Submitted by sandy craine on Sun, 12/05/2013 - 7:19pm
Min Tang1, Mithat Gonen2, Alfonso Quintas-Cardama3, Jorge Cortes3, Hagop Kantarjian3, Chani Field4, Timothy P. Hughes4, Susan Branford4, and Franziska Michor1
Min Tang1, Mithat Gonen2, Alfonso Quintas-Cardama3, Jorge Cortes3, Hagop Kantarjian3, Chani Field4, Timothy P. Hughes4, Susan Branford4, and Franziska Michor1
Submitted by sandy craine on Fri, 26/04/2013 - 1:53pm
Blood First Edition Paper, prepublished online April 25, 2013; DOI 10.1182/blood-2013-03-490003
Blood First Edition Paper, prepublished online April 25, 2013; DOI 10.1182/blood-2013-03-490003
Submitted by sandy craine on Wed, 17/04/2013 - 5:53pm
Michael Kaufman | March 26, 2013
'While WT1 is overexpressed in leukemias and other cancers, including myeloma, and breast, ovarian, and colorectal cancers, it is found in few healthy cells, which makes side effects less likely to occur from drugs that target it. “This is a new approach for attacking WT1, an important cancer target, with an antibody therapy,” said lead author David A. Scheinberg, MD, PhD, chair of the Sloan-Kettering Institute's molecular pharmacology and chemistry program and an inventor of the antibody. “This is something that was previously not possible. There has not been a way to make small-molecule drugs that can inhibit WT1 function. Our research shows that you can use a monoclonal antibody to recognize a cancer-associated protein inside a cell, and it will destroy the cell.”
Michael Kaufman | March 26, 2013
'While WT1 is overexpressed in leukemias and other cancers, including myeloma, and breast, ovarian, and colorectal cancers, it is found in few healthy cells, which makes side effects less likely to occur from drugs that target it. “This is a new approach for attacking WT1, an important cancer target, with an antibody therapy,” said lead author David A. Scheinberg, MD, PhD, chair of the Sloan-Kettering Institute's molecular pharmacology and chemistry program and an inventor of the antibody. “This is something that was previously not possible. There has not been a way to make small-molecule drugs that can inhibit WT1 function. Our research shows that you can use a monoclonal antibody to recognize a cancer-associated protein inside a cell, and it will destroy the cell.”
Submitted by sandy craine on Wed, 17/04/2013 - 4:13pm
Charles A. Schiffer, MD1 | October 12, 2012
Charles A. Schiffer, MD1 | October 12, 2012
Submitted by sandy craine on Wed, 17/04/2013 - 4:01pm
Dave Levitan | April 12, 2013
Chronic myeloid leukemia (CML) patients treated with nilotinib(Drug information on nilotinib) had fewer treatment-emergent BCR-ABL mutations than those treated with imatinib(Drug information on imatinib), and among patients who did have a mutation, those treated with nilotinib had reduced rates of progression to accelerated phase and blast phase of the disease, according to results from the phase III ENESTnd trial.
Dave Levitan | April 12, 2013
Chronic myeloid leukemia (CML) patients treated with nilotinib(Drug information on nilotinib) had fewer treatment-emergent BCR-ABL mutations than those treated with imatinib(Drug information on imatinib), and among patients who did have a mutation, those treated with nilotinib had reduced rates of progression to accelerated phase and blast phase of the disease, according to results from the phase III ENESTnd trial.
Submitted by sandy craine on Wed, 17/04/2013 - 3:21pm
Dave Levitan | April 16, 2013
A study of patients with chronic myeloid leukemia (CML) treated with imatinib found that chronic fatigue is the major factor that limits health-related quality of life (HRQOL).
Dave Levitan | April 16, 2013
A study of patients with chronic myeloid leukemia (CML) treated with imatinib found that chronic fatigue is the major factor that limits health-related quality of life (HRQOL).
Submitted by sandy craine on Wed, 17/04/2013 - 3:19pm
By Leah Lawrence | April 15, 2013
A majority of patients on imatinib(Drug information on imatinib) for treatment of gastrointestinal stromal tumor (GIST) or chronic myelogenous leukemia (CML) had low or absent levels of osteocalcin, a bone marker secreted by osteoblasts, and about 50% of patients had a decrease in bone mineral density, signaling that long-term treatment may affect bone health in these patients.
