The Experts below are selected from a list of 1686972 Experts worldwide ranked by ideXlab platform
Hagop M Kantarjian - One of the best experts on this subject based on the ideXlab platform.
-
survival benefit with imatinib mesylate versus interferon α based regimens in newly diagnosed chronic phase chronic myelogenous leukemia
Blood, 2006Co-Authors: Hagop M Kantarjian, Moshe Talpaz, Susan Obrien, Dan Jones, Francis J Giles, Guillermo Garciamanero, Stefan Faderl, Farhad Ravandi, Mary Beth Rios, Jianqin ShanAbstract:A survival benefit for imatinib mesylate versus Interferon-Alpha therapy could not be demonstrated in the randomized study in newly diagnosed Philadelphia chromosome (Ph)-positive chronic-phase chronic myelogenous leukemia (CML) due to the high rate of crossover (90%) from Interferon-Alpha to imatinib mesylate within a year of study entry. We compared survival in 279 patients with newly diagnosed CML treated with imatinib mesylate at our institution (2000-2004) to 650 patients treated with Interferon-Alpha (1982-1997). The complete cytogenetic response rates were 87% with imatinib mesylate and 28% with Interferon-Alpha (P < .001). The estimated 3-year survival rates were 96% with imatinib mesylate and 81% with Interferon-Alpha (P < .01). Survival rates with imatinib mesylate were significantly better than with Interferon-Alpha within each of the CML prognostic risks groups. By multivariate analysis, imatinib mesylate therapy was identified as an independent favorable prognostic factor, after accounting for the impact of pretreatment factors (hazard ratio, 0.44; P < .01). By landmark analysis at 12 months, survival within each cytogenetic response category was similar with imatinib mesylate or Interferon-Alpha, suggesting that the survival benefit of imatinib mesylate (versus Interferon-Alpha in newly diagnosed CML) is through improving cytogenetic response.
-
Acute pancreatitis associated with interferon alpha therapy for chronic myelogenous leukemia
Leukemia & Lymphoma, 2000Co-Authors: Nizar M. Tannir, Moshe Talpaz, Hassan Ghazal, Subhash Proothi, Hagop M KantarjianAbstract:Acute pancreatitis related to interferon alpha therapy is very rare. We report two patients with chronic myelogenous leukemia (CML) who developed acute pancreatitis following treatment with interferon alpha. A review of the literature on the association of pancreatitis and interferon alpha is provided. Possible pathophysiologic mechanisms are also discussed.
Goran Levan - One of the best experts on this subject based on the ideXlab platform.
-
assignment of 12 loci to rat chromosome 5 evidence that this chromosome is homologous to mouse chromosome 4 and to human chromosomes 9 and 1 1p arm
Genomics, 1990Co-Authors: Claude Szpirer, Michele Riviere, Josiane Szpirer, Myriam Genet, Pierre Luc Dreze, Mozaffarul Quamrul Islam, Goran LevanAbstract:Twelve loci have been assigned to rat chromosome 5: aldolase B (ALDOB), atrial natriuretic factor (ANF = pronatriodilatin, PND), D4RP1, DSI1, galactosyltransferase (GGTB2), glucose transporter (GLUT1), interferon alpha 1 and related interferon alpha (INFA), interferon beta (INFB), lymphocyte-specific protein-tyrosine kinase (LCK), oncogene MOS, alpha 2U-globulin (major urinary protein, MUP), and orosomucoid (ORM, also called alpha 1-acid glycoprotein, AGP). Among these, the interferon alpha and beta genes map in the q22-23 region, which also contains a transformation suppressor gene (SAI1). The other loci reside outside this region. This study also indicated that the rat genome contains 2 LCK genes, unlike the human and murine genomes. These new assignments on rat chromosome 5 demonstrate that this chromosome is highly homologous to mouse chromosome 4 and carries synteny groups conserved on human chromosome 9 (interferon alpha and beta, galactosyltransferase, orosomucoid, and aldolase B genes) and on the short arm of human chromosome 1 (MYCL, glucose transporter, protein kinase LCK, and atrial natriuretic factor genes).
Jianqin Shan - One of the best experts on this subject based on the ideXlab platform.
