Evidence map›Paper›PMID 27468191›Full record

ReviewWorld journal of gastroenterology2016

Pancreatic cancer stem cell markers and exosomes - the incentive push.

Sarah Heiler, Zhe Wang, Margot Zöller

Open access · bronzeAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in World journal of gastroenterology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
6.6field-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

48 citing papers in PubMed, 91 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Small extracellular vesicles (sEVs) in pancreatic cancer progression and diagnosis.Journal of controlled release : official journal of the Controlled Release Society · 2025
    Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Harnessing cancer stem cell-derived exosomes to improve cancer therapy.Journal of experimental & clinical cancer research : CR · 2023
    Review
  11. Review
  12. Review
  13. Review
  14. Review
  15. Article
  16. Review
  17. Article
  18. Review
  19. Review
  20. Review
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

3 authors at 2 institutions in 1 country.

Sarah HeilerSarah Heiler, Zhe Wang, Margot Zöller, Tumor Cell Biology, University Hospital of Surgery, D 69120 Heidelberg, Germany.
Zhe WangSarah Heiler, Zhe Wang, Margot Zöller, Tumor Cell Biology, University Hospital of Surgery, D 69120 Heidelberg, Germany.
Margot ZöllerSarah Heiler, Zhe Wang, Margot Zöller, Tumor Cell Biology, University Hospital of Surgery, D 69120 Heidelberg, Germany.
Heidelberg University · DEUniversity Hospital Heidelberg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pancreatic cancer (PaCa) has the highest death rate and incidence is increasing. Poor prognosis is due to late diagnosis and early metastatic spread, which is ascribed to a minor population of so called cancer stem cells (CSC) within the mass of the primary tumor. CSC are defined by biological features, which they share with adult stem cells like longevity, rare cell division, the capacity for self renewal, differentiation, drug resistance and the requirement for a niche. CSC can also be identified by sets of markers, which for pancreatic CSC (Pa-CSC) include CD44v6, c-Met, Tspan8, alpha6beta4, CXCR4, CD133, EpCAM and claudin7. The functional relevance of CSC markers is still disputed. We hypothesize that Pa-CSC markers play a decisive role in tumor progression. This is fostered by the location in glycolipid-enriched membrane domains, which function as signaling platform and support connectivity of the individual Pa-CSC markers. Outside-in signaling supports apoptosis resistance, stem cell gene expression and tumor suppressor gene repression as well as miRNA transcription and silencing. Pa-CSC markers also contribute to motility and invasiveness. By ligand binding host cells are triggered towards creating a milieu supporting Pa-CSC maintenance. Furthermore, CSC markers contribute to the generation, loading and delivery of exosomes, whereby CSC gain the capacity for a cell-cell contact independent crosstalk with the host and neighboring non-CSC. This allows Pa-CSC exosomes (TEX) to reprogram neighboring non-CSC towards epithelial mesenchymal transition and to stimulate host cells towards preparing a niche for metastasizing tumor cells. Finally, TEX communicate with the matrix to support tumor cell motility, invasion and homing. We will discuss the possibility that CSC markers are the initial trigger for these processes and what is the special contribution of CSC-TEX.

Indexed as

Gene Expression Regulation, NeoplasticAdenocarcinomaBiomarkers, TumorEpithelial-Mesenchymal TransitionExosomesHumansMicroRNAsNeoplastic Stem CellsPancreatic NeoplasmsBiomarkers, TumorMicroRNAsCancer stem cellsCrosstalkExosomesPancreatic cancerStem cell markers

Identifiers

PMID27468191
PMCPMC4948278
OpenAlexW2490991344

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.