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- 12 June 2002 |
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Green tea blocks HIV-related cancer
11 June 2002 8:00 GMT by Julie Clayton, BioMedNet News
The unpublished findings, from Adriana Albini, of the Italian National Institute for Cancer Research and the University of Genoa, add to the list of health claims for this popular drink, she told delegates to the 7th European Conference on Experimental AIDS Research here. With a taste for alternative approaches, Albini added green tea from the plant Camellia sinensis, or its flavanoid extract, epigallocatechin gallate (EGCG), to the drinking water of mice that had been injected with human Kaposi's sarcoma tumor cells a few days earlier. The mice were "nude," a strain that lacks the ability to reject transplanted tissues from other species. Albini found that the treatment reduced tumor formation by about 70%, compared with that of control animals, she told a workshop on novel therapies. This "strong and significant" result is consistent with epidemiological findings linking a reduced incidence of oesophageal, stomach, colon and other human cancers to the regular consumption of green tea, she noted. It also extends previous findings by Albini's group that EGCG represses angiogenesis by blocking the matrix metalloprotease enzymes, MMP-2 and MMP-9. In the US, the field of cancer chemoprevention is "blooming," said Albini, who added that Kaposi's sarcoma could now be added to the list of other types of cancer being investigated in clinical trials. According to Dorothee von Laer, a virologist at the Georg-Speyer-Haus Institute in Frankfurt who chaired the workshop, "[Albini's] data were good. Many people just throw stuff in culture and say it inhibits, but this was well controlled. And she looked at which substances were active. What we need now is a clinical trial." Von Laer added: "The main problem about these kinds of drugs is that there's not much interest from pharmaceutical companies because everyone can buy it routinely." In April this year, Albini published in the journal AIDS that EGCG directly inhibited, in a dose-dependent manner, the HIV replication enzyme, reverse transcriptase (RT), derived from cultures of blood cells infected with HIV variants associated with both early and late stages of HIV infection (known as R5 and X4 viruses). She also found that EGCG reduced the concentration of the viral coat protein, p24, indicating a direct inhibitory effect on viral production. These findings extended previous observations that EGCD blocks casein kinase II, a host cell enzyme that HIV exploits to activate RT, and another viral enzyme, protease, which is also a target for current HIV drugs. "Since it's a nontoxic drug, it would be interesting to see if it could be used in combinations," said Albini. "And as green tea, it's something that could be available in situations where expensive drugs are not available," particularly where there is endemic infection with both HIV and the herpes virus HHV8, which synergizes with HIV to cause Kaposi's sarcoma, she noted. Alternatively, chemical modification could lead to more potent substitutes, she concluded.
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See also:
Tea: A rich brew of anti-cancer magic bullets? [News] Kathryn Senior Drug Discovery Today, 2001, 6:21:1079-1080 Proteasome inhibitors: From research tools to drug candidates [Review] Alexei F. Kisselev and Alfred L. Goldberg Chemistry & Biology, 2001, 8:8:739-758 Antiangiogenic and antivascular therapy for cancer [Review] Giulia Taraboletti and Barbara Margosio Current Opinion in Pharmacology, 2001, 1:4:378-384 The social life of actin and microtubules: Interaction versus cooperation [Review] Frederic Yarm, Isabelle Sagot and David Pellman Current Opinion in Microbiology, 2001, 4:6:696-702 |
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Today's News Stories News Archive |
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Genoa
- In a supermarket near you could be lurking a safe nontoxic
treatment for the tumor associated with HIV infection: green tea.
Both the tea, and an extracted compound, block the growth of
Kaposi's sarcoma, as well as HIV itself, but without the side
effects of current antiretroviral drugs, reported an Italian
immunologist yesterday.