Evidence map›Paper›PMID 36911757›Full record

ArticleJournal of cellular signaling2023

Augmenting Venetoclax Activity Through Signal Transduction in AML.

Ian Michael Bouligny, Keri Renee Maher, Steven Grant

Open access · hybridAbstract read
In one paragraph

Article in Journal of cellular signaling, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.5field-weighted citation impact, top 17% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

4 citing papers in PubMed, 5 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Ian Michael BoulignyVirginia Commonwealth University Massey Cancer Center, Division of Hematology and Oncology, Department of Internal Medicine, 1300 E. Marshall St., Richmond, VA, USA.
Keri Renee MaherVirginia Commonwealth University Massey Cancer Center, Division of Hematology and Oncology, Department of Internal Medicine, 1300 E. Marshall St., Richmond, VA, USA.
Steven GrantVirginia Commonwealth University Massey Cancer Center, Division of Hematology and Oncology, Department of Internal Medicine, 1300 E. Marshall St., Richmond, VA, USA.
Virginia Commonwealth University · US

Funding

Virus Vector Shared ResourceP30CA016059 · NCI · VIRGINIA COMMONWEALTH UNIVERSITY · PI Renato Martins · 1985 to 2026
$51.0M
Princess Margaret Phase I Consorium (PMP1C)UM1CA186644 · NCI · UNIVERSITY HEALTH NETWORK · PI Philippe Bedard, Kevin D Courtney · 2014 to 2026
$16.6M
NCI NIH HHS P30 CA016059NCI NIH HHS UM1 CA186644
6 · The paper itself

Abstract

Venetoclax, a small-molecule B-cell lymphoma 2 (BCL-2) inhibitor, selectively eradicates leukemic stem cells (LSCs). While venetoclax has revolutionized the treatment of acute myeloid leukemia (AML), treatment failure and disease relapse are common. Mechanisms underlying venetoclax resistance are surprisingly heterogeneous. Venetoclax resistance encompasses a spectrum of genetic and epigenetic changes, with numerous pathways contributing to the upregulation of additional anti-apoptotic proteins. In this review, we address the mechanisms of venetoclax resistance in the context of signal transduction. We emphasize how aberrant cell signaling impairs apoptosis and predisposes to venetoclax failure. Commonly activated pathways, such as FLT3, PI3K/AKT/mTOR, and RAS, contribute to upregulated anti-apoptotic mediators and are frequently responsible for refractory disease or disease relapse. We highlight novel combination strategies aimed at disabling constitutively active signal transduction to augment response and overcome venetoclax resistance.

Indexed as

Acute myeloid leukemiaAkt pathwayApoptotic pathwaysB-cell lymphoma 2FMS-like tyrosine kinase 3Isocitrate dehydrogenase 1Isocitrate dehydrogenase 2MAPK pathway cell signalingSignal transduction cascades

Identifiers

PMID36911757
PMCPMC9997087
OpenAlexW4323352072

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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 Socratic graph.