Evidence map›Paper›PMID 31416286›Full record

ReviewCells2019

Gap Junction Intercellular Communication in the Carcinogenesis Hallmarks: Is This a Phenomenon or Epiphenomenon?

Roberto Zefferino, Claudia Piccoli, Sante Di Gioia, Nazzareno Capitanio, Massimo Conese

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.0field-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

27 citing papers in PubMed, 46 citations in OpenAlex.

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  18. Computational toxicology (Amsterdam, Netherlands) · 2021
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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

5 authors at 1 institution in 1 country.

Roberto ZefferinoDepartment of Medical and Surgical Sciences, University of Foggia, Via L. Pinto, 1-71122 Foggia, Italy. roberto.zefferino@unifg.it.
Claudia PiccoliDepartment of Clinical and Experimental Medicine, University of Foggia, Via L. Pinto, 1-71122 Foggia, Italy.
Sante Di GioiaDepartment of Medical and Surgical Sciences, University of Foggia, Via L. Pinto, 1-71122 Foggia, Italy.
Nazzareno CapitanioDepartment of Clinical and Experimental Medicine, University of Foggia, Via L. Pinto, 1-71122 Foggia, Italy.
Massimo ConeseDepartment of Medical and Surgical Sciences, University of Foggia, Via L. Pinto, 1-71122 Foggia, Italy.
University of Foggia · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

If occupational tumors are excluded, cancer causes are largely unknown. Therefore, it appeared useful to work out a theory explaining the complexity of this disease. More than fifty years ago the first demonstration that cells communicate with each other by exchanging ions or small molecules through the participation of connexins (Cxs) forming Gap Junctions (GJs) occurred. Then the involvement of GJ Intercellular Communication (GJIC) in numerous physiological cellular functions, especially in proliferation control, was proven and accounts for the growing attention elicited in the field of carcinogenesis. The aim of the present paper is to verify and discuss the role of Cxs, GJs, and GJIC in cancer hallmarks, pointing on the different involved mechanisms in the context of the multi-step theory of carcinogenesis. Functional GJIC acts both as a tumor suppressor and as a tumor enhancer in the metastatic stage. On the contrary, lost or non-functional GJs allow the uncontrolled proliferation of stem/progenitor initiated cells. Thus, GJIC plays a key role in many biological phenomena or epiphenomena related to cancer. Depending on this complexity, GJIC can be considered a tumor suppressor in controlling cell proliferation or a cancer ally, with possible preventive or therapeutic implications in both cases.

Indexed as

CarcinogenesisCell CommunicationAnimalsCell Line, TumorConnexinsGap JunctionsHumansMiceNeoplasmsStem CellsTumor MicroenvironmentConnexinsangiogenesiscancerconnexinshallmarkinflammationmetastasismicroenvironmentstem cells

Identifiers

PMID31416286
PMCPMC6721698
OpenAlexW2966984224

What OpenQuestion holds

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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.