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ASCO 2012:

PACE: Robust and Durable Antileukemic Responses With Ponatinib in Patients With Heavily Pretreated, Refractory CML or Ph+ ALL Posting Date: June 06, 2012 Updated analysis of PACE: single-arm phase II trial[1] Summary of Key Conclusions: www.clinicaloptions.com/Oncology/Conference>

clinicaloptions.com/Oncology/Conference%20Coverage/Clin%20Onc%20June%202012/Tracks/Chronic%20Myeloid%20Leukemia/Capsules/6503.aspx">www.clinicaloptions.com/Oncology/Conference>

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ASCO: 'New, Exciting Era' for Research and Treatment of CLL
By Hagop Kantarjian, MD1 | 18 June 2012
Department of Leukemia, The University of Texas M.D. Anderson Cancer Center, Houston, Texas
Interviewed by Michael Kaufman

CancerNetwork speaks with Hagop Kantarjian, MD, chair of the department of leukemia at the University of Texas M.D. Anderson Cancer Center in Houston, who shares his impressions of some of the highlights of this year's ASCO meeting with regard to hematologic malignancies.

Scroll down to the middle of the first page to where Dr. Kantarjian speaks about what he considers to be the exciting news for CML.

Snip:
"...The second area is chronic myeloid leukemia (CML). There were updates of the two front-line randomized studies looking at the second generation TKIs, nilotinib and dasatinib vs the standard of care, which is imatinib. And in both of these updates the investigators report that the second-generation TKIs continue to show an advantage in terms of the early surrogate endpoints—incidence of major molecular response, complete molecular response, and reduction in incidence of transformation to accelerated and blastic phase. So nothing much new in these two updates of the ENESTnd trial for nilotinib vs imatinib, or the DECISION trial for dasatinib vs imatinib, but it is reassuring that the updates continue to show a benefit for the second-generation TKIs.
I think the more important study is the one with ponatinib, which is also a BCR-ABL tyrosine kinase inhibitor, but in contrast to the other two drugs it is also active against the T315I mutation.........." read more here
www.cancernet.com/conferencereports/asco2012>