Evidence map›Paper›PMID 30990165›Full record

ArticleeLife2019

CCL5 promotes breast cancer recurrence through macrophage recruitment in residual tumors.

Andrea Walens, Ashley V DiMarco, Ryan Lupo, Benjamin R Kroger, Jeffrey S Damrauer, James V Alvarez

Open access · goldAbstract read
In one paragraph

Article in eLife, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 125 papers.

0numbers the graph read from it
0cells of the map it votes in
125citing papers in PubMed
11.1field-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

125 citing papers in PubMed, 194 citations in OpenAlex.

  1. Article
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  5. Immunity and Beyond: Emerging Roles of Monocytes and Macrophages in Cancer.Advances in experimental medicine and biology · 2026
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  19. Regulation of ROS signaling by TIGAR induces cancer-modulating responses in the tumor microenvironment.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  20. Article

65 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

6 authors at 1 institution in 1 country.

Andrea WalensDepartment of Pharmacology and Cancer Biology, Duke University, Durham, United States.
Ashley V DiMarcoDepartment of Pharmacology and Cancer Biology, Duke University, Durham, United States.
Ryan LupoDepartment of Pharmacology and Cancer Biology, Duke University, Durham, United States.
Benjamin R KrogerDepartment of Pharmacology and Cancer Biology, Duke University, Durham, United States.
Jeffrey S DamrauerDepartment of Pharmacology and Cancer Biology, Duke University, Durham, United States.ORCID 0000-0001-8148-0285
James V AlvarezDepartment of Pharmacology and Cancer Biology, Duke University, Durham, United States.ORCID 0000-0003-2910-7621
Duke University · US

Funding

Viral Oncology Training GrantT32CA009111 · NCI · DUKE UNIVERSITY · PI LUFTIG, MICAH A. · 1985 to 2023
$8.9M
Par-4 Regulation and Function in Breast Cancer Dormancy and RecurrenceR01CA208042 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI ALVAREZ, JAMES V · 2016 to 2020
$2.1M
Awakening the dormant tumor: the role of the tumor microenvironment in breast cancer recurrenceF31CA220957 · NCI · DUKE UNIVERSITY · PI WALENS, ANDREA NICOLE · 2017 to 2018
$69k
NCI NIH HHS F31 CA220957NCI NIH HHS R01 CA208042NCI NIH HHS T32 CA009111
6 · The paper itself

Abstract

Over half of breast-cancer-related deaths are due to recurrence 5 or more years after initial diagnosis and treatment. This latency suggests that a population of residual tumor cells can survive treatment and persist in a dormant state for many years. The role of the microenvironment in regulating the survival and proliferation of residual cells following therapy remains unexplored. Using a conditional mouse model for Her2-driven breast cancer, we identify interactions between residual tumor cells and their microenvironment as critical for promoting tumor recurrence. Her2 downregulation leads to an inflammatory program driven by TNFα/NFκB signaling, which promotes immune cell infiltration in regressing and residual tumors. The cytokine CCL5 is elevated following Her2 downregulation and remains high in residual tumors. CCL5 promotes tumor recurrence by recruiting CCR5-expressing macrophages, which may contribute to collagen deposition in residual tumors. Blocking this TNFα-CCL5-macrophage axis may be efficacious in preventing breast cancer recurrence.

Indexed as

AnimalsBreast NeoplasmsChemokine CCL5Disease Models, AnimalErb-b2 Receptor Tyrosine KinasesMacrophagesMiceNeoplasm, ResidualRecurrenceTumor Necrosis Factor-alphaCcl5 protein, mouseChemokine CCL5Erbb2 protein, mouseErb-b2 Receptor Tyrosine KinasesTumor Necrosis Factor-alphabreast cancercancer biologyCCL5collagenimmunologyinflammationmacrophagemouse

Identifiers

PMID30990165
PMCPMC6478432
OpenAlexW2923540337

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.