Submitted by sandy craine on Tue, 22/01/2013 - 1:50pm
On 17 January 2013, the Committee for Medicinal Products for Human Use (CHMP) adopted a positive opinion, recommending the granting of a conditional marketing authorisation for the medicinal product Bosulif 100 mg and 500 mg film-coated tablets intended for the treatment of chronic myelogenous leukaemia (CML). Bosulif was designated as an orphan medicinal product on 4 August 2010.
On 17 January 2013, the Committee for Medicinal Products for Human Use (CHMP) adopted a positive opinion, recommending the granting of a conditional marketing authorisation for the medicinal product Bosulif 100 mg and 500 mg film-coated tablets intended for the treatment of chronic myelogenous leukaemia (CML). Bosulif was designated as an orphan medicinal product on 4 August 2010.
Submitted by sandy craine on Tue, 08/01/2013 - 11:47am
Evaluation of the Impact of Switching CML Patients Treated with a First-line Tyrosine Kinase Inhibitor to Ponatinib
CAMBRIDGE, Mass. & LONDON--(BUSINESS WIRE)--Jan. 7, 2013-- ARIAD Pharmaceuticals, Inc. (NASDAQ: ARIA) and Newcastle University, U.K., on behalf of the U.K. National Cancer Research Institute (NCRI) CML Working Group, today announced an agreement to collaborate on a multicenter, randomized Phase 3 trial, named SPIRIT 3, to assess the impact of switching patients with chronic myeloid leukemia (CML) being treated with a first-line tyrosine kinase inhibitor, upon suboptimal response or treatment failure, to ponatinib. The NCRI expects to begin enrollment in the trial of 1,000 patients at approximately 172 clinical research sites in the U.K. in the second quarter of 2013.
Evaluation of the Impact of Switching CML Patients Treated with a First-line Tyrosine Kinase Inhibitor to Ponatinib
CAMBRIDGE, Mass. & LONDON--(BUSINESS WIRE)--Jan. 7, 2013-- ARIAD Pharmaceuticals, Inc. (NASDAQ: ARIA) and Newcastle University, U.K., on behalf of the U.K. National Cancer Research Institute (NCRI) CML Working Group, today announced an agreement to collaborate on a multicenter, randomized Phase 3 trial, named SPIRIT 3, to assess the impact of switching patients with chronic myeloid leukemia (CML) being treated with a first-line tyrosine kinase inhibitor, upon suboptimal response or treatment failure, to ponatinib. The NCRI expects to begin enrollment in the trial of 1,000 patients at approximately 172 clinical research sites in the U.K. in the second quarter of 2013.
Submitted by sandy craine on Fri, 04/01/2013 - 12:50pm
Paper:3782 'Change in Chronic Low-Grade Non-hematologic Adverse Events (AEs) and Quality of Life (QoL) in Adult Patients (pts) with Philadelphia Chromosome–Positive (Ph+) Chronic Myeloid Leukemia in Chronic Phase (CML-CP) Switched From Imatinib (IM) to Nilotinib (NIL)'
Jorge E. Cortes, MD1, Jeffrey H. Lipton, MD, PhD2, Carole B. Miller, MD3*, Sikander Ailawadhi, MD4, Luke Akard, MD5, Javier Pinilla-Ibarz, MD, PhD6*, Felice P. Lin, PharmD7*, Solveig G. Ericson, MD, PhD7 and Michael J. Mauro, MD8
Paper:3782 'Change in Chronic Low-Grade Non-hematologic Adverse Events (AEs) and Quality of Life (QoL) in Adult Patients (pts) with Philadelphia Chromosome–Positive (Ph+) Chronic Myeloid Leukemia in Chronic Phase (CML-CP) Switched From Imatinib (IM) to Nilotinib (NIL)'
Jorge E. Cortes, MD1, Jeffrey H. Lipton, MD, PhD2, Carole B. Miller, MD3*, Sikander Ailawadhi, MD4, Luke Akard, MD5, Javier Pinilla-Ibarz, MD, PhD6*, Felice P. Lin, PharmD7*, Solveig G. Ericson, MD, PhD7 and Michael J. Mauro, MD8
Submitted by sandy craine on Fri, 21/12/2012 - 10:30am
Winning the battle against leukaemia: positive early results in clinical trial for DNA vaccine: News Release from University of Southampton.
Winning the battle against leukaemia: positive early results in clinical trial for DNA vaccine: News Release from University of Southampton.
Submitted by sandy craine on Wed, 19/12/2012 - 7:11pm
There are a number of approaches for selective targeting of leukemic stem cells (LSCs). These include targeting stem-cell properties, such as self-renewal, inducing cycling of quiescent LSCs to sensitize them to conventional agents, employing or inducing immune-based mechanisms, and targeting tumor-specific physiology. Agents such as parthenolide inhibit the ability of leukemic stem cells to respond to oxidative stress and make leukemic stem cells and bulk leukemic cells susceptible to cell death, while normal stem cells remain relatively unharmed by these agents. The major mechanism of action of these small molecules appears to revolve around the aberrant glutathione metabolism pathway found in leukemic cells.
There are a number of approaches for selective targeting of leukemic stem cells (LSCs). These include targeting stem-cell properties, such as self-renewal, inducing cycling of quiescent LSCs to sensitize them to conventional agents, employing or inducing immune-based mechanisms, and targeting tumor-specific physiology. Agents such as parthenolide inhibit the ability of leukemic stem cells to respond to oxidative stress and make leukemic stem cells and bulk leukemic cells susceptible to cell death, while normal stem cells remain relatively unharmed by these agents. The major mechanism of action of these small molecules appears to revolve around the aberrant glutathione metabolism pathway found in leukemic cells.
