Introduction: The T315I mutation in patients with chronic myeloid leukemia (CML) has been associated with therapeutic resistance and an unfavourable prognosis.
Aim: To study the frequency of T315I mutation in patients with CML, BCR-ABL (+), their clinical characteristics, disease evolution, and median survival.
Patients And Methods: We studied 75 patients with CML and BCR-ABL1 (+).
Background: Management of beta-thalassemia major (TM) requires life-long hemotransfusions leading to iron overload. Iron elimination is enhanced by the use of modern chelators.
Aim: To assess the effect of modern chelation therapy by dynamics of serum ferritin concentration and liver MRI T2*.
Chronic myeloid leukemia (CML) arises from the fusion of the BCR and the ABL1 genes. The BCR gene (chromosome 22q11.2) and the ABL1 gene (chromosome 9q34) fuse together due to reciprocal chromosome translocation forming the Philadelphia chromosome (Ph).
View Article and Find Full Text PDFOlder patients with haemophilia (PWH) face many challenges related not only to haemophilia but also to general comorbidities associated with ageing. This article discusses the clinical experience published about the high prevalence of diseases in older PWH. These conditions are managed in the general population by healthcare workers with little training in haemophilia.
View Article and Find Full Text PDFSerum levels of OPG and RANKL and their clinical correlations were analyzed in 66 newly-diagnosed patients with multiple myeloma (MM). RANKL and RANKL /OPG ratio were significantly increased in advanced clinical stages and high grade myeloma bone disease (MBD), while OPG showed a tendency to decrease. Renal failure modified the expression of OPG.
View Article and Find Full Text PDFProteasome inhibitors are emerging as a promising class of anti-cancer therapeutic agents. The first of this new class of drugs with a clinical significance, bortezomib (PS 341, Velcade), is a modified dipeptidyl boronic acid. Bortezomib reduces the NF-kappaB translocation / transcription and blocks the drug-related signalling pathways critical to basic vital functions of myeloma cells.
View Article and Find Full Text PDFMultiple myeloma has recently been found to induce considerable imbalance in the newly identified system of osteoprotegerin (OPG), receptor activator of nuclear factor KB ligand (RANKL) and RANK. The binding of RANKL to RANK on the surface of osteoclastic precursors in the presence of m-CSF activates the signalling pathways for differentiation and proliferation of an osteoclastic line. OPG is a decoy circulating receptor for RANKL which blocks its binding to RANK.
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