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Department of Dermatology, University of Wisconsin Medical Sciences Center, Madison, Wisconsin 53706
Letter
I read with great interest the article by Leone et al. (1) showing a strong link between the anticancer activities of tea polyphenols and inhibition of Bcl-2 family of proteins, which are implicated in the development of many human malignancies. However, it is disappointing to note that the authors ignored a large amount of published work showing inhibition of Bcl-2 family proteins by tea polyphenols. A simple PubMed search using "Bcl-2" and "tea" as keywords reveals 14 papers, and a similar search using "tea polyphenols" and "Bcl" as keywords reveals 6 papers. Among these papers, our recently published study in the July 31, 2003 issue of Oncogene (2) and several other papers published in FASEB Journal (3) , Carcinogenesis (4) Breast Cancer Research and Treatment (5) , Journal of Biological Chemistry (6) , Clinical Cancer Research (7) and Life Sciences (8) really stand out. None of these prior published works (2, 3, 4, 5, 6, 7, 8) is cited in the publication of Leone et al. (1) . Hiding prior published work to get your work published has been used by many authors, but sooner or later this practice catches authors. Leone et al. (1) wrote: "In conclusion, our findings provide unprecedented insights into the mechanism of action of the major natural products present in the most widely consumed beverage, next to water." Although this study is interesting, I wonder what is new in this publication of Leone et al. (1) .
Received 12/26/03. Accepted 1/ 7/04.
REFERENCES
B in epigallocatechin-3-gallate-induced apoptosis of LNCaP cells. Oncogene, 22: 4851-9, 2003.[CrossRef][Medline]
The Burnham Institute, La Jolla, California 92037
To date, there are no papers reporting on direct inhibition of Bcl-2 and Bcl-xL by tea polyphenols, hence the results presented in our paper (1)
are novel and unprecedented. Dr. Mukhtar is grossly confounding direct inhibition with down-regulation of these proteins. In fact, Dr. Mukhtar’s paper (2)
reports on the effect of one particular green tea component on the inhibition of "two important transcription factors p53 and NF-B, causing a change in the ratio of Bax/Bcl-2 in a manner that favors apoptosis. This altered expression of Bcl-2 family members... " would cause apoptosis (2)
. Several related papers report on the possible inhibition of other proteins by tea polyphenols (mostly EGCG) at micromolar concentrations. Our findings that the antiapoptotic proteins Bcl-2 and Bcl-xL can be directly antagonized by a variety of tea polyphenols at nanomolar concentrations are novel and provide unprecedented insights on the possible mechanism of action of these compounds. We must conclude, from his comments, that Dr. Mukhtar has not carefully read our paper, therefore we report here again our main conclusion: "Whereas tea polyphenols conceivably could affect apoptosis through multiple mechanisms, our findings indicate that tea polyphenols may act as apoptosis-promoting cancer antagonists by binding to and suppressing Bcl-2-family proteins" (1)
.
Therefore, the paper from Dr. Mukhtar (2) and the others he has mentioned do not diminish the novelty or the significance of our findings.
Received 1/20/04. Accepted 1/23/04.
REFERENCES
B in epigallocatechin-3-gallate-induced apoptosis of LNCaP cells. Oncogene, 22: 4851-9, 2003.[CrossRef][Medline]
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