-
survival benefit with imatinib mesylate versus interferon α based regimens in newly diagnosed chronic phase chronic myelogenous leukemia
Blood, 2006Co-Authors: Hagop M Kantarjian, Moshe Talpaz, Susan Obrien, Dan Jones, Francis J Giles, Guillermo Garciamanero, Stefan Faderl, Farhad Ravandi, Mary Beth Rios, Jianqin ShanAbstract:A survival benefit for imatinib mesylate versus Interferon-Alpha therapy could not be demonstrated in the randomized study in newly diagnosed Philadelphia chromosome (Ph)-positive chronic-phase chronic myelogenous leukemia (CML) due to the high rate of crossover (90%) from Interferon-Alpha to imatinib mesylate within a year of study entry. We compared survival in 279 patients with newly diagnosed CML treated with imatinib mesylate at our institution (2000-2004) to 650 patients treated with Interferon-Alpha (1982-1997). The complete cytogenetic response rates were 87% with imatinib mesylate and 28% with Interferon-Alpha (P < .001). The estimated 3-year survival rates were 96% with imatinib mesylate and 81% with Interferon-Alpha (P < .01). Survival rates with imatinib mesylate were significantly better than with Interferon-Alpha within each of the CML prognostic risks groups. By multivariate analysis, imatinib mesylate therapy was identified as an independent favorable prognostic factor, after accounting for the impact of pretreatment factors (hazard ratio, 0.44; P < .01). By landmark analysis at 12 months, survival within each cytogenetic response category was similar with imatinib mesylate or Interferon-Alpha, suggesting that the survival benefit of imatinib mesylate (versus Interferon-Alpha in newly diagnosed CML) is through improving cytogenetic response.
Moshe Talpaz - One of the best experts on this subject based on the ideXlab platform.
-
survival benefit with imatinib mesylate versus interferon α based regimens in newly diagnosed chronic phase chronic myelogenous leukemia
Blood, 2006Co-Authors: Hagop M Kantarjian, Moshe Talpaz, Susan Obrien, Dan Jones, Francis J Giles, Guillermo Garciamanero, Stefan Faderl, Farhad Ravandi, Mary Beth Rios, Jianqin ShanAbstract:A survival benefit for imatinib mesylate versus Interferon-Alpha therapy could not be demonstrated in the randomized study in newly diagnosed Philadelphia chromosome (Ph)-positive chronic-phase chronic myelogenous leukemia (CML) due to the high rate of crossover (90%) from Interferon-Alpha to imatinib mesylate within a year of study entry. We compared survival in 279 patients with newly diagnosed CML treated with imatinib mesylate at our institution (2000-2004) to 650 patients treated with Interferon-Alpha (1982-1997). The complete cytogenetic response rates were 87% with imatinib mesylate and 28% with Interferon-Alpha (P < .001). The estimated 3-year survival rates were 96% with imatinib mesylate and 81% with Interferon-Alpha (P < .01). Survival rates with imatinib mesylate were significantly better than with Interferon-Alpha within each of the CML prognostic risks groups. By multivariate analysis, imatinib mesylate therapy was identified as an independent favorable prognostic factor, after accounting for the impact of pretreatment factors (hazard ratio, 0.44; P < .01). By landmark analysis at 12 months, survival within each cytogenetic response category was similar with imatinib mesylate or Interferon-Alpha, suggesting that the survival benefit of imatinib mesylate (versus Interferon-Alpha in newly diagnosed CML) is through improving cytogenetic response.
-
Acute pancreatitis associated with interferon alpha therapy for chronic myelogenous leukemia
Leukemia & Lymphoma, 2000Co-Authors: Nizar M. Tannir, Moshe Talpaz, Hassan Ghazal, Subhash Proothi, Hagop M KantarjianAbstract:Acute pancreatitis related to interferon alpha therapy is very rare. We report two patients with chronic myelogenous leukemia (CML) who developed acute pancreatitis following treatment with interferon alpha. A review of the literature on the association of pancreatitis and interferon alpha is provided. Possible pathophysiologic mechanisms are also discussed.
Bernd W Scheithauer - One of the best experts on this subject based on the ideXlab platform.
-
phase ii trial of recombinant interferon alpha 2a and eflornithine in patients with recurrent glioma
Journal of Neuro-oncology, 1998Co-Authors: Janet C Buckner, Terrence L Cascino, Judith R Ofallon, Patrick A Burch, Bernd W ScheithauerAbstract:Interferons alpha and beta have been reported to cause tumor regression in a small proportion of patients with recurrent glioma. Eflornithine, an irreversible inhibitor of ornithine decarboxylase, reduces cellular polyamine levels and has also been reported to cause tumor regression in patients with recurrent anaplastic astrocytoma and glioblastoma multiforme. In vitro evidence suggests that interferon and eflornithine are synergistic. In this phase II trial, we investigated the combination of recombinant alpha interferon (36 × 106 units/m2 subcutaneously days 3 to 7) and eflornithine (2.25 g/m2 QID PO days 1 to 7) repeated every 28 days. All 29 patients entered in the study were evaluable for toxicity and efficacy. Toxicity consisted primarily of fever, chills, myalgia, weakness and fatigue as well as cortical dysfunction including somnolence, confusion, and exacerbation of underlying neurologic deficits. One patient died from cerebral herniation attributable to interferon. None of the patients experienced objective tumor regression. Seven patients (24%) were stable for more than six months, but the disease stability could also be explained by indolent underlying disease or inability to distinguish recurrent tumor from delayed radiation effects. Intermittent high-dose recombinant interferon alpha plus eflornithine demonstrated no definite antitumor effects in this trial.