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Some more information that has come to my atttention that may be of interest to

some of you.....

Last modified December 2007. ADDING TIPIFARNIB after imatinib failure in

CML restores antitumor efficacy. Dr. Cortes and colleagues at The

University of Texas M. D. Cancer Center in Houston treated 26 patients

with chronic phase CML, half with Abl kinase domain mutations, with the

combination of imatinib and tipifarnib, after an initial course of imatinib

treatment failed.

http://www.oncolink.upenn.edu/resources/article.cfm?c=3 & s=8 & ss=23 & id=14881 & month\

=12 & year=2007

MODELING predicts impact of cellular QUIESCENCE on CML therapy. " Data

indicate that the presence of certain 'sleeping' or quiescent cancer stem cells

can be an obstacle to treatment, because they are not killed by the drug(s), "

study co-author Dr. Dominik Wodarz told Reuters Health. However, more and more

of these cells are activated over time, regaining susceptibility to drug

therapy.

http://www.oncolink.upenn.edu/resources/article.cfm?c=3 & s=8 & ss=23 & id=14668 & month\

=10 & year=2007

GENETICALLY unstable stem cells confer drug resistance in CML. To

understand the mechanisms involved, the research team at the Terry Fox

Laboratory in Vancouver, British Columbia obtained blood samples from five

patients with chronic phase CML who had not been treated with imatinib. Control

samples of blood and bone marrow from healthy individuals were also collected.

They used fluorescence-activated cell sorting to isolate patients' CML stem

cells, and then generated BCR-ABL cDNA for sequencing and comparison with normal

control cells. The results showed that the BCR-ABL oncogene in CML stem cells is

highly unstable, the researchers report, and have a high frequency of mutations,

even when cloned in vitro and in the absence of imatinib exposure.

http://www.oncolink.upenn.edu/resources/article.cfm?c=3 & s=8 & ss=23 & id=14157 & month\

=05 & year=2007

Blessings,

Lottie

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