Evidence map›Paper›PMID 23147254›Full record

ReviewLeukemia2013

The ASXL-BAP1 axis: new factors in myelopoiesis, cancer and epigenetics.

O Abdel-Wahab, A Dey

Abstract readReview
PubMed Publisher
In one paragraph

Review in Leukemia, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed, 2 pooled it
5.1field-weighted citation impact, top 4% 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

50 citing papers in PubMed, 2 syntheses or guidelines pooled it, 90 citations in OpenAlex.

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  18. Chronic Myelogenous Leukemia in Childhood.Current oncology reports · 2021
    Review
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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

2 authors at 1 institution in 1 country.

O Abdel-WahabHuman Oncology and Pathogenesis Program and Leukemia Service, Memorial Sloan-Kettering Cancer Center, New York, NY, USA. abdelwao@mskcc.org
A Dey
Memorial Sloan Kettering Cancer Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The recent identification of germline and somatic mutations in BAP1 as well as in multiple members of the ASXL (additional sex combs-like) family of genes has highlighted the role of these proteins in a diverse array of biological functions. A diverse number of possible functions have previously been ascribed to ASXL1 in non-hematopoietic contexts, including physical co-operativity with HP1a and LSD1. Here we discuss new evidence for a BAP1-independent function of ASXL1 in regulating histone H3 lysine 27 methylation through interactions with the Polycomb-repressive complex 2 (PRC2). BAP1, a nuclear-localized deubiquitinase, has been shown to interact with a number of proteins, including ASXL1 and/or ASXL2, but the functional importance of this interaction has remained elusive. Here, we highlight recent work revealing the critical function of BAP1 in restricting myelopoiesis and in regulating hematopoietic stem cell function. These data provide evidence that BAP1 and ASXL1 function as a novel class of tumor suppressors in myeloid malignancies. BAP1 functions through effects on stability of host cell factor-1, and O-GlcNAcylation, and ASXL1 impacts histone post-translational modifications through interaction with PRC2. Future studies investigating the mechanism of transformation by loss of BAP1 and ASXL1 may result in new therapeutic approaches to treat hematological malignancies.

Indexed as

EpigenomicsCell Transformation, NeoplasticHumansMyelopoiesisNeoplasmsRepressor ProteinsTumor Suppressor ProteinsUbiquitin ThiolesteraseASXL1 protein, humanBAP1 protein, humanRepressor ProteinsTumor Suppressor ProteinsUbiquitin Thiolesterase

Identifiers

PMID23147254
OpenAlexW2090150670

What OpenQuestion holds

Textmetadata
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 OpenQuestion graph.