Evidence map›Paper›PMID 34273006›Full record

ReviewJournal of cancer research and clinical oncology2021

Gut microbiota-derived metabolites in CRC progression and causation.

Nishu Dalal, Rekha Jalandra, Nitin Bayal, Amit K Yadav, Harshulika, Minakshi Sharma, Govind K Makharia, Pramod Kumar, Rajeev Singh, Pratima R Solanki and 1 more

Open access · greenAbstract readReview
In one paragraph

Review in Journal of cancer research and clinical oncology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed
5.6field-weighted citation impact, top 3% 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

70 citing papers in PubMed, 93 citations in OpenAlex.

  1. Review
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  7. Crosstalk between mFrontiers in immunology · 2026
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10 more citing papers are in PubMed but not listed here.

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

11 authors at 6 institutions in 1 country.

Nishu Dalal *Gene Regulation Laboratory, National Institute of Immunology, New Delhi, 110067, India.
Rekha Jalandra *Gene Regulation Laboratory, National Institute of Immunology, New Delhi, 110067, India.
Nitin BayalGene Regulation Laboratory, National Institute of Immunology, New Delhi, 110067, India.
Amit K YadavSpecial Centre for Nanoscience, Jawaharlal Nehru University, New Delhi, 110067, India.
HarshulikaMinistry of Environment, Forest and Climate Change, New Delhi, 110003, India.
Minakshi SharmaDepartment of Zoology, Maharshi Dayanand University, Rohtak, 124001, India.
Govind K MakhariaDepartment of Gastroenterology and Human Nutrition, AIIMS, New Delhi, 110029, India.
Pramod KumarSri Aurobindo College, Delhi University, New Delhi, 110067, India.
Rajeev SinghDepartment of Environmental Science, Satyawati College, Delhi University, Delhi, 110052, India.
Pratima R SolankiSpecial Centre for Nanoscience, Jawaharlal Nehru University, New Delhi, 110067, India. partima@mail.jnu.ac.in.
Anil KumarGene Regulation Laboratory, National Institute of Immunology, New Delhi, 110067, India. anilk@nii.ac.in.ORCID http://orcid.org/0000-0002-8785-6033
National Institute of Immunology · INUniversity of Delhi · INJawaharlal Nehru University · INAll India Institute of Medical Sciences Raipur · INMaharshi Dayanand University · INMinistry of Environment, Forests and Climate Change · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundBased on recent research reports, dysbiosis and improper concentrations of microbial metabolites in the gut may result into the carcinogenesis of colorectal cancer. Recent advancement also highlights the involvement of bacteria and their secreted metabolites in the cancer causation. Gut microbial metabolites are functional output of the host-microbiota interactions and produced by anaerobic fermentation of food components in the diet. They contribute to influence variety of biological mechanisms including inflammation, cell signaling, cell-cycle disruption which are majorly disrupted in carcinogenic activities. PURPOSE: In this review, we intend to discuss recent updates and possible molecular mechanisms to provide the role of bacterial metabolites, gut bacteria and diet in the colorectal carcinogenesis. Recent evidences have proposed the role of bacteria, such as Fusobacterium nucleaturm, Streptococcus bovis, Helicobacter pylori, Bacteroides fragilis and Clostridium septicum, in the carcinogenesis of CRC. Metagenomic study confirmed that these bacteria are in increased abundance in CRC patient as compared to healthy individuals and can cause inflammation and DNA damage which can lead to development of cancer. These bacteria produce metabolites, such as secondary bile salts from primary bile salts, hydrogen sulfide, trimethylamine-N-oxide (TMAO), which are likely to promote inflammation and subsequently cancer development.

conclusionRecent studies suggest that gut microbiota-derived metabolites have a role in CRC progression and causation and hence, could be implicated in CRC diagnosis, prognosis and therapy.

Indexed as

AnimalsColorectal NeoplasmsDisease ProgressionGastrointestinal MicrobiomeGram-Negative BacteriaGram-Positive BacteriaHumansMetagenomicsColorectal cancerCRC inflammationGastrointestinal diseasesGut microbiotaMicrobial metabolites

Identifiers

PMID34273006
PMCPMC11801839
OpenAlexW3180464509

What OpenQuestion holds

Textmetadata
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.