Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Protein phosphatase 2A inactivation induces microsatellite instability, neoantigen production and immune response

15 Dec 2021

Abstract excerpt

Microsatellite-instable (MSI), a predictive biomarker for immune checkpoint blockade (ICB) response, is caused by mismatch repair deficiency (MMRd) that occurs through genetic or epigenetic silencing of MMR genes. Here, we report a mechanism of MMRd and demonstrate that protein phosphatase 2A (PP2A) deletion or inactivation converts cold microsatellite-stable (MSS) into MSI tumours through two orthogonal...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Cancer Immunotherapy and Biomarkers
Share to Ferroptosis and cancer prognosis
Share to Genetic factors in colorectal cancer

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 34911954
DOI: 10.1038/s41467-021-27620-x

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 8 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Protein phosphatase 2A inactivation induces microsatellite instability, neoantigen production and immune responsePMID 34911954Read ↗

Immunotherapy of MSI Cancer: Facts and HopesSemantic proximity Read ↗

Mismatch Repair Proteins Initiate Epigenetic Alterations during Inflammation-Driven TumorigenesisSemantic proximity Read ↗

Effect of MisMatch Repair Deficiency on metastasis occurrence modelized in a syngeneic mouse modelSemantic proximity Read ↗

Microsatellite instability-high colorectal cancer patient-derived xenograft models for cancer immunity research.Semantic proximity Read ↗

Inactivation of the mouse Msh2 gene results in mismatch repair deficiency, methylation tolerance, hyperrecombination, and predisposition to cancer.Semantic proximity Read ↗

Genetic and epigenetic analysis of the beta-2-microglobulin gene in microsatellite instable colorectal cancer.Semantic proximity Read ↗

Inducing mismatch repair deficiency sensitizes immune-cold neuroblastoma to anti-CTLA4 and generates broad anti-tumor immune memorySemantic proximity Read ↗

Parallel High-Throughput RNA Interference Screens Identify PINK1 as a Potential Therapeutic Target for the Treatment of DNA Mismatch Repair–Deficient CancersSemantic proximity Read ↗

Genetic and pharmacological modulation of DNA mismatch repair heterogeneous tumors promotes immune surveillanceSemantic proximity Read ↗

<i>MSH2</i> Dysregulation Is Triggered by Proinflammatory Cytokine Stimulation and Is Associated with Liver Cancer DevelopmentSemantic proximity Read ↗

Consequences of the Hsp110DE9 mutation in tumorigenesis and the 5-fluorouracil-based chemotherapy response in Msh2-deficient mice.Semantic proximity Read ↗

Mismatch repair proteins recruit DNA methyltransferase 1 to sites of oxidative DNA damageSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.