Evidence map›Paper›PMID 36010993›Full record

ReviewCancers2022

The Extracellular Matrix: A Key Accomplice of Cancer Stem Cell Migration, Metastasis Formation, and Drug Resistance in PDAC.

Dan Wang, Yuqiang Li, Heming Ge, Tarik Ghadban, Matthias Reeh, Cenap Güngör

Open access · goldAbstract readReview
In one paragraph

Review in Cancers, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
6.7field-weighted citation impact, top 2% 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

47 citing papers in PubMed, 67 citations in OpenAlex.

  1. Review
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  7. Matrix stiffness induces CaExperimental hematology & oncology · 2026
    Article
  8. Article
  9. Review
  10. Review
  11. Exploring the interactions of integrins and CEACAM6 (Review).Experimental and therapeutic medicine · 2025
    Review
  12. Review
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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 at 1 institution in 1 country.

Dan WangDepartment of General Visceral and Thoracic Surgery, University Medical Center Hamburg-Eppendorf, 20251 Hamburg, Germany.
Yuqiang LiDepartment of General Visceral and Thoracic Surgery, University Medical Center Hamburg-Eppendorf, 20251 Hamburg, Germany.
Heming GeDepartment of General Visceral and Thoracic Surgery, University Medical Center Hamburg-Eppendorf, 20251 Hamburg, Germany.
Tarik GhadbanDepartment of General Visceral and Thoracic Surgery, University Medical Center Hamburg-Eppendorf, 20251 Hamburg, Germany.ORCID 0000-0002-1894-9893
Matthias ReehDepartment of General Visceral and Thoracic Surgery, University Medical Center Hamburg-Eppendorf, 20251 Hamburg, Germany.ORCID 0000-0001-9111-3905
Cenap GüngörDepartment of General Visceral and Thoracic Surgery, University Medical Center Hamburg-Eppendorf, 20251 Hamburg, Germany.ORCID 0000-0002-5173-9492
Universität Hamburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pancreatic ductal adenocarcinoma (PDAC) is rich in dense fibrotic stroma that are composed of extracellular matrix (ECM) proteins. A disruption of the balance between ECM synthesis and secretion and the altered expression of matrix remodeling enzymes lead to abnormal ECM dynamics in PDAC. This pathological ECM promotes cancer growth, survival, invasion, and alters the behavior of fibroblasts and immune cells leading to metastasis formation and chemotherapy resistance, which contribute to the high lethality of PDAC. Additionally, recent evidence highlights that ECM, as a major structural component of the tumor microenvironment, is a highly dynamic structure in which ECM proteins establish a physical and biochemical niche for cancer stem cells (CSCs). CSCs are characterized by self-renewal, tumor initiation, and resistance to chemotherapeutics. In this review, we will discuss the effects of the ECM on tumor biological behavior and its molecular impact on the fundamental signaling pathways in PDAC. We will also provide an overview of how the different ECM components are able to modulate CSCs properties and finally discuss the current and ongoing therapeutic strategies targeting the ECM. Given the many challenges facing current targeted therapies for PDAC, a better understanding of molecular events involving the interplay of ECM and CSC will be key in identifying more effective therapeutic strategies to eliminate CSCs and ultimately to improve survival in patients that are suffering from this deadly disease.

Indexed as

cancer stem cellschemotherapy resistanceextracellular matrixmetastasispancreatic ductal adenocarcinoma

Identifiers

PMID36010993
PMCPMC9406497
OpenAlexW4293778265

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.