Evidence map›Paper›PMID 25887413›Full record

ArticleBreast cancer research : BCR2015

Mesenchymal stem cells mediate the clinical phenotype of inflammatory breast cancer in a preclinical model.

Lara Lacerda, Bisrat G Debeb, Daniel Smith, Richard Larson, Travis Solley, Wei Xu, Savitri Krishnamurthy, Yun Gong, Lawrence B Levy, Thomas Buchholz and 3 more

Open access · goldAbstract read
In one paragraph

Article in Breast cancer research : BCR, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed, 1 pooled it
2.9field-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

43 citing papers in PubMed, 1 synthesis or guideline pooled it, 59 citations in OpenAlex.

  1. Pooled it
  2. Reprogramming the Immune Landscape of Inflammatory Breast Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Review
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  16. Article
  17. Breast cancer resistance mechanisms: challenges to immunotherapy.Breast cancer research and treatment · 2021
    Review
  18. Review
  19. Article
  20. Review
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

13 authors at 1 institution in 1 country.

Lara LacerdaDepartment of Radiation Oncology, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Blvd., Houston, TX, 77030, USA. lcalvarez@mdanderson.org.
Bisrat G DebebDepartment of Radiation Oncology, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Blvd., Houston, TX, 77030, USA. bgdebeb@mdanderson.org.
Daniel SmithDepartment of Radiation Oncology, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Blvd., Houston, TX, 77030, USA. dlsmith2@mdanderson.org.
Richard LarsonDepartment of Radiation Oncology, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Blvd., Houston, TX, 77030, USA. ralarson@mdanderson.org.
Travis SolleyDepartment of Radiation Oncology, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Blvd., Houston, TX, 77030, USA. tnsolley@mdanderson.org.
Wei XuDepartment of Radiation Oncology, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Blvd., Houston, TX, 77030, USA. weixu@mdanderson.org.
Savitri KrishnamurthyMorgan Welch Inflammatory Breast Cancer Program, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Blvd., Houston, TX, 77030, USA. skrishna@mdanderson.org.
Yun GongMorgan Welch Inflammatory Breast Cancer Program, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Blvd., Houston, TX, 77030, USA. yungong@mdanderson.org.
Lawrence B LevyDepartment of Radiation Oncology, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Blvd., Houston, TX, 77030, USA. lblevy@mdanderson.org.
Thomas BuchholzDepartment of Radiation Oncology, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Blvd., Houston, TX, 77030, USA. tbuchhol@mdanderson.org.
Naoto T UenoMorgan Welch Inflammatory Breast Cancer Program, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Blvd., Houston, TX, 77030, USA. nueno@mdanderson.org.
Ann KloppDepartment of Radiation Oncology, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Blvd., Houston, TX, 77030, USA. aklopp@mdanderson.org.
Wendy A WoodwardDepartment of Radiation Oncology, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Blvd., Houston, TX, 77030, USA. wwoodward@mdanderson.org.
The University of Texas MD Anderson Cancer Center · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
Human Breast Cancer Stem Cell SurrogatesR01CA138239 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI CRISTOFANILLI, MASSIMO, REUBEN, JAMES MARTIN · 2008 to 2012
$2.8M
(PQD4) SIGNS OF INFLAMMATORY BREAST CANCER ARE CAUSED BY STROMAL FIELD EFFECTSR01CA180061 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI WOODWARD, WENDY A · 2013 to 2016
$1.9M
NCI NIH HHS 1R01CA180061-01NCI NIH HHS CA016672NCI NIH HHS P30 CA016672NCI NIH HHS R01 CA138239NCI NIH HHS R01CA138239-01NCI NIH HHS R01 CA180061
6 · The paper itself

Abstract

introductionInflammatory breast cancer (IBC) is an aggressive type of breast cancer, characterized by very rapid progression, enlargement of the breast, skin edema causing an orange peel appearance (peau d'orange), erythema, thickening, and dermal lymphatic invasion. It is characterized by E-cadherin overexpression in the primary and metastatic disease, but to date no robust molecular features that specifically identify IBC have been reported. Further, models that recapitulate all of these clinical findings are limited and as a result no studies have demonstrated modulation of these clinical features as opposed to simply tumor cell growth.

methodsHypothesizing the clinical presentation of IBC may be mediated in part by the microenvironment, we examined the effect of co-injection of IBC xenografts with mesenchymal stem/stromal cells (MSCs).

resultsMSCs co-injection significantly increased the clinical features of skin invasion and metastasis in the SUM149 xenograft model. Primary tumors co-injected with MSCs expressed higher phospho-epidermal growth factor receptor (p-EGFR) and promoted metastasis development after tumor resection, effects that were abrogated by treatment with the epidermal growth factor receptor (EGFR) inhibitor, erlotinib. E-cadherin expression was maintained in primary tumor xenografts with MSCs co-injection compared to control and erlotinib treatment dramatically decreased this expression in control and MSCs co-injected tumors. Tumor samples from patients demonstrate correlation between stromal and tumor p-EGFR staining only in IBC tumors.

conclusionsOur findings demonstrate that the IBC clinical phenotype is promoted by signaling from the microenvironment perhaps in addition to tumor cell drivers.

Indexed as

PhenotypeAnimalsAntineoplastic AgentsCadherinsCell Line, TumorCell ProliferationCell Transformation, NeoplasticCulture Media, ConditionedDisease Models, AnimalErbB ReceptorsErlotinib HydrochlorideFemaleHeterograftsHumansInflammatory Breast NeoplasmsMesenchymal Stem CellsAntineoplastic AgentsCadherinsCulture Media, ConditionedErbB ReceptorsErlotinib Hydrochloride

Identifiers

PMID25887413
PMCPMC4389342
OpenAlexW2137922932

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.