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【bio-news】砷触发罕见白血病病发的独特机制

Dartmouth Researchers Find that Arsenic Triggers Unique Mechanism in Rare Leukemia

01/08/07 -- Dartmouth Medical School (DMS) researchers have identified a new way that arsenite, a form of arsenic, acts in treating a rare cancer known as APL, or acute promyelocytic leukemia. Their study is published in the Jan. 3 issue of the Journal of the National Cancer Institute.


"We knew that arsenite was particularly effective against this cancer, and we wanted to figure out why," says Sutisak Kitareewan, an author on this paper and an instructor of pharmacology and toxicology at DMS. "Now we know that arsenite destabilizes lysosomes, a part of a cell that contains certain enzymes, which, when released, often kill APL cells."

APL is caused by the swapping of chromosomes 15 and 17, which forms a fusion protein. This fusion protein prevents certain blood cells from maturing and leads to an accumulation of immature leukemia cells. Researchers found that arsenite causes rapid destabilization of the lysosome in cells, and that breaks the lysosome apart, releasing enzymes that destroy these particular kinds of leukemia cells.

"We hope this finding will be used to inform further research into treating APL," says co-author Ethan Dmitrovsky, professor of medicine and of pharmacology and toxicology, who is also affiliated with the Norris Cotton Cancer Center at Dartmouth-Hitchcock Medical Center. "We also hope that further studies examine if this same mode of action is the basis for arsenic toxicity."

In addition to Kitareewan and Dmitrovsky, the other authors on the paper include B.D. Roebuck, professor of pharmacology and toxicology; Eugene Demidenko, research professor of community and family medicine in the area of biostatistics; and Roger Sloboda, the Ira Allen Eastman Professor of Biological Sciences. Dmitrovsky also holds the Andrew G. Wallace Professorship at Dartmouth.

This research was supported by funds from the National Institutes of Health and the National Science Foundation.

Source: Dartmouth College

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Dartmouth Researchers Find that Arsenic Triggers Unique Mechanism in Rare Leukemia
Dartmouth研究人员发现砷治疗APL的独特机制

01/08/07 -- Dartmouth Medical School (DMS) researchers have identified a new way that arsenite, a form of arsenic, acts in treating a rare cancer known as APL, or acute promyelocytic leukemia. Their study is published in the Jan. 3 issue of the Journal of the National Cancer Institute.
01/08/07—Dartmouth医学院(DMS)研究人员明确了一种亚砷酸盐,即砷在治疗罕见白血病急性早幼粒细胞白血病(APL)治疗方面的新机制。他们的研究成果发表在一月三日的国立癌症研究杂志上。

"We knew that arsenite was particularly effective against this cancer, and we wanted to figure out why," says Sutisak Kitareewan, an author on this paper and an instructor of pharmacology and toxicology at DMS. "Now we know that arsenite destabilizes lysosomes, a part of a cell that contains certain enzymes, which, when released, often kill APL cells."
文章作者、DMS药理学及毒理学讲师Sutisak Kitareewan 说:“我们已经知道砷对APL极为有效,但我们想明确为什么有效。现在我们明白,砷可以使溶酶体不稳定。后者是一种细胞成份,包含特定的酶,当这些酶释放时,可以杀灭APL细胞。”

APL is caused by the swapping of chromosomes 15 and 17, which forms a fusion protein. This fusion protein prevents certain blood cells from maturing and leads to an accumulation of immature leukemia cells. Researchers found that arsenite causes rapid destabilization of the lysosome in cells, and that breaks the lysosome apart, releasing enzymes that destroy these particular kinds of leukemia cells.
APL由15号及17号染色体异位、形成融合蛋白所导致。这一融合蛋白阻止特定血液细胞分化成熟,使幼稚细胞堆积。研究人员发现砷可以在短时间内使细胞中的溶酶体变得不稳定,从而使其分解并释放出酶,杀灭APL细胞。

"We hope this finding will be used to inform further research into treating APL," says co-author Ethan Dmitrovsky, professor of medicine and of pharmacology and toxicology, who is also affiliated with the Norris Cotton Cancer Center at Dartmouth-Hitchcock Medical Center. "We also hope that further studies examine if this same mode of action is the basis for arsenic toxicity."
共同作者、DMS药理学及毒理学教授Ethan Dmitrovsky说:“我们希望这一发现可以促进有关APL治疗的研究。我们也希望更进一步的研究能证实这一作用方式是否为砷对APL细胞毒性的基础。”他同时也是Dartmouth-Hitchcock 医学中心Norris Cotton癌症中心成员。

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作者:admin@医学,生命科学    2011-03-10 05:11
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