Evidence map›Paper›PMID 24752443›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2014

Murine B-1 B cell progenitors initiate B-acute lymphoblastic leukemia with features of high-risk disease.

Encarnacion Montecino-Rodriguez, Katy Li, Michael Fice, Kenneth Dorshkind

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

17 citing papers in PubMed, 23 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

4 authors at 1 institution in 1 country.

Encarnacion Montecino-RodriguezDepartment of Pathology and Laboratory Medicine, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA 90095.
Katy LiDepartment of Pathology and Laboratory Medicine, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA 90095.
Michael FiceDepartment of Pathology and Laboratory Medicine, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA 90095.
Kenneth DorshkindDepartment of Pathology and Laboratory Medicine, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA 90095 kdorshki@mednet.ucla.edu.
University of California, Los Angeles · US

Funding

Women's CancersP30CA016042 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Samuel Wheeler French · 1985 to 2026
$134.5M
Virology CoreP30AI028697 · NIAID · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI ANTON, PETER A · 1991 to 2018
$39.9M
Immunobiology of B Cell DifferentiationR37AI021256 · NIAID · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI DORSHKIND, KENNETH ALLAN · 2009 to 2018
$3.8M
IMMUNOBIOLOGY OF B CELL DIFFERENTIATIONR01AI021256 · NIAID · UNIVERSITY OF CALIFORNIA RIVERSIDE · PI DORSHKIND, KENNETH ALLAN · 1985 to 2007
$2.3M
Impact of B-Cell Lineage on Progression of B-Acute Lymphoblastic LeukemiaR21CA173028 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI DORSHKIND, KENNETH ALLAN, KOGAN, SCOTT C. · 2013 to 2014
$380k
NCI NIH HHS CA16042NCI NIH HHS CA173028NCI NIH HHS P30 CA016042NCI NIH HHS R21 CA173028NIAID NIH HHS AI021256NIAID NIH HHS AI28697NIAID NIH HHS P30 AI028697NIAID NIH HHS R01 AI021256NIAID NIH HHS R37 AI021256
6 · The paper itself

Abstract

B-1 and B-2 B cells derive from distinct progenitors that emerge in overlapping waves of development. The number of murine B-1 progenitors peaks during fetal development whereas B-2 B cell production predominates in adult bone marrow. Many genetic mutations that underlie B-acute lymphoblastic leukemia (B-ALL) occur in the fetus, at which time B-1 progenitor numbers are high. However, whether B-ALL can initiate in B-1 progenitors is unknown. In the present study, we report that BCR-ABL-transformed murine B-1 progenitors can be B-ALL cells of origin and demonstrate that they initiate disease more rapidly than do oncogene-expressing B-2 progenitors. We further demonstrate that B-1 progenitors exhibit relative resistance to apoptosis and undergo significant growth following oncogene expression, and we propose that these properties underlie the accelerated kinetics with which they initiate leukemia. These results provide a developmental perspective on the origin of B-ALL and indicate B cell lineage as a factor influencing disease progression.

Indexed as

AnimalsB-Lymphocyte SubsetsCell Transformation, NeoplasticFusion Proteins, bcr-ablMiceMice, KnockoutPrecursor B-Cell Lymphoblastic Leukemia-LymphomaPrecursor Cells, B-LymphoidFusion Proteins, bcr-abl

Identifiers

PMID24752443
PMCPMC4028370
OpenAlexW2159136295

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.