Evidence map›Paper›PMID 31292161›Full record

ReviewCancer research2019

Recent Advances Targeting CCR5 for Cancer and Its Role in Immuno-Oncology.

Xuanmao Jiao, Omar Nawab, Tejal Patel, Andrew V Kossenkov, Niels Halama, Dirk Jaeger, Richard G Pestell

Open access · bronzeAbstract readReview
In one paragraph

Review in Cancer research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 141 papers.

0numbers the graph read from it
0cells of the map it votes in
141citing papers in PubMed
11.3field-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

141 citing papers in PubMed, 227 citations in OpenAlex.

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  14. Searching for a HIV-1 Cure.Theranostics · 2026
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81 more citing papers are in PubMed but not listed here.

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

7 authors at 4 institutions in 2 countries.

Xuanmao JiaoPennsylvania Cancer and Regenerative Medicine Research Center, Baruch S. Blumberg Institute, Pennsylvania Biotechnology Center, Wynnewood, Pennsylvania.
Omar NawabPennsylvania Cancer and Regenerative Medicine Research Center, Baruch S. Blumberg Institute, Pennsylvania Biotechnology Center, Wynnewood, Pennsylvania.
Tejal PatelXavier University School of Medicine, Woodbury, New York.
Andrew V KossenkovWistar Institute, Philadelphia, Pennsylvania.
Niels HalamaDepartment of Medical Oncology, National Center for Tumor Diseases (NCT) Heidelberg, Heidelberg University Hospital, Heidelberg, Germany.ORCID 0000-0003-0344-6027
Dirk JaegerDepartment of Medical Oncology, National Center for Tumor Diseases (NCT) Heidelberg, Heidelberg University Hospital, Heidelberg, Germany.
Richard G PestellPennsylvania Cancer and Regenerative Medicine Research Center, Baruch S. Blumberg Institute, Pennsylvania Biotechnology Center, Wynnewood, Pennsylvania. Richard.Pestell@bblumberg.org.
Heidelberg University · DEThe Wistar Institute · USWoodbury University · USBaruch S. Blumberg Institute · US

Funding

DACH1/Eya Cell fate determination factor and mammary tumorigenesisR01CA132115 · NCI · THOMAS JEFFERSON UNIVERSITY · PI PESTELL, RICHARD G · 2009 to 2018
$3.1M
Integrative Approach to Comprehensive Analysis of High Throughput Data on a Cancer Center LevelR50CA211199 · NCI · WISTAR INSTITUTE · PI Andrew V Kossenkov · 2016 to 2026
$1.6M
NCI NIH HHS R01 CA132115NCI NIH HHS R50 CA211199
6 · The paper itself

Abstract

Experiments of nature have revealed the peculiar importance of the G-protein-coupled receptor, C-C chemokine receptor type 5 (CCR5), in human disease since ancient times. The resurgence of interest in heterotypic signals in the onset and progression of tumorigenesis has led to the current focus on CCR5 as an exciting new therapeutic target for metastatic cancer with clinical trials now targeting breast and colon cancer. The eutopic expression of CCR5 activates calcium signaling and thereby augments regulatory T cell (Treg) differentiation and migration to sites of inflammation. The misexpression of CCR5 in epithelial cells, induced upon oncogenic transformation, hijacks this migratory phenotype. CCR5 reexpression augments resistance to DNA-damaging agents and is sufficient to induce cancer metastasis and "stemness". Recent studies suggest important cross-talk between CCR5 signaling and immune checkpoint function. Because CCR5 on Tregs serves as the coreceptor for human immunodeficiency virus (HIV) entry, CCR5-targeted therapeutics used in HIV, [small molecules (maraviroc and vicriviroc) and a humanized mAb (leronlimab)], are now being repositioned in clinical trials as cancer therapeutics. As CCR5 is expressed on a broad array of tumors, the opportunity for therapeutic repositioning and the rationale for combination therapy approaches are reviewed herein.

Indexed as

AnimalsCarcinogenesisHumansImmunotherapyNeoplasmsReceptors, CCR5CCR5 protein, humanReceptors, CCR5

Identifiers

PMID31292161
PMCPMC6810651
OpenAlexW2959034083

What OpenQuestion holds

Textmetadata
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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.