Evidence map›Paper›PMID 21248315›Full record

ArticleScience translational medicine2011

Stromal endothelial cells directly influence cancer progression.

Joseph W Franses, Aaron B Baker, Vipul C Chitalia, Elazer R Edelman

Abstract read
In one paragraph

Article in Science translational medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 107 papers.

0numbers the graph read from it
0cells of the map it votes in
107citing papers in PubMed
–field-weighted citation impact
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

107 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Clinical Implications and Molecular Features of Extracellular Matrix Networks in Soft Tissue Sarcomas.Clinical cancer research : an official journal of the American Association for Cancer Research · 2024
    Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. EndothelialCells · 2022
    Article
  19. Article
  20. Review

47 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

4 authors.

Joseph W FransesBiomedical Engineering Center, Harvard-MIT Division of Health Sciences and Technology, Massachusetts Institute of Technology, E25-438, Cambridge, MA 02139, USA.
Aaron B Baker
Vipul C Chitalia
Elazer R Edelman

Funding

Medical Scientist Training ProgramT32GM007753 · NIGMS · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI WALENSKY, LOREN DAVID · 1985 to 2021
$50.0M
Vascular Drug Delivery - Supplement for EquipmentR01GM049039 · NIGMS · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI EDELMAN, ELAZER R · 1994 to 2019
$8.9M
Role of Wnt signaling in uremia-induced entothelial dysfunctionK08DK080946 · NIDDK · BOSTON MEDICAL CENTER · PI CHITALIA, VIPUL C · 2009 to 2013
$746k
NIDDK NIH HHS 1K08DK080946NIDDK NIH HHS K08 DK080946NIGMS NIH HHS R01 GM049039NIGMS NIH HHS R01 GM49039NIGMS NIH HHS T32 GM007753
6 · The paper itself

Abstract

Cancer growth and metastasis are regulated in part by stromal cells such as fibroblasts and immune cells within the tumor microenvironment. Endothelial cells (ECs) are also ubiquitous within tumors because tumors are vascular, and yet, the impact of tumor-resident ECs is less well understood. Through paracrine regulation, ECs modulate a diverse spectrum of pathophysiologic processes in normal and hyperplastic tissues. We hypothesized that ECs offer similar paracrine regulatory control of cancer biology. Indeed, secretions from quiescent ECs muted the proliferative and invasive phenotype of lung and breast cancer cells in vitro and reduced cancer cell protumorigenic and proinflammatory signaling. EC perlecan silencing significantly changed this regulatory relationship, eliminating the ability of ECs to inhibit cancer cell invasiveness via increased interleukin-6 secretion. Moreover, implanting ECs embedded within porous matrices slowed adjacent xenograft tumor growth and prevented architectural degeneration, with a concomitant reduction in proliferative and tumorigenic markers. Finally, lung carcinoma cells pretreated with intact EC-conditioned media, but not media conditioned with perlecan-silenced ECs, exhibited reduced micrometastatic burden after tail vein injection. These findings add to an emerging appreciation of EC-regulatory effects that transcend their structural roles and pave the way for improved characterization and control of EC-cancer cross-talk interactions for diagnosis, prognosis, and treatment of cancer.

Indexed as

AnimalsCell Line, TumorCulture Media, ConditionedDisease ProgressionEndothelial CellsHeparan Sulfate ProteoglycansHumansInterleukin-6Lung NeoplasmsMiceNeoplasm MetastasisNeoplasmsNeoplasm TransplantationStromal CellsCulture Media, ConditionedHeparan Sulfate ProteoglycansInterleukin-6perlecan

Identifiers

PMID21248315
PMCPMC3076139

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.