Evidence map›Paper›PMID 31831021›Full record

ReviewJournal of experimental & clinical cancer research : CR2019

Metformin in colorectal cancer: molecular mechanism, preclinical and clinical aspects.

Muhamad Noor Alfarizal Kamarudin, Md Moklesur Rahman Sarker, Jin-Rong Zhou, Ishwar Parhar

Open access · goldAbstract readReview
In one paragraph

Review in Journal of experimental & clinical cancer research : CR, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 112 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
112citing papers in PubMed, 6 pooled it
7.5field-weighted citation impact, top 2% 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

112 citing papers in PubMed, 6 syntheses or guidelines pooled it, 187 citations in OpenAlex.

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52 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

4 authors at 3 institutions in 3 countries.

Muhamad Noor Alfarizal KamarudinBrain Research Institute Monash Sunway (BRIMS), Jeffrey Cheah School of Medicine and Health Sciences, Monash University Malaysia, 47500, Bandar Sunway, Selangor, Malaysia. MuhamadNoor.Alfarizal@monash.edu.ORCID http://orcid.org/0000-0003-2505-1018
Md Moklesur Rahman SarkerDepartment of Pharmacy, State University of Bangladesh, 77 Satmasjid Road, Dhanmondi, Dhaka, 1205, Bangladesh. moklesur2002@yahoo.com.ORCID https://orcid.org/0000-0001-9795-0608
Jin-Rong ZhouDepartment of Surgery, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, 02215, USA.
Ishwar ParharBrain Research Institute Monash Sunway (BRIMS), Jeffrey Cheah School of Medicine and Health Sciences, Monash University Malaysia, 47500, Bandar Sunway, Selangor, Malaysia.
Monash University Malaysia · MYBeth Israel Deaconess Medical Center · USState University of Bangladesh · BD

Funding

Brain Research Institute Monash Sunway (BRIMS) and Jeffrey Cheah School of Medicine and Health Sciences, Monash University Malaysia. -
6 · The paper itself

Abstract

Growing evidence showed the increased prevalence of cancer incidents, particularly colorectal cancer, among type 2 diabetic mellitus patients. Antidiabetic medications such as, insulin, sulfonylureas, dipeptyl peptidase (DPP) 4 inhibitors and glucose-dependent insulinotropic peptide (GLP-1) analogues increased the additional risk of different cancers to diabetic patients. Conversely, metformin has drawn attention among physicians and researchers since its use as antidiabetic drug exhibited beneficial effect in the prevention and treatment of cancer in diabetic patients as well as an independent anticancer drug. This review aims to provide the comprehensive information on the use of metformin at preclinical and clinical stages among colorectal cancer patients. We highlight the efficacy of metformin as an anti-proliferative, chemopreventive, apoptosis inducing agent, adjuvant, and radio-chemosensitizer in various colorectal cancer models. This multifarious effects of metformin is largely attributed to its capability in modulating upstream and downstream molecular targets involved in apoptosis, autophagy, cell cycle, oxidative stress, inflammation, metabolic homeostasis, and epigenetic regulation. Moreover, the review highlights metformin intake and colorectal cancer risk based on different clinical and epidemiologic results from different gender and specific population background among diabetic and non-diabetic patients. The improved understanding of metformin as a potential chemotherapeutic drug or as neo-adjuvant will provide better information for it to be used globally as an affordable, well-tolerated, and effective anticancer agent for colorectal cancer.

Indexed as

AnimalsAntineoplastic AgentsCell ProliferationCell SurvivalClinical Trials as TopicColorectal NeoplasmsHumansMetforminAntineoplastic AgentsMetforminAnticancerCancerChemopreventiveColorectal cancerMetforminType 2 diabetes mellitus

Identifiers

PMID31831021
PMCPMC6909457
OpenAlexW2996301762

What Socratic 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 Socratic graph.