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

CD44 loss of function sensitizes AML cells to the BCL-2 inhibitor venetoclax by decreasing CXCL12-driven survival cues

3 Jun 2021

Abstract excerpt

Acute myeloid leukemia (AML) has a poor prognosis under the current standard of care. In recent years, venetoclax, a BCL-2 inhibitor, was approved to treat patients who are ineligible for intensive induction chemotherapy. However, complete remission rates with venetoclax-based therapies are hampered by minimal residual disease (MRD) in a proportion of patients, leading to relapse. MRD is a result of leukemic stem...

Read the complete abstract on PubMed

Topics

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

Share to Acute Myeloid Leukemia Research
Share to Hematopoietic Stem Cell Transplantation
Share to Immune Cell Function and Interaction

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 34115113
DOI: 10.1182/blood.2020006343

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

CD44 loss of function sensitizes AML cells to the BCL-2 inhibitor venetoclax by decreasing CXCL12-driven survival cuesPMID 34115113Read ↗

AML under the Scope: Current Strategies and Treatment Involving FLT3 Inhibitors and Venetoclax-Based Regimens.Semantic proximity Read ↗

Targeting Bcl-2 Proteins in Acute Myeloid LeukemiaSemantic proximity Read ↗

Venetoclax resistance: mechanistic insights and future strategiesSemantic proximity Read ↗

Ex vivo characterization of acute myeloid leukemia patients undergoing hypomethylating agents and venetoclax regimen reveals a venetoclax-specific effect on non-suppressive regulatory T cells and bona fide PD-1+TIM3+ exhausted CD8+ T cellsSemantic proximity Read ↗

Anlotinib Induced Venetoclax-resistant Acute Myeloid Leukemia Stem Cells Apoptosis through Downregulating Mcl-1-mediated Anti-apoptoeic PathwaySemantic proximity Read ↗

Unraveling Venetoclax Resistance: Navigating the Future of HMA/Venetoclax-Refractory AML in the Molecular EraSemantic proximity Read ↗

Venetoclax durable response in adult relapsed/refractory Philadelphia-negative acute lymphoblastic leukemia with JAK/STAT pathway alterationsSemantic proximity Read ↗

Venetoclax Resistance in Acute Myeloid LeukemiaSemantic proximity Read ↗

The UBE2J2/UBE2K-MARCH5 ubiquitination machinery regulates apoptosis in response to venetoclax in acute myeloid leukemiaSemantic proximity Read ↗

CXCR4 as a therapeutic target in acute myeloid leukemia.Semantic proximity Read ↗

A Novel MCL1 Inhibitor Combined with Venetoclax Rescues Venetoclax-Resistant Acute Myelogenous LeukemiaSemantic proximity Read ↗

Venetoclax-Resistant T-ALL Cells Display Distinct Cancer Stem Cell Signatures and Enrichment of Cytokine SignalingSemantic proximity Read ↗

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