Evidence map›Paper›PMID 28835371›Full record

ArticleMolecular cancer research : MCR2017

B-cell Receptor Signaling Regulates Metabolism in Chronic Lymphocytic Leukemia.

Hima V Vangapandu, Ondrej Havranek, Mary L Ayres, Benny Abraham Kaipparettu, Kumudha Balakrishnan, William G Wierda, Michael J Keating, R Eric Davis, Christine M Stellrecht, Varsha Gandhi

Open access · bronzeAbstract read
In one paragraph

Article in Molecular cancer research : MCR, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

33 citing papers in PubMed, 50 citations in OpenAlex.

  1. Article
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  3. PD-1 expression identifies proliferating malignant CLL B cells and is a potential biomarker of response to BTK inhibitor therapy.Proceedings of the National Academy of Sciences of the United States of America · 2025
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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

10 authors at 2 institutions in 1 country.

Hima V VangapanduDepartment of Experimental Therapeutics, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Ondrej HavranekMD Anderson Cancer Center UT Health Graduate School of Biomedical Sciences, Houston, Texas.
Mary L AyresDepartment of Experimental Therapeutics, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Benny Abraham KaipparettuDepartment of Molecular and Human Genetics, Baylor College of Medicine, Houston, Texas.
Kumudha BalakrishnanDepartment of Experimental Therapeutics, The University of Texas MD Anderson Cancer Center, Houston, Texas.
William G WierdaDepartment of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Michael J KeatingDepartment of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, Texas.
R Eric DavisMD Anderson Cancer Center UT Health Graduate School of Biomedical Sciences, Houston, Texas.
Christine M StellrechtDepartment of Experimental Therapeutics, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Varsha GandhiDepartment of Experimental Therapeutics, The University of Texas MD Anderson Cancer Center, Houston, Texas. vgandhi@mdanderson.org.
The University of Texas MD Anderson Cancer Center · USBaylor Genetics · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
Tissue CoreP01CA081534 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI KIPPS, THOMAS J · 2000 to 2016
$59.5M
NCI NIH HHS P01 CA081534NCI NIH HHS P30 CA016672
6 · The paper itself

Abstract

Peripheral blood chronic lymphocytic leukemia (CLL) cells are quiescent but have active transcription and translation processes, suggesting that these lymphocytes are metabolically active. Based on this premise, the metabolic phenotype of CLL lymphocytes was investigated by evaluating the two intracellular ATP-generating pathways. Metabolic flux was assessed by measuring glycolysis as extracellular acidification rate (ECAR) and mitochondrial oxidative phosphorylation as oxygen consumption rate (OCR) and then correlated with prognostic factors. Further, the impact of B-cell receptor signaling (BCR) on metabolism was determined by genetic ablation and pharmacological inhibitors. Compared with proliferative B-cell lines, metabolic fluxes of oxygen and lactate were low in CLL cells. ECAR was consistently low, but OCR varied considerably in human patient samples (

Indexed as

PrognosisAdenosine TriphosphateApoptosisCell Line, TumorCell ProliferationClass I Phosphatidylinositol 3-KinasesGlycolysisHumansLeukemia, Lymphocytic, Chronic, B-CellMetabolic Networks and PathwaysOxidative PhosphorylationOxygen ConsumptionReceptors, Antigen, B-CellZAP-70 Protein-Tyrosine KinaseAdenosine TriphosphateClass I Phosphatidylinositol 3-KinasesPIK3CD protein, humanReceptors, Antigen, B-CellZAP-70 Protein-Tyrosine Kinase

Identifiers

PMID28835371
PMCPMC5714317
OpenAlexW2745688238

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.