ArticleCell cycle (Georgetown, Tex.)2013
Genetic variants and mutations of PPM1D control the response to DNA damage.
Article in Cell cycle (Georgetown, Tex.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
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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.
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Who cites it
30 citing papers in PubMed, 44 citations in OpenAlex.
- Trial
- Review
- Next-generation sequencing identifies the presence of protein phosphatase 1D, PPM1D, as a potential biomarker of resistance to PARP inhibition in metastatic castration-resistant prostate cancer.American journal of clinical and experimental urology · 2025Article
- [The role of clonal hematopoiesis in the molecular diagnostics of solid tumors].Magyar onkologia · 2024Review
- PPM1D/Wip1 is amplified, overexpressed, and mutated in human non-Hodgkin's lymphomas.Molecular biology reports · 2024Article
- Whole exome/genome sequencing in cyclic vomiting syndrome reveals multiple candidate genes, suggesting a model of elevated intracellular cations and mitochondrial dysfunction.Frontiers in neurology · 2023Article
- PPM1D in Solid and Hematologic Malignancies: Friend and Foe?Molecular cancer research : MCR · 2022Article
- Molecular Pathways in Clonal Hematopoiesis: From the Acquisition of Somatic Mutations to Transformation into Hematologic Neoplasm.Life (Basel, Switzerland) · 2022Review
- Somatic Mutations in Cardiovascular Disease.Circulation research · 2022Review
- Exploring the Associations Between Clonal Hematopoiesis of Indeterminate Potential, Myeloid Malignancy, and Atherosclerosis.Methods in molecular biology (Clifton, N.J.) · 2022Review
- Article
- High Expression ofCancers · 2021Article
- Inhibition of the DNA damage response phosphatase PPM1D reprograms neutrophils to enhance anti-tumor immune responses.Nature communications · 2021Article
- Arctigenin suppresses fibroblast activity and extracellular matrix deposition in hypertrophic scarring by reducing inflammation and oxidative stress.Molecular medicine reports · 2020Article
- Review
- Silencing of PPM1D inhibits cell proliferation and invasion through the p38 MAPK and p53 signaling pathway in papillary thyroid carcinoma.Oncology reports · 2020Article
- Spinal cord high-grade infiltrating gliomas in adults: clinico-pathological and molecular evaluation.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2019Article
- Inhibition of mutant PPM1D enhances DNA damage response and growth suppressive effects of ionizing radiation in diffuse intrinsic pontine glioma.Neuro-oncology · 2019Article
- Absence of EIF1AX, PPM1D, and CHEK2 mutations reported in Thyroid Cancer Genome Atlas (TCGA) in a large series of thyroid cancer.Endocrine · 2019Article
- PPM1D Mutations Drive Clonal Hematopoiesis in Response to Cytotoxic Chemotherapy.Cell stem cell · 2018Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
The Wip1 phosphatase is an oncogene that is overexpressed in a variety of primary human cancers. We were interested in identifying genetic variants that could change Wip1 activity. We identified 3 missense SNPs of the human Wip1 phosphatase, L120F, P322Q, and I496V confer a dominant-negative phenotype. On the other hand, in primary human cancers, PPM1D mutations commonly result in a gain-of-function phenotype, leading us to identify a hot-spot truncating mutation at position 525. Surprisingly, we also found a significant number of loss-of-function mutations of PPM1D in primary human cancers, both in the phosphatase domain and in the C terminus. Thus, PPM1D has evolved to generate genetic variants with lower activity, potentially providing a better fitness for the organism through suppression of multiple diseases. In cancer, however, the situation is more complex, and the presence of both activating and inhibiting mutations requires further investigation to understand their contribution to tumorigenesis.
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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.