Evidence map›Paper›PMID 35704091›Full record

ReviewInternational journal of colorectal disease2022

The role of gut microbiota in the development of colorectal cancer: a review.

Navami Koyande, Madhusree Gangopadhyay, Shashidhar Thatikonda, Aravind Kumar Rengan

Abstract readReview
PubMed Publisher
In one paragraph

Review in International journal of colorectal disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
–field-weighted citation impact
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

13 citing papers in PubMed.

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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

4 authors.

Navami KoyandeDepartment of Biomedical Engineering, Indian Institute of Technology Hyderabad, Kandi, Sangareddy- 502284, India.
Madhusree GangopadhyayDepartment of Biomedical Engineering, Indian Institute of Technology Hyderabad, Kandi, Sangareddy- 502284, India.
Shashidhar ThatikondaDepartment of Civil Engineering, Indian Institute of Technology Hyderabad, Kandi, Sangareddy- 502284, India.
Aravind Kumar RenganDepartment of Biomedical Engineering, Indian Institute of Technology Hyderabad, Kandi, Sangareddy- 502284, India. aravind@bme.iith.ac.in.

Funding

Department of Biotechnology, Ministry of Science and Technology, India DBT/CE/F064/2020-21/G307
6 · The paper itself

Abstract

purposeColorectal cancer (CRC) is the cancer of the colon and rectum. Recent research has found a link between CRC and human gut microbiota. This review explores the effect of gut microbiota on colorectal carcinogenesis and the development of chemoresistance.

methodsA literature overview was performed to identify the gut microbiota species that showed altered abundance in CRC patients and the mechanisms by which some of them aid in the development of chemoresistance.

resultsTypes of gut microbiota present and methods of analyzing them were discussed. We observed that numerous microbiota showed altered abundance in CRC patients and could act as a biomarker for CRC diagnosis and treatment. Further, it was demonstrated that microbes also have a role in the development of chemoresistance by mechanisms like immune system activation, drug modification, and autophagy modulation. Finally, the key issue of the growing global problem of antimicrobial resistance and its relationship with CRC was highlighted.

conclusionThis review discussed the role of gut microbiota dysbiosis on colorectal cancer progression and the development of chemoresistance.

Indexed as

Colorectal NeoplasmsGastrointestinal MicrobiomeMicrobiotaDysbiosisHumansAntimicrobial resistanceChemoresistanceColorectal cancerDysbiosisGut bacteria

Identifiers

PMID35704091

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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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.