Evidence map›Paper›PMID 26291921›Full record

ReviewConnective tissue research2015

Cancer stem cells and the tumor microenvironment: interplay in tumor heterogeneity.

Adriana Albini, Antonino Bruno, Cristina Gallo, Giorgio Pajardi, Douglas M Noonan, Katiuscia Dallaglio

Abstract readReview
In one paragraph

Review in Connective tissue research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
91citing papers in PubMed, 1 pooled it
–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

91 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. PRX5 as a critical driver of colorectal cancer stemness and tumorigenicity.Redox report : communications in free radical research · 2026
    Article
  3. Article
  4. The metabolic profiles of cancer stem cells.Stem cell research & therapy · 2026
    Review
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
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  14. Adenosinergic Signalling in Cervical Cancer Microenvironment.Expert reviews in molecular medicine · 2025
    Review
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. Article

31 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

6 authors.

Adriana Albinia Department of Research and Statistics , IRCCS Arcispedale Santa Maria Nuova , Reggio Emilia , Italy .
Antonino Brunob Scientific and Technology Park, IRCCS MultiMedica , Milan , Italy .
Cristina Galloa Department of Research and Statistics , IRCCS Arcispedale Santa Maria Nuova , Reggio Emilia , Italy .
Giorgio Pajardic Department of Hand Surgery , San Giuseppe MultiMedica Hospital of Milan , Milan , Italy .
Douglas M Noonanb Scientific and Technology Park, IRCCS MultiMedica , Milan , Italy .
Katiuscia Dallaglioa Department of Research and Statistics , IRCCS Arcispedale Santa Maria Nuova , Reggio Emilia , Italy .

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tumor cells able to recapitulate tumor heterogeneity have been tracked, isolated and characterized in different tumor types, and are commonly named Cancer Stem Cells or Cancer Initiating Cells (CSC/CIC). CSC/CIC are disseminated in the tumor mass and are resistant to anti-cancer therapies and adverse conditions. They are able to divide into another stem cell and a "proliferating" cancer cell. They appear to be responsible for disease recurrence and metastatic dissemination even after apparent eradication of the primary tumor. The modulation of CSC/CIC activities by the tumor microenvironment (TUMIC) is still poorly known. CSC/CIC may mutually interact with the TUMIC in a special and unique manner depending on the TUMIC cells or proteins encountered. The TUMIC consists of extracellular matrix components as well as cellular players among which endothelial, stromal and immune cells, providing and responding to signals to/from the CSC/CIC. This interplay can contribute to the mechanisms through which CSC/CIC may reside in a dormant state in a tissue for years, later giving rise to tumor recurrence or metastasis in patients. Different TUMIC components, including the connective tissue, can differentially activate CIC/CSC in different areas of a tumor and contribute to the generation of cancer heterogeneity. Here, we review possible networking activities between the different components of the tumor microenvironment and CSC/CIC, with a focus on its role in tumor heterogeneity and progression. We also summarize novel therapeutic options that could target both CSC/CIC and the microenvironment to elude resistance mechanisms activated by CSC/CIC, responsible for disease recurrence and metastases.

Indexed as

AnimalsCell DifferentiationExtracellular MatrixHumansNeoplasm MetastasisNeoplasmsNeoplastic Stem CellsTumor MicroenvironmentCancer initiating cellscancer stem cellsconnective tissueheterogeneitytumor microenvironment

Identifiers

PMID26291921
PMCPMC4673538

What OpenQuestion holds

Textmetadata
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.