Evidence map›Paper›PMID 27334834›Full record

ArticleClinical cancer research : an official journal of the American Association for Cancer Research2016

Colony-Stimulating Factor-1 Receptor Is Required for Nurse-like Cell Survival in Chronic Lymphocytic Leukemia.

Avery Polk, Ye Lu, Tianjiao Wang, Erlene Seymour, Nathanael G Bailey, Jack W Singer, Philip S Boonstra, Megan S Lim, Sami Malek, Ryan A Wilcox

Open access · bronzeAbstract read
In one paragraph

Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.6field-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

35 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

10 authors at 1 institution in 1 country.

Avery PolkDepartment of Internal Medicine, Division of Hematology and Oncology, University of Michigan, Ann Arbor, Michigan.
Ye LuDepartment of Internal Medicine, Division of Hematology and Oncology, University of Michigan, Ann Arbor, Michigan.
Tianjiao WangDepartment of Internal Medicine, Division of Hematology and Oncology, University of Michigan, Ann Arbor, Michigan.
Erlene SeymourDepartment of Internal Medicine, Division of Hematology and Oncology, University of Michigan, Ann Arbor, Michigan.
Nathanael G BaileyDepartment of Pathology, University of Michigan, Ann Arbor, Michigan.
Jack W SingerCTI Biopharma, Seattle, Washington.
Philip S BoonstraDepartment of Biostatistics, University of Michigan, Ann Arbor, Michigan.
Megan S LimDepartment of Pathology, University of Michigan, Ann Arbor, Michigan.
Sami MalekDepartment of Internal Medicine, Division of Hematology and Oncology, University of Michigan, Ann Arbor, Michigan.
Ryan A WilcoxDepartment of Internal Medicine, Division of Hematology and Oncology, University of Michigan, Ann Arbor, Michigan. rywilcox@med.umich.edu.
University of Michigan–Ann Arbor · US

Funding

XenograftP30CA046592 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI THEODORE S LAWRENCE · 1988 to 2026
$178.2M
Research Education CoreP30AG024824 · NIA · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Neil Alexander · 2004 to 2026
$29.2M
The role of GATA-3 in T-cell lymphomasK08CA172215 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI WILCOX, RYAN A · 2013 to 2017
$893k
NCI NIH HHS K08 CA172215NCI NIH HHS P30 CA046592NIA NIH HHS P30 AG024824
6 · The paper itself

Abstract

purposeMonocytes and their progeny are abundant constituents of the tumor microenvironment in lymphoproliferative disorders, including chronic lymphocytic leukemia (CLL). Monocyte-derived cells, including nurse-like cells (NLC) in CLL, promote lymphocyte proliferation and survival, confer resistance to chemotherapy, and are associated with more rapid disease progression. Colony-stimulating factor-1 receptor (CSF-1R) regulates the homeostatic survival of tissue-resident macrophages. Therefore, we sought to determine whether CSF-1R is similarly required for NLC survival. EXPERIMENTAL

designCSF-1R expression by NLC was examined by flow cytometry and IHC. CSF-1R blocking studies were performed using an antagonistic mAb to examine its role in NLC generation and in CLL survival. A rational search strategy was performed to identify a novel tyrosine kinase inhibitor (TKI) targeting CSF-1R. The influence of TKI-mediated CSF-1R inhibition on NLC and CLL viability was examined.

resultsWe demonstrated that the generation and survival of NLC in CLL is dependent upon CSF-1R signaling. CSF-1R blockade is associated with significant depletion of NLC and consequently inhibits CLL B-cell survival. We found that the JAK2/FLT3 inhibitor pacritinib suppresses CSF-1R signaling, thereby preventing the generation and survival of NLC and impairs CLL B-cell viability.

conclusionsCSF-1R is a novel therapeutic target that may be exploited in lymphoproliferative disorders, like CLL, that are dependent upon lymphoma-associated macrophages. Clin Cancer Res; 22(24); 6118-28. ©2016 AACR.

Indexed as

B-LymphocytesCell ProliferationCell SurvivalHumansLeukemia, Lymphocytic, Chronic, B-CellMacrophagesMonocytesProtein Kinase InhibitorsReceptor, Macrophage Colony-Stimulating FactorReceptor Protein-Tyrosine KinasesReceptors, Granulocyte-Macrophage Colony-Stimulating FactorSignal TransductionCSF1R protein, humanProtein Kinase InhibitorsReceptor, Macrophage Colony-Stimulating FactorReceptor Protein-Tyrosine KinasesReceptors, Granulocyte-Macrophage Colony-Stimulating Factor

Identifiers

PMID27334834
PMCPMC5161678
OpenAlexW2467219218

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.