Evidence map›Paper›PMID 24811161›Full record

ReviewCurrent opinion in hematology2014

Targeting the B-cell receptor signaling pathway in B lymphoid malignancies.

Maike Buchner, Markus Müschen

Open access · greenAbstract readReview
In one paragraph

Review in Current opinion in hematology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

29 citing papers in PubMed, 42 citations in OpenAlex.

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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.

Maike BuchnerDepartment of Laboratory Medicine, University of California, San Francisco, San Francisco, California, USA.
Markus Müschen
University of California, San Francisco · US

Funding

Targeted activation of autoimmune checkpoints in B cell malignanciesR01CA157644 · NCI · YALE UNIVERSITY · PI Markus Müschen · 2011 to 2026
$5.7M
PRE-B CELL RECEPTOR SIGNALING IN ACUTE LYMPHOBLASTIC LEUKEMIAR01CA137060 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI MÜSCHEN, MARKUS · 2009 to 2016
$2.7M
AID-mediated genetic instability in BCR-ABL1-transformed B cell lineage leukemiaR01CA139032 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI MÜSCHEN, MARKUS · 2009 to 2013
$1.6M
Negative feedback signaling in tyrosine kinase-driven leukemiaR01CA172558 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI MÜSCHEN, MARKUS · 2013 to 2015
$972k
Targeting BCL6 in tyrosine kinase-driven leukemiaR01CA169458 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI MÜSCHEN, MARKUS · 2013 to 2015
$972k
Cancer Research UK 18131NCI NIH HHS R01 CA137060NCI NIH HHS R01CA137060NCI NIH HHS R01 CA139032NCI NIH HHS R01CA139032NCI NIH HHS R01 CA157644NCI NIH HHS R01CA157644NCI NIH HHS R01 CA169458NCI NIH HHS R01CA169458NCI NIH HHS R01 CA172558NCI NIH HHS R01CA172558Wellcome Trust 101880Wellcome Trust 101880Z/13/Z
6 · The paper itself

Abstract

purpose of reviewNormal B cells that have failed to productively rearrange immunoglobulin V region genes encoding a functional B-cell receptor (BCR) are destined to die. Likewise, the majority of B-cell malignancies remain dependent on functional BCR signaling, whereas in some subtypes BCR expression is missing and, apparently, counterselected. Here, we summarize the recent experimental evidence for the importance of BCR signaling and clinical concepts to target the BCR pathway in B-cell leukemia and lymphoma. RECENT

findingsAlthough the dependency on pre-BCR signaling in pre-B acute lymphoblastic leukemia (ALL) seems to be limited to few ALL subtypes (e.g. TCF3-PBX1), most mature B-cell lymphomas rely on BCR signaling provided by different stimuli, for example tonic B-cell signaling, chronic (auto)-antigen exposure, and self-binding properties of the BCR. The finding that in chronic lymphocytic leukemia, BCRs bind to an epitope on the BCR itself unravels a novel concept for chronic lymphocytic leukemia pathogenesis. SUMMARY: Targeting of the B-cell receptor tyrosine kinases spleen tyrosine kinase, Bruton's tyrosine kinase, and phosphatidylinositol 3-kinase achieve promising clinical responses in various mature B-cell malignancies and might also be useful in defined subsets of ALL. However, further understanding of the BCR signal integration in the different disease groups is required to accurately predict which groups of patients will benefit from BCR pathway inhibition.

Indexed as

Signal TransductionAnimalsCell Transformation, NeoplasticHumansLeukemia, B-CellLymphoma, B-CellMolecular Targeted TherapyReceptors, Antigen, B-CellReceptors, Antigen, B-Cell

Identifiers

PMID24811161
PMCPMC4136419
OpenAlexW2031362256

What OpenQuestion holds

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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.