Evidence map›Paper›PMID 21827739›Full record

ReviewBiochemical pharmacology2011

Green tea catechin, epigallocatechin-3-gallate (EGCG): mechanisms, perspectives and clinical applications.

Brahma N Singh, Sharmila Shankar, Rakesh K Srivastava

Registry-linked trialAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Biochemical pharmacology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02329600 (Evaluation of Systemic Administration of Green Tea Polyphenols as a Supportive Antioxidant Agent in the Management of Oral Lichen Planus), which is not on this map. Cited by 607 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
607citing papers in PubMed, 5 pooled it
43.5field-weighted citation impact, top 1% 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.

NCT02329600 phase3completednot on this mapstarted 2013, after this paper: background citation

Evaluation of Systemic Administration of Green Tea Polyphenols as a Supportive Antioxidant Agent in the Management of Oral Lichen Planus

TypeinterventionalSponsorCairo UniversityRan2013 to 2014Enrolled40ConditionsOral Lichen PlanusArmsgreen tea tablets (Green tea extract 5:1) 200 mg, Triamcinolone Acetonide
3 · Its place in the literature

Who cites it

607 citing papers in PubMed, 5 syntheses or guidelines pooled it, 1,549 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Pooled it
  6. Trial
  7. Trial
  8. Trial
  9. Article
  10. Review
  11. Review
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Review
  18. Review
  19. Article
  20. Review

547 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

3 authors at 1 institution in 1 country.

Brahma N SinghDepartment of Pharmacology, Toxicology and Therapeutics, and Medicine, The University of Kansas Cancer Center, The University of Kansas Medical Center, Kansas City, KS 66160, United States.
Sharmila Shankar
Rakesh K Srivastava
University of Kansas Medical Center · US

Funding

Chemoprevention of Pancreatic Cancer by EGCGR01CA125262 · NCI · UNIVERSITY OF TEXAS HLTH CTR AT TYLER · PI DHAR, ANIMESH · 2008 to 2012
$1.7M
Mechanisms of Chemoprevention by ResveratrolR01CA114469 · NCI · UNIVERSITY OF TEXAS HLTH CTR AT TYLER · PI SRIVASTAVA, RAKESH K. · 2005 to 2009
$726k
NCI NIH HHS R01 CA114469NCI NIH HHS R01CA114469NCI NIH HHS R01 CA125262NCI NIH HHS R01CA125262NCI NIH HHS R01CA125262-02S1
6 · The paper itself

Abstract

An expanding body of preclinical evidence suggests EGCG, the major catechin found in green tea (Camellia sinensis), has the potential to impact a variety of human diseases. Apparently, EGCG functions as a powerful antioxidant, preventing oxidative damage in healthy cells, but also as an antiangiogenic and antitumor agent and as a modulator of tumor cell response to chemotherapy. Much of the cancer chemopreventive properties of green tea are mediated by EGCG that induces apoptosis and promotes cell growth arrest by altering the expression of cell cycle regulatory proteins, activating killer caspases, and suppressing oncogenic transcription factors and pluripotency maintain factors. In vitro studies have demonstrated that EGCG blocks carcinogenesis by affecting a wide array of signal transduction pathways including JAK/STAT, MAPK, PI3K/AKT, Wnt and Notch. EGCG stimulates telomere fragmentation through inhibiting telomerase activity. Various clinical studies have revealed that treatment by EGCG inhibits tumor incidence and multiplicity in different organ sites such as liver, stomach, skin, lung, mammary gland and colon. Recent work demonstrated that EGCG reduced DNMTs, proteases, and DHFR activities, which would affect transcription of TSGs and protein synthesis. EGCG has great potential in cancer prevention because of its safety, low cost and bioavailability. In this review, we discuss its cancer preventive properties and its mechanism of action at numerous points regulating cancer cell growth, survival, angiogenesis and metastasis. Therefore, non-toxic natural agent could be useful either alone or in combination with conventional therapeutics for the prevention of tumor progression and/or treatment of human malignancies.

Indexed as

Antineoplastic AgentsAntioxidantsApoptosisCamellia sinensisCatechinCell ProliferationCell Transformation, NeoplasticHumansMolecular StructureNeoplasmsSignal TransductionAntineoplastic AgentsAntioxidantsCatechinepigallocatechin gallate

Identifiers

PMID21827739
PMCPMC4082721
OpenAlexW2070785261

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

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.