Evidence map›Paper›PMID 35070037›Full record

ReviewWorld journal of gastrointestinal oncology2021

Diabetes mellitus contribution to the remodeling of the tumor microenvironment in gastric cancer.

Armando Rojas, Cristian Lindner, Iván Schneider, Ileana Gonzàlez, Hernan Araya, Erik Morales, Milibeth Gómez, Nelson Urdaneta, Paulina Araya, Miguel Angel Morales

Open access · diamondAbstract readReview
In one paragraph

Review in World journal of gastrointestinal oncology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed, 1 pooled it
0.4field-weighted citation impact, top 45% 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

5 citing papers in PubMed, 1 synthesis or guideline pooled it, 11 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. 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

10 authors at 1 institution in 1 country.

Armando RojasBiomedical Research Lab., Medicine Faculty, Catholic University of Maule, Talca 34600000, Chile. arojasr@ucm.cl.
Cristian LindnerBiomedical Research Lab., Medicine Faculty, Catholic University of Maule, Talca 34600000, Chile.
Iván SchneiderBiomedical Research Lab., Medicine Faculty, Catholic University of Maule, Talca 34600000, Chile.
Ileana GonzàlezBiomedical Research Lab., Medicine Faculty, Catholic University of Maule, Talca 34600000, Chile.
Hernan ArayaDepartment of Clinical Sciences, Medicine Faculty, Catholic University of Maule, Talca 34600000, Chile.
Erik MoralesBiomedical Research Lab., Medicine Faculty, Catholic University of Maule, Talca 34600000, Chile.
Milibeth GómezDepartment of Clinical Sciences, Medicine Faculty, Catholic University of Maule, Talca 34600000, Chile.
Nelson UrdanetaDepartment of Clinical Sciences, Medicine Faculty, Catholic University of Maule, Talca 34600000, Chile.
Paulina ArayaBiomedical Research Lab., Medicine Faculty, Catholic University of Maule, Talca 34600000, Chile.
Miguel Angel MoralesDepartment of Molecular and Clinical Pharmacology Program, Institute of Biomedical Sciences, University of Chile, Santiago 8320000, Chile.
University of Chile · CL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Compelling pieces of evidence derived from both clinical and experimental research has demonstrated the crucial contribution of diabetes mellitus (DM) as a risk factor associated with increased cancer incidence and mortality in many human neoplasms, including gastric cancer (GC). DM is considered a systemic inflammatory disease and therefore, this inflammatory status may have profound effects on the tumor microenvironment (TME), particularly by driving many molecular mechanisms to generate a more aggressive TME. DM is an active driver in the modification of the behavior of many cell components of the TME as well as altering the mechanical properties of the extracellular matrix (ECM), leading to an increased ECM stiffening. Additionally, DM can alter many cellular signaling mechanisms and thus favoring tumor growth, invasion, and metastatic potential, as well as key elements in regulating cellular functions and cross-talks, such as the microRNAs network, the production, and cargo of exosomes, the metabolism of cell stroma and resistance to hypoxia. In the present review, we intend to highlight the mechanistic contributions of DM to the remodeling of TME in GC.

Indexed as

Chronic inflammationDiabetes mellitusGastric cancerHyperglycemiaTumor microenvironment

Identifiers

PMID35070037
PMCPMC8713306
OpenAlexW4200257675

What Socratic holds

Textmetadata
LicenceCC BY-NC
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 Socratic graph.