Evidence map›Paper›PMID 25026286›Full record

ArticleOncotarget2014

Surgery-induced wound response promotes stem-like and tumor-initiating features of breast cancer cells, via STAT3 signaling.

Ilenia Segatto, Stefania Berton, Maura Sonego, Samuele Massarut, Tiziana Perin, Erica Piccoli, Alfonso Colombatti, Andrea Vecchione, Gustavo Baldassarre, Barbara Belletti

Abstract read
In one paragraph

Article in Oncotarget, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing 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

43 citing papers in PubMed.

  1. Trial
  2. Trial
  3. Trial
  4. Trial
  5. Review
  6. Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Wound fluid sampling methods for proteomic studies: A scoping review.Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society · 2022
    Article
  14. 3D printed drug-loaded implantable devices for intraoperative treatment of cancer.Journal of controlled release : official journal of the Controlled Release Society · 2022
    Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. Article
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

10 authors.

Ilenia SegattoDivision of Experimental Oncology 2, CRO, National Cancer Institute, Aviano 33081, Italy.
Stefania BertonDivision of Experimental Oncology 2, CRO, National Cancer Institute, Aviano 33081, Italy.
Maura SonegoDivision of Experimental Oncology 2, CRO, National Cancer Institute, Aviano 33081, Italy.
Samuele MassarutBreast Surgery Unit, CRO, National Cancer Institute, Aviano 33081, Italy.
Tiziana PerinPathology Unit, CRO, National Cancer Institute, Aviano 33081, Italy.
Erica PiccoliBreast Surgery Unit, CRO, National Cancer Institute, Aviano 33081, Italy.
Alfonso ColombattiDivision of Experimental Oncology 2, CRO, National Cancer Institute, Aviano 33081, Italy; Department of Scienze Biologiche e Mediche, MATI Center of Excellence, University of Udine, 33100 Udine, Italy.
Andrea VecchioneDivision of Pathology, II University of Rome "La Sapienza", Santo Andrea Hospital, Rome 00189, Italy.
Gustavo BaldassarreDivision of Experimental Oncology 2, CRO, National Cancer Institute, Aviano 33081, Italy.
Barbara BellettiDivision of Experimental Oncology 2, CRO, National Cancer Institute, Aviano 33081, Italy.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inflammation is clinically linked to cancer but the mechanisms are not fully understood. Surgery itself elicits a range of inflammatory responses, suggesting that it could represent a perturbing factor in the process of local recurrence and/or metastasis. Post-surgery wound fluids (WF), drained from breast cancer patients, are rich in cytokines and growth factors, stimulate the in vitro growth of breast cancer cells and are potent activators of the STAT transcription factors. We wondered whether STAT signaling was functionally involved in the response of breast cancer cells to post-surgical inflammation. We discovered that WF induced the enrichment of breast cancer cells with stem-like phenotypes, via activation of STAT3. In vitro, WF highly stimulated mammosphere formation and self-renewal of breast cancer cells. In vivo, STAT3 signaling was critical for breast cancer cell tumorigenicity and for the formation of local relapse after surgery. Overall, we demonstrate here that surgery-induced inflammation promotes stem-like phenotypes and tumor-initiating abilities of breast cancer cells. Interfering with STAT3 signaling with a peri-surgical treatment was sufficient to strongly suppress this process. The understanding of the crosstalk between breast tumor-initiating cells and their microenvironment may open the way to successful targeting of these cells in their initial stages of growth and be eventually curative.

Indexed as

AnimalsBreast NeoplasmsCell Line, TumorCell ProliferationFemaleHumansInflammationMCF-7 CellsMiceMice, NudeNeoplasm Recurrence, LocalNeoplastic Stem CellsPhosphorylationSignal TransductionSTAT3 Transcription FactorTumor MicroenvironmentSTAT3 protein, humanSTAT3 Transcription Factor

Identifiers

PMID25026286
PMCPMC4171628

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.