Evidence map›Paper›PMID 19200260›Full record

ArticleCancer science2009

Catechin, green tea component, causes caspase-independent necrosis-like cell death in chronic myelogenous leukemia.

Reo Iwasaki, Kinji Ito, Takaomi Ishida, Makoto Hamanoue, Souichi Adachi, Toshiki Watanabe, Yuko Sato

Open access · greenAbstract read
In one paragraph

Article in Cancer science, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 18% 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

19 citing papers in PubMed, 1 synthesis or guideline pooled it, 53 citations in OpenAlex.

  1. Tea consumption and leukemia risk: a meta-analysis.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014
    Pooled it
  2. Article
  3. Article
  4. Review
  5. Flavonoids as Chemosensitizers in Leukemias.Advances in experimental medicine and biology · 2025
    Review
  6. Review
  7. Anticarcinogenic potentials of tea catechins.Frontiers in nutrition · 2022
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Role of Bax/Bcl-2 family members in green tea polyphenol induced necroptosis of p53-deficient Hep3B cells.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014
    Article
  16. Article
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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

7 authors at 4 institutions in 1 country.

Reo IwasakiLaboratory of Tumor Cell Biology, Department of Medical Genome Sciences, Graduate School of Frontier Sciences, University of Tokyo, 4-6-1 Shiroganedai, Minato-ku, Tokyo, Japan.
Kinji Ito
Takaomi Ishida
Makoto Hamanoue
Souichi Adachi
Toshiki Watanabe
Yuko Sato
Saitama International Medical Center · JPThe University of Tokyo · JPKyoto University · JPToho University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Management strategies of chronic phase chronic myelogenous leukemia (CML) have been revolutionized due to the discovery of a selective tyrosine kinase inhibitor, imatinib (Gleevec, STI571), which is substantially improving median survival. However, emergence of imatinib-resistance has put up a serious problem that requires novel treatment methods. Catechins, polyphenolic compounds in green tea, are gathering much attention due to their potential antitumor effects. So far (-)-epigallocatechin-3-gallate (EGCG), the most abundant component of catechin, has been shown to cause typical apoptosis in several tumor cell lines in most cases through activation of caspases. In this study, we showed that EGCG predominantly caused necrosis-like cell death via a caspase-independent mechanism in CML cells, K562 and C2F8, whereas imatinib induced the typical apoptotic cell death. Moreover, this caspase-independent cell death partially mediated the release of apoptosis-inducing factor, AIF, and serine protease, HtrA2/Omi, from the mitochondria to cytosol. In addition, EGCG enhanced the imatinib-induced cell death (P < 0.01) resulting in additive cell death in K562 cells and EGCG alone, effectively reduced the viability of imatinib-resistant K562 cells (P < 0.01). Catechin is a possible candidate for an antitumor agent that causes cell death in CML cells via a caspase-independent mechanism.

Indexed as

Anticarcinogenic AgentsApoptosisBlotting, WesternCaspasesCatechinCell Line, TumorCell ProliferationHumansImmunoenzyme TechniquesLeukemia, Myelogenous, Chronic, BCR-ABL PositiveMembrane Potential, MitochondrialNecrosisSubcellular FractionsTeaAnticarcinogenic AgentsCaspasesCatechinepigallocatechin gallateTea

Identifiers

PMID19200260
PMCPMC11159957
OpenAlexW2038518074

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.