Evidence map›Paper›PMID 22282653›Full record

ArticleCancer research2012

Myeloid progenitor cells in the premetastatic lung promote metastases by inducing mesenchymal to epithelial transition.

Dingcheng Gao, Natasha Joshi, Hyejin Choi, Seongho Ryu, Mary Hahn, Raul Catena, Helen Sadik, Pedram Argani, Patrick Wagner, Linda T Vahdat and 6 more

Open access · hybridAbstract read
In one paragraph

Article in Cancer research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 172 papers.

0numbers the graph read from it
0cells of the map it votes in
172citing 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

172 citing papers in PubMed, 304 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Metastasis-promoting functions of myeloid cells.Cancer metastasis reviews · 2025
    Review
  9. Article
  10. Review
  11. The Roles of Myeloid Cells in Breast Cancer Progression.Advances in experimental medicine and biology · 2025
    Review
  12. Review
  13. MDSC: a new potential breakthrough in CAR-T therapy for solid tumors.Cell communication and signaling : CCS · 2024
    Review
  14. Review
  15. Review
  16. Review
  17. Article
  18. KRT17high/CXCL8+ Tumor Cells Display Both Classical and Basal Features and Regulate Myeloid Infiltration in the Pancreatic Cancer Microenvironment.Clinical cancer research : an official journal of the American Association for Cancer Research · 2024
    Article
  19. Review
  20. Article

112 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

16 authors at 2 institutions in 1 country.

Dingcheng GaoDepartment of Cardiothoracic Surgery and Neuberger Berman Lung Cancer Center, Weill Cornell Medical College of Cornell University, New York, New York, USA.
Natasha Joshi
Hyejin Choi
Seongho Ryu
Mary Hahn
Raul Catena
Helen Sadik
Pedram Argani
Patrick Wagner
Linda T Vahdat
Jeffrey L Port
Brendon Stiles
Saraswati Sukumar
Nasser K Altorki
Shahin Rafii
Vivek Mittal
Cornell University · USSidney Kimmel Comprehensive Cancer Center · US

Funding

TRANS-NETWORK PROJECTSU54CA143876 · NCI · CORNELL UNIVERSITY · PI SHULER, MICHAEL L · 2009 to 2014
$12.6M
The role of endothelial progenitor cells in tumor growth and metastasisR01CA107429 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI BENEZRA, ROBERT I, MITTAL, VIVEK · 2004 to 2015
$5.5M
Molecular mechanisms of tumor-initiated premetastatic niche formation in lung strR01CA135417 · NCI · WEILL MEDICAL COLL OF CORNELL UNIV · PI MITTAL, VIVEK, WATNICK, RANDOLPH S · 2010 to 2014
$2.6M
NCI NIH HHS R01 CA107429NCI NIH HHS R01 CA135417NCI NIH HHS U54 CA143876NCI NIH HHS U54CA143876
6 · The paper itself

Abstract

Tumors systemically initiate metastatic niches in distant target metastatic organs. These niches, composed of bone marrow-derived hematopoietic cells, provide permissive conditions for future metastases. However, the mechanisms by which these cells mediate outgrowth of metastatic tumor cells are not completely known. Using mouse models of spontaneous breast cancer, we show enhanced recruitment of bone marrow-derived CD11b(+)Gr1(+) myeloid progenitor cells in the premetastatic lungs. Gene expression profiling revealed that the myeloid cells from metastatic lungs express versican, an extracellular matrix proteoglycan. Notably, versican in metastatic lungs was mainly contributed by the CD11b(+)Ly6C(high) monocytic fraction of the myeloid cells and not the tumor cells or other stromal cells. Versican knockdown in the bone marrow significantly impaired lung metastases in vivo, without impacting their recruitment to the lungs or altering the immune microenvironment. Versican stimulated mesenchymal to epithelial transition of metastatic tumor cells by attenuating phospho-Smad2 levels, which resulted in elevated cell proliferation and accelerated metastases. Analysis of clinical specimens showed elevated versican expression within the metastatic lung of patients with breast cancer. Together, our findings suggest that selectively targeting tumor-elicited myeloid cells or versican represents a potential therapeutic strategy for combating metastatic disease.

Indexed as

Epithelial-Mesenchymal TransitionAnimalsBreast NeoplasmsCD11b AntigenCell Line, TumorCell ProliferationFemaleGene Expression ProfilingGene Expression Regulation, NeoplasticGene Knockdown TechniquesHumansLung NeoplasmsMaleMammary Neoplasms, AnimalMiceMice, TransgenicCD11b AntigenSmad2 ProteinVersicans

Identifiers

PMID22282653
PMCPMC8543151
OpenAlexW2065678781

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.