Evidence map›Paper›PMID 23243021›Full record

ArticleCancer research2013

Myeloid-derived suppressor cells function as novel osteoclast progenitors enhancing bone loss in breast cancer.

Anandi Sawant, Jessy Deshane, Joel Jules, Carnella M Lee, Brittney A Harris, Xu Feng, Selvarangan Ponnazhagan

Abstract read
In one paragraph

Article in Cancer research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 122 papers.

0numbers the graph read from it
0cells of the map it votes in
122citing papers in PubMed
5.6field-weighted citation impact, top 3% 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

122 citing papers in PubMed, 178 citations in OpenAlex.

  1. Article
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  12. Review
  13. Osteoimmunology in bone malignancies: a symphony with evil.Journal of the National Cancer Center · 2024
    Review
  14. Immune mediated support of metastasis: Implication for bone invasion.Cancer communications (London, England) · 2024
    Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Tristetraprolin regulates the skeletal phenotype and osteoclastogenic potential through monocytic myeloid-derived suppressor cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024
    Article
  20. Review

62 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 1 institution in 1 country.

Anandi SawantDepartment of Pathology, The University of Alabama at Birmingham, Birmingham, Alabama 35294-2182, USA.
Jessy Deshane
Joel Jules
Carnella M Lee
Brittney A Harris
Xu Feng
Selvarangan Ponnazhagan
University of Alabama at Birmingham · US

Funding

University of Alabama at Birmingham's Diabetes Research CenterP30DK079626 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI Kirk Michael Habegger · 2013 to 2026
$19.5M
ROS Modulation of Innate and Adaptive Immunity in RAP30AR048311 · NIAMS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI MOUNTZ, JOHN D · 2001 to 2017
$9.5M
UAB Core Center for Musculoskeletal DisordersP30AR046031 · NIAMS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI GILBERT, SHAWN ROBERT · 2001 to 2010
$5.6M
Targeted Stem Cell Therapy Coupling Angiogenesis and Osteogenesis for Bone DefectR01AR060948 · NIAMS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI PONNAZHAGAN, SELVARANGAN · 2011 to 2016
$1.6M
rAAV vaccine vectorR01CA132077 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI PONNAZHAGAN, SELVARANGAN · 2008 to 2012
$1.5M
Gene-Engineered and Targeted Stem Cell Therapy for MyelomaR01CA133737 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI PONNAZHAGAN, SELVARANGAN · 2009 to 2013
$1.5M
AAV-Mediated Gene Therapy for Metabolic Bone DiseaseR01AR050251 · NIAMS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI PONNAZHAGAN, SELVARANGAN · 2005 to 2009
$1.4M
NCI NIH HHS CA132077NCI NIH HHS CA133737NCI NIH HHS R01 CA132077NCI NIH HHS R01 CA133737NIAMS NIH HHS AR050251NIAMS NIH HHS AR560948NIAMS NIH HHS P30 AR046031NIAMS NIH HHS P30 AR048311NIAMS NIH HHS P30 AR48311NIAMS NIH HHS R01 AR050251NIAMS NIH HHS R01 AR060948NIDDK NIH HHS P30 DK079626
6 · The paper itself

Abstract

Enhanced bone destruction is a hallmark of various carcinomas such as breast cancer, where osteolytic bone metastasis is associated with increased morbidity and mortality. Immune cells contribute to osteolysis in cancer growth, but the factors contributing to aggressive bone destruction are not well understood. In this study, we show the importance of myeloid-derived suppressor cells (MDSC) in this process at bone metastatic sites. Because MDSC originate from the same myeloid lineage as macrophages, which are osteoclast precursors, we hypothesized that MDSC may undergo osteoclast differentiation and contribute to enhanced bone destruction and tumor growth. Using an immunocompetent mouse model of breast cancer bone metastasis, we confirmed that MDSC isolated from the tumor-bone microenvironment differentiated into functional osteoclasts both in vitro and in vivo. Mechanistic investigations revealed that nitric oxide signaling was critical for differentiation of MDSC into osteoclasts. Remarkably, osteoclast differentiation did not occur in MDSC isolated from control or tumor-bearing mice that lacked bone metastasis, signifying the essential cross-talk between tumor cells and myeloid progenitors in the bone microenvironment as a requirement for osteoclast differentiation of MDSC. Overall, our results identify a wholly new facet to the multifunctionality of MDSC in driving tumor progression, in this case as a novel osteoclast progenitor that specifically drives bone metastasis during cancer progression.

Indexed as

Bone ResorptionAnimalsBone NeoplasmsBreast NeoplasmsCell DifferentiationCell Line, TumorFemaleHumansMiceMice, Inbred BALB CMyeloid CellsNitric OxideOsteoclastsOsteolysisNitric Oxide

Identifiers

PMID23243021
PMCPMC3548966
OpenAlexW2120312714

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.