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Giving imatinib a hand

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Researchers have discovered a new a way to make the anticancer drug imatinib more effective... Imatinib is currently the most popular targeted therapy for CML... The leukemia is associated with the abnormal fusion of BCR with a kinase gene, ABL, which results in a perpetually active kinase known as BCR-ABL... But the drug doesn't work in everyone and patients often relapse, most likely because the drug only targets mature cells, leaving CML stem cells behind... Mutated versions of the recently identified protein AHI-1, whose function is unknown, have been shown to be highly expressed in leukemic stem cells—the same cells that express BCR-ABL in patients with CML... Here, Zhou et al. show that expressing AHI-1 in stem cells turns the cells cancerous in vitro, and these cells caused lethal leukemia when transferred into mice... When expressed in BCR-ABL–positive cells, AH1-1 exacerbated the growth-promoting effects of the fusion protein... Indeed, blocking AHI-1 in cells from imatinib-resistant CML patients restored the cells' sensitivity to the drug... With this finding, the race is on to find a drug to block AH1-1... As other studies have recently suggested, the cure for CML and other leukemias may not lie in a miracle drug, but rather in a carefully concocted cocktail of targeted therapies.

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A combination of imatinib and an AHI-1 blocker (red) killed more cells from imatinib-resistant CML patients than did imatinib alone (purple).
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fig1: A combination of imatinib and an AHI-1 blocker (red) killed more cells from imatinib-resistant CML patients than did imatinib alone (purple).


Giving imatinib a hand
A combination of imatinib and an AHI-1 blocker (red) killed more cells from imatinib-resistant CML patients than did imatinib alone (purple).
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2571918&req=5

fig1: A combination of imatinib and an AHI-1 blocker (red) killed more cells from imatinib-resistant CML patients than did imatinib alone (purple).

View Article: PubMed Central

AUTOMATICALLY GENERATED EXCERPT
Please rate it.

Researchers have discovered a new a way to make the anticancer drug imatinib more effective... Imatinib is currently the most popular targeted therapy for CML... The leukemia is associated with the abnormal fusion of BCR with a kinase gene, ABL, which results in a perpetually active kinase known as BCR-ABL... But the drug doesn't work in everyone and patients often relapse, most likely because the drug only targets mature cells, leaving CML stem cells behind... Mutated versions of the recently identified protein AHI-1, whose function is unknown, have been shown to be highly expressed in leukemic stem cells—the same cells that express BCR-ABL in patients with CML... Here, Zhou et al. show that expressing AHI-1 in stem cells turns the cells cancerous in vitro, and these cells caused lethal leukemia when transferred into mice... When expressed in BCR-ABL–positive cells, AH1-1 exacerbated the growth-promoting effects of the fusion protein... Indeed, blocking AHI-1 in cells from imatinib-resistant CML patients restored the cells' sensitivity to the drug... With this finding, the race is on to find a drug to block AH1-1... As other studies have recently suggested, the cure for CML and other leukemias may not lie in a miracle drug, but rather in a carefully concocted cocktail of targeted therapies.

No MeSH data available.