Evidence map›Paper›PMID 32781778›Full record

ReviewInternational journal of molecular sciences2020

CD36 and CD97 in Pancreatic Cancer versus Other Malignancies.

Cristiana Tanase, Ancuta-Augustina Gheorghisan-Galateanu, Ionela Daniela Popescu, Simona Mihai, Elena Codrici, Radu Albulescu, Mihail Eugen Hinescu

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.8field-weighted citation impact, top 13% 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

19 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
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  11. CD36 and Its Role in Regulating the Tumor Microenvironment.Current oncology (Toronto, Ont.) · 2022
    Review
  12. Article
  13. Article
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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

7 authors at 3 institutions in 1 country.

Cristiana TanaseVictor Babeș National Institute of Pathology, 99-101 Splaiul Independentei, 050096 Bucharest, Romania.
Ancuta-Augustina Gheorghisan-GalateanuDepartment of Cellular and Molecular Biology and Histology, Carol Davila University of Medicine and Pharmacy, 8 Eroilor Sanitari Str., 050474 Bucharest, Romania.
Ionela Daniela PopescuVictor Babeș National Institute of Pathology, 99-101 Splaiul Independentei, 050096 Bucharest, Romania.
Simona MihaiVictor Babeș National Institute of Pathology, 99-101 Splaiul Independentei, 050096 Bucharest, Romania.
Elena CodriciVictor Babeș National Institute of Pathology, 99-101 Splaiul Independentei, 050096 Bucharest, Romania.
Radu AlbulescuVictor Babeș National Institute of Pathology, 99-101 Splaiul Independentei, 050096 Bucharest, Romania.ORCID 0000-0002-3765-8207
Mihail Eugen HinescuVictor Babeș National Institute of Pathology, 99-101 Splaiul Independentei, 050096 Bucharest, Romania.ORCID 0000-0002-7740-9336
Institutul National Victor Babes · ROCarol Davila University of Medicine and Pharmacy · ROTitu Maiorescu University · RO

Funding

Romanian Ministry of Education and Research, UEFISCDI 7PFE/16.10.2018; PN 19.29.01.04; POC-A.1.1.4-E, P_37_794
6 · The paper itself

Abstract

Starting from the recent identification of CD36 and CD97 as a novel marker combination of fibroblast quiescence in lung during fibrosis, we aimed to survey the literature in search for facts about the separate (or concomitant) expression of clusters of differentiation CD36 and CD97 in either tumor- or pancreatic-cancer-associated cells. Here, we provide an account of the current knowledge on the diversity of the cellular functions of CD36 and CD97 and explore their potential (common) contributions to key cellular events in oncogenesis or metastasis development. Emphasis is placed on quiescence as an underexplored mechanism and/or potential target in therapy. Furthermore, we discuss intricate signaling mechanisms and networks involving CD36 and CD97 that may regulate different subpopulations of tumor-associated cells, such as cancer-associated fibroblasts, adipocyte-associated fibroblasts, tumor-associated macrophages, or neutrophils, during aggressive pancreatic cancer. The coexistence of quiescence and activated states in cancer-associated cell subtypes during pancreatic cancer should be better documented, in different histological forms. Remodeling of the local microenvironment may also change the balance between growth and dormant state. Taking advantage of the reported data in different other tissue types, we explore the possibility to induce quiescence (similar to that observed in normal cells), as a therapeutic option to delay the currently observed clinical outcome.

Indexed as

CD36 AntigensCell Line, TumorDrug Resistance, NeoplasmHumansNeoplasm MetastasisPancreatic NeoplasmsReceptors, G-Protein-CoupledCD36 AntigensReceptors, G-Protein-Coupledcancer-associated fibroblastsCD36CD97pancreatic cancerpancreatic ductal adenocarcinoma (PDAC)quiescence

Identifiers

PMID32781778
PMCPMC7460590
OpenAlexW3047119758

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.