iris/tyrosine

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Gleevec as Maintenance Therapy After Cytogenetic Response With Nilotinib in Newly Diagnosed Chronic Myelogenous Leukemia

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Imatinib mesylate selectively targets the causative BCR-ABL oncogene in CML. The results of the IRIS trial indicate that in patients with chronic phase CML treated with first line imatinib, achievement of a complete or partial cytogenetic response (CCyR or PCyR) at 12 months is associated with a

Nitisinone for Type 1B Oculocutaneous Albinism

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Objective: The primary objective of this study is to evaluate oral nitisinone as a treatment that improves ocular pigmentation in adult participants with oculocutaneous albinism, type 1B (OCA1B). Secondary objectives of this study are to determine whether the selected outcome measures are robust

Fractalkine, a CX3C Chemokine, Act as a Mediator of Ocular Angiogenesis

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Fractalkine (FKN), the sole member of the CX3C chemokine family, is named for its fractal geometry. The CX3C motif, with three amino acids between the two terminal cysteines, makes fractalkine distinct from other chemokines.The structure of fractalkine, a membrane-bound glycoprotein with the

Front-line Nilotinib Treatment of BCR-ABL+ Chronic Myeloid Leukaemia in Chronic Phase

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The primary objective of the study is to describe the stability of molecular response with NIL as frontline therapy in newly diagnosed, unselected, CP CML patients, in an independent, investigator-initiated observational study. Imatinib mesylate (IM), a protein tyrosine kinase inhibitor (TKI)

Chart Review Study of Chronic Myelogenous Leukemia (CML) Patients Treated With Imatinib Outside of a Clinical Trial

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PATIENT POPULATION: All patients with CML in any phase of the disease (chronic, accelerated or blast phase) that has received treatment with any tyrosine kinase inhibitor (eg, imatinib, dasatinib, nilotinib) regardless of prior treatment history that has had at least one clinic visit at MDACC will

Efficacy of Nilotinib Versus Imatinib in Ph+ CML in Early CP Who Have a Suboptimal Molecular Response to Imatinib

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Imatinib mesylate (imatinib) binds to the inactive conformation of Bcr-Abl tyrosine kinase suppressing the Ph+ clone in CML (Giles et al, 2005). It is effective in CML and is a major advance in therapy. With standard dose imatinib, the MMR and complete molecular response (CMR) rates are 35% to 40%

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