Evidence map›Paper›PMID 16809610›Full record

ArticleBlood2006

Specific killing of multiple myeloma cells by (-)-epigallocatechin-3-gallate extracted from green tea: biologic activity and therapeutic implications.

Masood A Shammas, Paola Neri, Hemanta Koley, Ramesh B Batchu, Robert C Bertheau, Vidit Munshi, Rao Prabhala, Mariateresa Fulciniti, Yu Tzu Tai, Steven P Treon and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
6.6field-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

61 citing papers in PubMed, 165 citations in OpenAlex.

  1. Trial
  2. Review
  3. Review
  4. Article
  5. Article
  6. Integrative Hematology: State of the Art.International journal of molecular sciences · 2023
    Review
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Src Mediates Epigallocatechin-3-Molecules (Basel, Switzerland) · 2020
    Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Review
  18. Article
  19. Review
  20. Future in the Past:International journal of molecular sciences · 2018
    Article

1 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

13 authors at 1 institution in 1 country.

Masood A ShammasVeterans Administration Boston Health Care System, and Dana Farber Cancer Institute/Harvard Medical School, 44 Binney Street, D1B25, Boston, MA 02115, USA.
Paola Neri
Hemanta Koley
Ramesh B Batchu
Robert C Bertheau
Vidit Munshi
Rao Prabhala
Mariateresa Fulciniti
Yu Tzu Tai
Steven P Treon
Raj K Goyal
Kenneth C Anderson
Nikhil C Munshi
Dana-Farber Cancer Institute · US

Funding

PHYSIOLOGY AND PATHOPHYSIOLOGY OF ESOPHAGEAL MOTILITYR01DK031092 · NIDDK · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI GOYAL, RAJ K · 1994 to 2002
$1.3M
PHYSIOLOGY &PATHOPHYSIOLOGY OF ESOPHAGEAL MOTILITYR37DK031092 · NIDDK · BETH ISRAEL DEACONESS MEDICAL CENTER · PI GOYAL, RAJ K · 1986 to 1993
–
NIDDK NIH HHS DK 031092PHS HHS P01 78378PHS HHS P50 100007
6 · The paper itself

Abstract

Epigallocatechin-3-gallate (EGCG), a polyphenol extracted from green tea, is an antioxidant with chemopreventive and chemotherapeutic actions. Based on its ability to modulate growth factor-mediated cell proliferation, we evaluated its efficacy in multiple myeloma (MM). EGCG induced both dose- and time-dependent growth arrest and subsequent apoptotic cell death in MM cell lines including IL-6-dependent cells and primary patient cells, without significant effect on the growth of peripheral blood mononuclear cells (PBMCs) and normal fibroblasts. Treatment with EGCG also led to significant apoptosis in human myeloma cells grown as tumors in SCID mice. EGCG interacts with the 67-kDa laminin receptor 1 (LR1), which is significantly elevated in myeloma cell lines and patient samples relative to normal PBMCs. RNAi-mediated inhibition of LR1 resulted in abrogation of EGCG-induced apoptosis in myeloma cells, indicating that LR1 plays an important role in mediating EGCG activity in MM while sparing PBMCs. Evaluation of changes in gene expression profile indicates that EGCG treatment activates distinct pathways of growth arrest and apoptosis in MM cells by inducing the expression of death-associated protein kinase 2, the initiators and mediators of death receptor-dependent apoptosis (Fas ligand, Fas, and caspase 4), p53-like proteins (p73, p63), positive regulators of apoptosis and NF-kappaB activation (CARD10, CARD14), and cyclin-dependent kinase inhibitors (p16 and p18). Expression of related genes at the protein level were also confirmed by Western blot analysis. These data demonstrate potent and specific antimyeloma activity of EGCG and provide the rationale for its clinical evaluation.

Indexed as

AnimalsAntineoplastic AgentsApoptosisCatechinCell Line, TumorGene Expression ProfilingHumansMiceMice, SCIDMultiple MyelomaNeoplasm TransplantationPhytotherapyReceptors, LamininRNA, Small InterferingTeaTransplantation, HeterologousAntineoplastic AgentsCatechinepigallocatechin gallateReceptors, LamininRNA, Small InterferingTea

Identifiers

PMID16809610
PMCPMC1895573
OpenAlexW2093789049

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.