Evidence map›Paper›PMID 41511497›Full record

ReviewCell biochemistry and biophysics2026

Unveiling the Influence of Polyphenols on Mitogen-activated Protein Kinases in Cancer.

Mugdha Tendulkar, Reshma Tendulkar

Abstract readReview
PubMed Publisher
In one paragraph

Review in Cell biochemistry and biophysics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

2 authors.

Mugdha TendulkarK. J. Somaiya Medical College & Research Centre, Mumbai, India. mugdhatendulkar14@gmail.com.ORCID http://orcid.org/0000-0001-7255-8351
Reshma TendulkarVivekanand Education Society's College of Pharmacy, Mumbai, India.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitogen-activated protein kinases are the most crucial pathways involved in cellular homeostasis. Aberrations in this signalling cascade have been implicated in the pathogenesis of neoplasia. They prove to be a key modulator in tumorigenesis as they extend their influence in all aspects of tumorigenesis. They further enhance cancer progression by accelerating neoplastic cell proliferation, differentiation, apoptosis inhibition, metastasis & invasion. In a nutshell, this pathway proves to be a prime hub for molecular targeting in combating cancer. Polyphenols are a class of compounds which play a potent role in impeding neoplastic progression. They are known to modulate each step of tumorigenesis thus hindering cancer metastasis as well as invasion. Research suggests that polyphenols exhibit promising results for the treatment of cancer by modulating the mitogen signalling pathway. Dietary polyphenols deserve a special emphasis for combating tumorigenesis with greater therapeutic efficacy. The fundamental objective of this manuscript is to meticulously analyse the role of mitogen-activated protein kinases in neoplasia & recognise possible sites for molecular targeting. It also extensively discusses how polyphenols hinder cancer progression and how this property can be exploited for the benefits of patients. The effect of polyphenols on the majority of cancers have been intricately discussed. The challenges & future prospects are also enumerated for clearly defining the research question for the future decades.

Indexed as

Mitogen-Activated Protein KinasesNeoplasmsPolyphenolsAnimalsHumansSignal TransductionMitogen-Activated Protein KinasesPolyphenolsCarcinogenesisChemotherapyMitogen-activated protein kinasesPolyphenols

Identifiers

PMID41511497

What OpenQuestion holds

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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.