these variants to better predict disease risk and prognosis?
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.