Submitted by sandy craine on Fri, 14/12/2012 - 8:09pm
FDA approves Iclusig to treat two rare types of leukemia
Drug approved 3 months ahead of schedule
The U.S. Food and Drug Administration today approved Iclusig (ponatinib) to treat adults with chronic myeloid leukemia (CML) and Philadelphia chromosome positive acute lymphoblastic leukemia (Ph+ ALL), two rare blood and bone marrow diseases.
FDA approves Iclusig to treat two rare types of leukemia
Drug approved 3 months ahead of schedule
The U.S. Food and Drug Administration today approved Iclusig (ponatinib) to treat adults with chronic myeloid leukemia (CML) and Philadelphia chromosome positive acute lymphoblastic leukemia (Ph+ ALL), two rare blood and bone marrow diseases.
Submitted by sandy craine on Fri, 14/12/2012 - 10:57am
The researchers report their findings December 9 in a plenary scientific session at the 54th American Society of Hematology Annual Meeting and Exposition in Atlanta.
The researchers report their findings December 9 in a plenary scientific session at the 54th American Society of Hematology Annual Meeting and Exposition in Atlanta.
Submitted by sandy craine on Mon, 03/12/2012 - 1:39pm
“This is another tool to fight this disease, but it’s the tool we’ve been waiting for,” said Brian Druker, M.D., director of the OHSU Knight Cancer Institute.
“This is another tool to fight this disease, but it’s the tool we’ve been waiting for,” said Brian Druker, M.D., director of the OHSU Knight Cancer Institute.
Submitted by sandy craine on Mon, 12/11/2012 - 12:25pm
Paper46810
3743 Long-Term Anti-Leukemic Activity of Ponatinib in Patients with Philadelphia Chromosome-Positive Leukemia: Updated Results from an Ongoing Phase 1 Study
Michael W Deininger, MD, PhD1,2, Jorge E. Cortes, MD3, Hagop M. Kantarjian, MD4*, Neil Shah, MD, PhD5, Dale Bixby, MD, PhD6*, Michael J. Mauro, MD7, Ian W. Flinn, MD, PhD8, Thomas O'Hare, PhD1,9, Simin Hu, PhD10*, David J. Dorer10*, Victor M. Rivera, PhD10*, Tim Clackson, PhD10, Christopher D. Turner, MD, FAAP10, Frank G Haluska, MD, PhD10, Brian J. Druker7 and Moshe Talpaz, MD6
Paper46810
3743 Long-Term Anti-Leukemic Activity of Ponatinib in Patients with Philadelphia Chromosome-Positive Leukemia: Updated Results from an Ongoing Phase 1 Study
Michael W Deininger, MD, PhD1,2, Jorge E. Cortes, MD3, Hagop M. Kantarjian, MD4*, Neil Shah, MD, PhD5, Dale Bixby, MD, PhD6*, Michael J. Mauro, MD7, Ian W. Flinn, MD, PhD8, Thomas O'Hare, PhD1,9, Simin Hu, PhD10*, David J. Dorer10*, Victor M. Rivera, PhD10*, Tim Clackson, PhD10, Christopher D. Turner, MD, FAAP10, Frank G Haluska, MD, PhD10, Brian J. Druker7 and Moshe Talpaz, MD6
Submitted by sandy craine on Thu, 08/11/2012 - 6:55pm
'A frequent question now is whether results such as the ones reported here mean that all patients should be treated with a second-generation TKI. Taken at face value, we should always aim in cancer treatment to use our best agent first to have the best chance of rendering our patient free of disease for the longest time, and cured if possible. Our first shot is always our best shot. Nonetheless, one cannot disregard some important facts: (1) most patients do well with imatinib, (2) most patients with resistance to imatinib are still in chronic phase and in generally good condition, and (3) many patients with resistance to imatinib respond to second-generation TKIs. If one adjusts for the sequential use of effective therapy, the current event-free survival is 88% at 7 years compared with the unadjusted rate of 81%.7 However, only 40% to 50% of patients with resistance to imatinib achieve a complete cytogenetic response with second-generation TKIs.8⇓–10 With growing awareness of the relevance of early responses, an argument can be made for using imatinib first and switch patients who are lagging behind early on. This is an attractive approach, but one without data that confirms that patients who fall behind on their response can catch up (in long-term outcome) after such intervention. Then there is the argument of what would we use if we start with a second-generation TKI and the patient develops resistance to it.'.....read full article here:
'A frequent question now is whether results such as the ones reported here mean that all patients should be treated with a second-generation TKI. Taken at face value, we should always aim in cancer treatment to use our best agent first to have the best chance of rendering our patient free of disease for the longest time, and cured if possible. Our first shot is always our best shot. Nonetheless, one cannot disregard some important facts: (1) most patients do well with imatinib, (2) most patients with resistance to imatinib are still in chronic phase and in generally good condition, and (3) many patients with resistance to imatinib respond to second-generation TKIs. If one adjusts for the sequential use of effective therapy, the current event-free survival is 88% at 7 years compared with the unadjusted rate of 81%.7 However, only 40% to 50% of patients with resistance to imatinib achieve a complete cytogenetic response with second-generation TKIs.8⇓–10 With growing awareness of the relevance of early responses, an argument can be made for using imatinib first and switch patients who are lagging behind early on. This is an attractive approach, but one without data that confirms that patients who fall behind on their response can catch up (in long-term outcome) after such intervention. Then there is the argument of what would we use if we start with a second-generation TKI and the patient develops resistance to it.'.....read full article here:
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