1,721,355 research outputs found
Clinical relevance of the association of interferon alfa to imatinib in chronic myeloid leukemia therapy
No full textAlpha(v)beta(3) integrin engagement enhances cell invasiveness in human multiple myeloma
No full textExpert Panel Consensus Statement for Proper Evaluation of First Relapse in Multiple Myeloma
No full textPURPOSE OF REVIEW: A working group of six expert physicians convened to assess the spectrum of multiple myeloma relapse presentations, discussed the features that can define the disease as aggressive and not aggressive, and established whether this information could help in selecting treatment together with the characteristics of disease and of patients and type of prior therapy. RECENT FINDINGS: The working group agreed that relapse should be distinguished between biochemical and clinical according to IMWG. Moreover, the expert panel defined "aggressive disease" as a clinical condition that requires therapy able to induce a rapid and as deep as possible response to release symptoms and to avoid impending danger of new events. According to this definition, relapse was considered aggressive if it presents with at least one of the following features: doubling of M protein rate over 2 months, renal insufficiency, hypercalcemia, extramedullary disease, elevated LDH, high plasma cell proliferative index, presence of plasma cells in peripheral blood, or skeletal-related complications. Moreover, the panel agreed that this classification can be useful to choose therapy in first relapse together with other patient, disease, and prior therapy characteristics. So, this item was included in a new therapeutic algorithm. The treatment choice in MM at relapse is wider than in the past with the availability of many new therapeutic regimens leading to increased diversity of approaches and relevant risk of inappropriate treatment decisions. A practical classification of relapses into aggressive or non-aggressive, included in a decisional algorithm on MM management at first relapse, could help to make the appropriate treatment decisions
BORTEZOMIB IS ABLE TO INACTIVATE NF-KB AND DOWN-REGULATE WT1 GENE IN P39 CELL LINE: A POSSIBLE USE IN HIGH-RISK MYELODYSPLASTIC SYNDROMES?
No full textBORTEZOMIB COMBINED WITH HISTONE DEACETYLASE INHIBITOR ITF2357 OR ARSENIC TRIOXIDE EXERTS SYNERGISTIC ANTI-PROLIF- ERATIVE AND PRO-APOPTOTIC EFFECTS IN P39 CELL LINE: A POSSI- BLE NEW APPROACH TO HIGH-RISK MYELODYSPLASTIC SYNDROMES
No full textStandard therapies versus novel therapies in Hodgkin lymphoma.
No full textThe prognostic models in Hodgkin lymphoma (HL) such as the International Prognostic Score (IPS), retrospectively constructed in the last twenty years from different cohorts of patients treated with ABVD or ABVD-equivalent regimens have been shown a limited predictive value on treatment outcome when applied to a prospective cohort of patients. In the turn of millennium a new class of prognostic factors has emerged, aimed to test the chemosensitivity to treatment in a single patient-basis, such as the minimal residual disease (MRD) assessment with molecular biology, or interim PET/CT performed early during treatment. The main challenge in the management of both early and advanced-stage HL is to achieve a durable remission or cure while minimizing therapy toxicity. An adaptive therapy strategy based on interim PET results could distinguish high from low-risk patients: the former with a potential benefit from an intensify regimen, the latter in whom treatment could be de-escalated or abbreviated for minimizing long-term adverse effects. Conversely, chemosensitivity evaluation in early-stage HL has been the underpinning of de-escalation trials aimed at assessing the safety and the efficacy of omitting radiotherapy in interim PET-negative patients. Brentuximab Vedotin (BV) is a novel antibody-drug conjugate targeting CD30 linked to a potent synthetic antitubulin chemotherapeutic agent, monomethyl auristatin E (MME). BV showed an impressive activity against refractory/relapsed HL and now is being incorporated in a modified ABVD schedule in first-line treatment of HL, with promising efficacy and a low toxicity profile. This novel therapeutic strategy will tell us if traditional ABVD or BEACOPP chemotherapy could be abandoned for the brand-new targeted therapy. Despite the brilliant results of HL treatment, which proved able to achieve a long-term disease control in 80-90% of the patients, the search of new prognostic has continued over the last two decades and the progress of the knowledge of the pathobiology of HL has led to a discovery of a series of markers related to microenvironment of HL tissue and molecular mechanisms to escape host immune reaction against the tumor. The strong association between the locus A of the human leukocyte antigen (HLA-A) system and EBV-positive HL suggests that both an abnormal antigen presentation and some specific EBV antigen per se could play a pivotal role in the pathogenesis of cHL. In EBV. +. HL patients, the susceptibility or the resistance to develop HL depends on the HLA allele A-*01 or A-*02, respectively. Tumor escape mechanism to block the immune response of the host against the neoplastic tissue is one of the property of a recently discovered subset of myeloid-derived suppressor cells (MDSC) that induce tumor vasculogenesis and escape from immunity via T cell suppression. Initially, these myeloid cells were identified as granulocytes or monocytes; however, MDSC derive from multipotent progenitor cells that can differentiate in the tissue as monocyte-derived MDSC (Mo-MDSC) with a phenotype CD14+/dull and granulocyte-derived MDSC (G-MDSC) expressing CD15 on cell surface. The latter were shown to produce arginase. Recent investigations suggest that MDSC present in the bone marrow in patients with several solid and hematological cancers in response to chemokine release in the tumor site are correlated with tumor-associated macrophages (TAM). Both TAM and MDSC have been strongly associated with a significantly worse prognosis in HL. As a consequence, several efforts are ongoing to standardize the methods to assess TAM and MDSC and prospective studies are being planned to validate their prognostic role
Trisomy 8 in Philadelphia Chromosome (Ph1)- Negative Cells in the Course of Ph1-Positive Chronic Myelocytic Leukemia
No full textA female patient with chronic myelocytic leukemia (CML) in chronic phase after busulfan and interferon treatment had four different cell lines in her bone marrow. In addition to cells with a normal karyotype there were cells with the Philadelphia chromosome (Ph1), cells with trisomy 8 and a Ph1, and cells with trisomy 8 as the sole anomaly
A paracrine loop in the vascular endothelial growth factor pathway triggers tumor angiogenesis and growth in multiple myeloma
No full textHISTONE DEACETYLASE INHIBITOR ITF2357 EXERT SIGNIFICANT ANTI-PROLIFERATIVE AND PRO-APOPTOTIC EFFECTS ON THE P39 CELL LINE: A GENE EXPRESSION STUDY
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