Evidence map›Paper›PMID 22878500›Full record

ArticleScience (New York, N.Y.)2012

Loss of the tumor suppressor BAP1 causes myeloid transformation.

Anwesha Dey, Dhaya Seshasayee, Rajkumar Noubade, Dorothy M French, Jinfeng Liu, Mira S Chaurushiya, Donald S Kirkpatrick, Victoria C Pham, Jennie R Lill, Corey E Bakalarski and 17 more

Open access · greenAbstract read
In one paragraph

Article in Science (New York, N.Y.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 258 papers.

0numbers the graph read from it
0cells of the map it votes in
258citing papers in PubMed
22.2field-weighted citation impact, top 1% 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

258 citing papers in PubMed, 416 citations in OpenAlex.

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198 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

27 authors at 2 institutions in 1 country.

Anwesha DeyDepartment of Physiological Chemistry, Genentech, 1 DNA Way, South San Francisco, CA 94080, USA.
Dhaya Seshasayee
Rajkumar Noubade
Dorothy M French
Jinfeng Liu
Mira S Chaurushiya
Donald S Kirkpatrick
Victoria C Pham
Jennie R Lill
Corey E Bakalarski
Jiansheng Wu
Lilian Phu
Paula Katavolos
Lindsay M LaFave
Omar Abdel-Wahab
Zora Modrusan
Somasekar Seshagiri
Ken Dong
Zhonghua Lin
Mercedesz Balazs
Rowena Suriben
Kim Newton
Sarah Hymowitz
Guillermo Garcia-Manero
Flavius Martin
Ross L Levine
Vishva M Dixit
Acentech (United States) · USThe University of Texas MD Anderson Cancer Center · US

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Nicholas D Socci · 1985 to 2026
$347.4M
Role of TET2 mutations in malignant transformation and acute myeloid leukemiaR01CA173636 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI AIFANTIS, IANNIS, LEVINE, ROSS L · 2013 to 2022
$6.3M
NCI NIH HHS P30 CA008748NCI NIH HHS R01 CA173636
6 · The paper itself

Abstract

De-ubiquitinating enzyme BAP1 is mutated in a hereditary cancer syndrome with increased risk of mesothelioma and uveal melanoma. Somatic BAP1 mutations occur in various malignancies. We show that mouse Bap1 gene deletion is lethal during embryogenesis, but systemic or hematopoietic-restricted deletion in adults recapitulates features of human myelodysplastic syndrome (MDS). Knockin mice expressing BAP1 with a 3xFlag tag revealed that BAP1 interacts with host cell factor-1 (HCF-1), O-linked N-acetylglucosamine transferase (OGT), and the polycomb group proteins ASXL1 and ASXL2 in vivo. OGT and HCF-1 levels were decreased by Bap1 deletion, indicating a critical role for BAP1 in stabilizing these epigenetic regulators. Human ASXL1 is mutated frequently in chronic myelomonocytic leukemia (CMML) so an ASXL/BAP1 complex may suppress CMML. A BAP1 catalytic mutation found in a MDS patient implies that BAP1 loss of function has similar consequences in mice and humans.

Indexed as

Cell Transformation, NeoplasticGenes, Tumor SuppressorAnimalsBone Marrow TransplantationChromatin ImmunoprecipitationEmbryonic DevelopmentGene DeletionGene Expression RegulationGene Knock-In TechniquesHematopoiesisHost Cell Factor C1HumansLeukemia, Myelomonocytic, ChronicMiceMice, KnockoutMyelodysplastic SyndromesAsxl1 protein, mouseASXL2 protein, mouseBAP1 protein, humanBAP1 protein, mouseHcfc1 protein, mouseHost Cell Factor C1N-AcetylglucosaminyltransferasesRepressor ProteinsTumor Suppressor ProteinsUbiquitin Thiolesterase

Identifiers

PMID22878500
PMCPMC5201002
OpenAlexW1989561383

What OpenQuestion holds

Textmetadata
LicenceTDM
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.