By Leah Lawrence | April 15, 2013
A majority of patients on imatinib(Drug information on imatinib) for treatment of gastrointestinal stromal tumor (GIST) or chronic myelogenous leukemia (CML) had low or absent levels of osteocalcin, a bone marker secreted by osteoblasts, and about 50% of patients had a decrease in bone mineral density, signaling that long-term treatment may affect bone health in these patients.
Submitted by sandy craine on Thu, 11/04/2013 - 12:05pm
S Mustjoki1, K Auvinen2,10, A Kreutzman1,10, P Rousselot3, S Hernesniemi1, T Melo4, A-M Lahesmaa-Korpinen5, S Hautaniemi5, S Bouchet6, M Molimard6, R Smykla7, F Y Lee7, J Vakkila1, S Jalkanen2,8, M Salmi2,9 and K Porkka1
Abstract
Tyrosine kinase inhibitors (TKIs) have potent effects on malignant cells, and they also target kinases in normal cells, which may have therapeutic implications.
S Mustjoki1, K Auvinen2,10, A Kreutzman1,10, P Rousselot3, S Hernesniemi1, T Melo4, A-M Lahesmaa-Korpinen5, S Hautaniemi5, S Bouchet6, M Molimard6, R Smykla7, F Y Lee7, J Vakkila1, S Jalkanen2,8, M Salmi2,9 and K Porkka1
Abstract
Tyrosine kinase inhibitors (TKIs) have potent effects on malignant cells, and they also target kinases in normal cells, which may have therapeutic implications.
Submitted by sandy craine on Fri, 05/04/2013 - 4:24pm
Pratap Neelakantan1, Gareth Gerrard1, Claire Lucas2, Dragana Milojkovic1, Philippa May1, Lihui Wang2, Christos Paliompeis1, Marco Bua1, Alistair Reid1, Katayoun Rezvani1, Stephen O'Brien3, Richard Clark2, John Goldman1, and David Marin1,
Abstract
Several groups have shown that that the BCR-ABL1 transcript level measured at 3 or 6 months after starting treatment with tyrosine kinase inhibitors strongly predicts for clinical outcomes for CML patients. In this work we asked whether the prognostic value of the 3-month transcript level could be improved by combining the 3- and 6- month results.
Pratap Neelakantan1, Gareth Gerrard1, Claire Lucas2, Dragana Milojkovic1, Philippa May1, Lihui Wang2, Christos Paliompeis1, Marco Bua1, Alistair Reid1, Katayoun Rezvani1, Stephen O'Brien3, Richard Clark2, John Goldman1, and David Marin1,
Abstract
Several groups have shown that that the BCR-ABL1 transcript level measured at 3 or 6 months after starting treatment with tyrosine kinase inhibitors strongly predicts for clinical outcomes for CML patients. In this work we asked whether the prognostic value of the 3-month transcript level could be improved by combining the 3- and 6- month results.
Submitted by sandy craine on Sun, 31/03/2013 - 7:45pm
Trying to Calculate the Economic Value of Dasatinib or Nilotinib for Imatinib-Resistant CML
Published Online: Thursday, March 28, 2013
Although it is now standard practice to utilize the second-generation tyrosine-kinase inhibitors dasatinib or nilotinib in patients whose chronic myeloid leukemia (CML) has recurred while taking imatinib treatment, published support for the economic value of this approach is lacking. Investigators from the University of Exeter, United Kingdom, conducted a review of the literature and produced an economic model to help fill this information gap.
Trying to Calculate the Economic Value of Dasatinib or Nilotinib for Imatinib-Resistant CML
Published Online: Thursday, March 28, 2013
Although it is now standard practice to utilize the second-generation tyrosine-kinase inhibitors dasatinib or nilotinib in patients whose chronic myeloid leukemia (CML) has recurred while taking imatinib treatment, published support for the economic value of this approach is lacking. Investigators from the University of Exeter, United Kingdom, conducted a review of the literature and produced an economic model to help fill this information gap.
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