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

Single-cell genomics reveals the genetic and molecular bases for escape from mutational epistasis in myeloid neoplasms.

Blood - 24 Sept 2020

Taylor Justin, Mi Xiaoli, North Khrystyna, Binder Moritz, Penson Alexander, Lasho Terra, Knorr Katherine, Haddadin Michael, Liu Bo, Pangallo Joseph, Benbarche Salima, Wiseman Daniel, Tefferi Ayalew, Halene Stephanie, Liang Yang, Patnaik Mrinal M, Bradley Robert K, Abdel-Wahab Omar

Abstract excerpt

Large-scale sequencing studies of hematologic malignancies have revealed notable epistasis among high-frequency mutations. One of the most striking examples of epistasis occurs for mutations in RNA splicing factors. These lesions are among the most common alterations in myeloid neoplasms and generally occur in a mutually exclusive manner, a finding attributed to their synthetic lethal interactions and/or...

Read the complete abstract on PubMed

Topics

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

Share to DNA Mutational Analysis
Share to Epistasis, Genetic

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Genomics

Share to Hematologic Neoplasms

Share to Leukemia, Myeloid

Share to RNA Splicing

Share to RNA Splicing Factors

Share to Single-Cell Analysis

Source

Open in PubMed Open full text

Identifiers

PMID: 32640014
DOI: 10.1182/blood.2020006868
PMCID: PMC7515689

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Single-cell genomics reveals the genetic and molecular bases for escape from mutational epistasis in myeloid neoplasms.PMID 32640014Read ↗

U2af1S34F and U2af1Q157R myeloid neoplasm-associated hotspot mutations induce distinct hematopoietic phenotypes in mice.Semantic proximity Read ↗

Rare and private spliceosomal gene mutations drive partial, complete, and dual phenocopies of hotspot alterations.Semantic proximity Read ↗

Clinical presentation and differential splicing of SRSF2, U2AF1 and SF3B1 mutations in patients with acute myeloid leukemia.Semantic proximity Read ↗

Co-mutation pattern, clonal hierarchy, and clone size concur to determine disease phenotype of SRSF2P95-mutated neoplasms.Semantic proximity Read ↗

Comprehensive genomic profiling reveals molecular subsets of ASXL1-mutated myeloid neoplasms.Semantic proximity Read ↗

SRSF2 mutations drive oncogenesis by activating a global program of aberrant alternative splicing in hematopoietic cells.Semantic proximity Read ↗

Impact of single versus multiple spliceosome mutations on myelodysplastic syndrome.Semantic proximity Read ↗

U2af1S34F and U2af1Q157R myeloid neoplasm-associated hotspot mutations induce distinct hematopoietic phenotypes in miceSemantic proximity Read ↗

Synthetic Lethal and Convergent Biological Effects of Cancer-Associated Spliceosomal Gene Mutations.Semantic proximity Read ↗

Complex landscape of alternative splicing in myeloid neoplasms.Semantic proximity Read ↗

Overcoming mutational complexity in acute myeloid leukemia by inhibition of critical pathways.Semantic proximity Read ↗

SpliceUp: Predicting <i>SF3B1</i> mutations in individual cells via aberrant splice site activation from scRNA-seq dataSemantic proximity Read ↗

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