ArticleMolecular cancer research : MCR2022
PPM1D in Solid and Hematologic Malignancies: Friend and Foe?
Article in Molecular cancer research : MCR, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 22 citations in OpenAlex.
- Cancer treatment alters mutant selection in normal esophagus.Nature genetics · 2026Article
- The NeuroWES project: lessons learned from comprehensive phenotyping and genetic analysis of neurodevelopmental disorders over a decade.Human genetics · 2026Article
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- Biphasic high-grade cerebellar glioma with epithelial-like components: challenges in integrated diagnosis imposed by limited sampling.Brain tumor pathology · 2026Article
- CDK4/6 inhibition mitigates chemotherapy-induced expansion of TP53-mutant clonal hematopoiesis.Nature genetics · 2026Article
- Multi-Level Profiling of MAPK-Associated Genes and MicroRNAs Uncovers Regulatory Networks in Breast Cancer Subtypes.International journal of molecular sciences · 2025Article
- Analysis and Interpretation of Somatic NMD-Escaping Variants in Oncogenes and Dual-Function Genes across Adult and Pediatric Cancer Cohorts.medRxiv : the preprint server for health sciences · 2025Article
- Article
- Identification of small molecule inhibitors of PPM1D using an integrated drug discovery platform.iScience · 2025Article
- The Role of P53 in Immune Evasion and Therapeutic Strategies in Hematologic Malignancies.Journal of Cancer · 2025Review
- Long-term breast cancer response to CDK4/6 inhibition defined by TP53-mediated geroconversion.Cancer cell · 2024Article
- PPM1D/Wip1 is amplified, overexpressed, and mutated in human non-Hodgkin's lymphomas.Molecular biology reports · 2024Article
- Distinct landscape and clinical implications of therapy-related clonal hematopoiesis.The Journal of clinical investigation · 2024Review
- Identification of Small Molecule Inhibitors of PPM1D Using a Novel Drug Discovery Platform.bioRxiv : the preprint server for biology · 2024Article
- PPM1D activity promotes the replication stress caused by cyclin E1 overexpression.Molecular oncology · 2024Article
- Associations Between Cancer Predisposition Mutations and Clonal Hematopoiesis in Patients With Solid Tumors.JCO precision oncology · 2023Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
In the face of constant genomic insults, the DNA damage response (DDR) is initiated to preserve genome integrity; its disruption is a classic hallmark of cancer. Protein phosphatase Mg2+/Mn2+-dependent 1D (PPM1D) is a central negative regulator of the DDR that is mutated or amplified in many solid cancers. PPM1D overexpression is associated with increased proliferative and metastatic behavior in multiple solid tumor types and patients with PPM1D-mutated malignancies have poorer prognoses. Recent findings have sparked an interest in the role of PPM1D in hematologic malignancies. Acquired somatic mutations may provide hematopoietic stem cells with a competitive advantage, leading to a substantial proportion of mutant progeny in the peripheral blood, an age-associated phenomenon termed "clonal hematopoiesis" (CH). Recent large-scale genomic studies have identified PPM1D to be among the most frequently mutated genes found in individuals with CH. While PPM1D mutations are particularly enriched in patients with therapy-related myeloid neoplasms, their role in driving leukemic transformation remains uncertain. Here, we examine the mechanisms through which PPM1D overexpression or mutation may drive malignancy by suppression of DNA repair, cell-cycle arrest, and apoptosis. We also discuss the divergent roles of PPM1D in the oncogenesis of solid versus hematologic cancers with a view to clinical implications and new therapeutic avenues.
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