Evidence map›Paper›PMID 30353617›Full record

ArticleStem cells (Dayton, Ohio)2019

Ovarian Carcinoma-Associated Mesenchymal Stem Cells Arise from Tissue-Specific Normal Stroma.

Lan G Coffman, Alexander T Pearson, Leonard G Frisbie, Zachary Freeman, Elizabeth Christie, David D Bowtell, Ronald J Buckanovich

Open access · bronzeAbstract read
In one paragraph

Article in Stem cells (Dayton, Ohio), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
5.2field-weighted citation impact, top 4% 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

53 citing papers in PubMed, 85 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

7 authors at 4 institutions in 2 countries.

Lan G CoffmanDivision of Hematology Oncology, Department of Internal Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, USA.ORCID 0000-0002-3753-1652
Alexander T PearsonDivision of Hematology Oncology, Department of Internal Medicine, University of Chicago, Illinois, USA.
Leonard G FrisbieDivision of Hematology Oncology, Department of Internal Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, USA.
Zachary FreemanUnit for Laboratory Animal Medicine, Rogel Cancer Center, University of Michigan, Ann Arbor, Michigan, USA.
Elizabeth ChristieResearch Division Peter MacCallum Cancer Centre, Parkville, Victoria, Australia.
David D BowtellResearch Division Peter MacCallum Cancer Centre, Parkville, Victoria, Australia.
Ronald J BuckanovichDivision of Hematology Oncology, Department of Internal Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, USA.
University of Pittsburgh · USPeter MacCallum Cancer Centre · AUUniversity of Illinois Chicago · USUniversity of Michigan · US

Funding

Targeting Ovarian Tumor Associated Myeloid Cells with Nanoparticles TherapeuticsR01CA163345 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI BUCKANOVICH, RONALD J · 2012 to 2016
$1.6M
Defining the formation and function of carcinoma-associated mesenchymal stem cells in the ovarian cancer microenvironmentK08CA211362 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI COFFMAN, LAN · 2016 to 2021
$918k
NCI NIH HHS K08 CA211362NCI NIH HHS R01 CA163345
6 · The paper itself

Abstract

Carcinoma-associated mesenchymal stem cells (CA-MSCs) are critical stromal progenitor cells within the tumor microenvironment (TME). We previously demonstrated that CA-MSCs differentially express bone morphogenetic protein family members, promote tumor cell growth, increase cancer "stemness," and chemotherapy resistance. Here, we use RNA sequencing of normal omental MSCs and ovarian CA-MSCs to demonstrate global changes in CA-MSC gene expression. Using these expression profiles, we create a unique predictive algorithm to classify CA-MSCs. Our classifier accurately distinguishes normal omental, ovary, and bone marrow MSCs from ovarian cancer CA-MSCs. Suggesting broad applicability, the model correctly classifies pancreatic and endometrial cancer CA-MSCs and distinguishes cancer associated fibroblasts from CA-MSCs. Using this classifier, we definitively demonstrate ovarian CA-MSCs arise from tumor mediated reprograming of local tissue MSCs. Although cancer cells alone cannot induce a CA-MSC phenotype, the in vivo ovarian TME can reprogram omental or ovary MSCs to protumorigenic CA-MSCs (classifier score of >0.96). In vitro studies suggest that both tumor secreted factors and hypoxia are critical to induce the CA-MSC phenotype. Interestingly, although the breast cancer TME can reprogram bone marrow MSCs into CA-MSCs, the ovarian TME cannot, demonstrating for the first time that tumor mediated CA-MSC conversion is tissue and cancer type dependent. Together these findings (a) provide a critical tool to define CA-MSCs and (b) highlight cancer cell influence on distinct normal tissues providing powerful insights into the mechanisms underlying cancer specific metastatic niche formation. Stem Cells 2019;37:257-269.

Indexed as

Cell DifferentiationCell Line, TumorCell ProliferationFemaleHumansMesenchymal Stem CellsOvarian NeoplasmsTumor MicroenvironmentHypoxiaMesenchymal stem cellOvarian cancerTumor microenvironment

Identifiers

PMID30353617
PMCPMC6392140
OpenAlexW2898454641

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.