359 research outputs found
Cardiovascular Toxicity of Antineoplastic Treatments in Hematological Diseases: Focus on Molecular Mechanisms to Improve Therapeutic Management
In recent years, advancements in the treatment of hematologic neoplasms have led to more effective and less toxic therapeutic schemes, resulting in prolonged patient life expectancy. However, the success of these treatments has also brought about an increased prevalence of cardiovascular adverse events, becoming a significant concern for the growing population of cancer survivors. Antineoplastic therapies, targeting both tumor and organ vessels, contribute to vascular toxicity, influenced by genetic factors and pre-existing vascular diseases. Chemotherapeutic agents and targeted treatments can induce cardiovascular toxicity by affecting endothelial cells and cardiomyocytes through various mechanisms, including hypoxia, vasculature abnormalities, and direct effects on cardiomyocytes. Cardiovascular adverse events encompass a wide range, from cardiac dysfunction to an elevated risk of arrhythmias. While early cardiac events are well-described in clinical trials, delayed toxicities are gaining relevance due to prolonged patient survival. The review focuses on the cardiac and vascular toxicity of antineoplastic drugs in hematological disorders, providing insights into the molecular physiopathology of cancer therapy-associated cardiotoxicity. Understanding how these drugs interact with the heart and blood vessels is essential for predicting, detecting, and managing chemotherapy-related heart issues
How to facilitate early diagnosis of CNS involvement in malignant lymphoma
Introduction: Making the diagnosis of secondary CNS involvement in lymphoma can be difficult due to unspecific signs and symptoms, limited accessibility of brain/myelon parenchyma and low sensitivity and/or specifity of imaging and cerebrospinal fluid (CSF) examination currently available. Areas covered: MRI of the total neuroaxis followed by CSF cytomorphology and flow cytometry are methods of choice when CNS lymphoma (CNSL) is suspected. To reduce the numerous pitfalls of these examinations several aspects should be considered. New CSF biomarkers might be of potential diagnostic value. Attempts to standardize response criteria are presented. Expert commentary: Diagnosing CNSL remains challenging. Until diagnostic methods combining high sensitivity with high specifity are routinely introduced, high level of awareness and optimal utilization of examinations currently available are needed to early diagnose this potentially devastating disease
Pegylated liposomal doxorubicin in combination with dexamethasone and bortezomib (VMD) or lenalidomide (RMD) in multiple myeloma pretreated patients
Bortezomib and liposomal doxorubicin are highly effective in obtaining the best possible response before autologous transplant for multiple myeloma
Fludarabine, Bortezomib, Myocet and rituximab chemotherapy in relapsed and refractory mantle cell lymphoma
Abstract
Based on the hypothesis that bortezomib may potentiate fludarabine activity by inhibiting DNA repair, we designed a phase I trial using this combination with rituximab in patients with relapsed and refractory indolent and mantle cell non-Hodgkin lymphoma. Twenty-four patients were enrolled. Non-Hodgkin lymphoma subtypes included 12 patients with follicular lymphoma, four with marginal zone lymphoma, three with lymphoplasmacytic lymphoma, three with mantle cell lymphoma and two with small lymphocytic/chronic lymphocytic leukaemia. Fludarabine and bortezomib were escalated in cohorts of three patients. Rituximab was added to the maximum tolerated dose of fludarabine and bortezomib and added significant dose-limiting myelosuppression. The maximum tolerated dose was fludarabine 25 mg/m(2) on days 1-3, bortezomib 1.3 mg/m(2) on days 1, 4, 8, 11, with rituximab 375 mg/m(2) on day 1 administered every 21 d. Clinical responses were observed in 11 patients, five of whom were refractory to their most recent treatment regimen. Six additional patients had stable disease for a median of 10 months (range 4-30+). Cumulative myelosuppression and neuropathy was observed. The combination of fludarabine, bortezomib, and rituximab appears to be an active regimen with manageable toxicity for relapsed NHL
Molecular Remission After VTD or TAD As Induction for Multiple Myeloma: Results with Two Different Methods of Analysis
Free light chains are needed for the follow up of multiple myeloma
Nonsecretory multiple myeloma (NSMM) is considered a rare variant of the classic form of MM that has a similar clinical and radiologic presentation and lack of M-protein in serum and/or urine on electrophoresis and immunofixation. We describe here, a case of a 29-year-old woman who came in our Hospital in 2010 with back pain and multiple osteolytic bone lesions. This woman had no other symptoms. A CT guide biopsy from the L1 vertebra showed massive infiltration of plasmocytes confirming the diagnosis of suspected NSMM, because she had normal serum and urine protein electrophoresis and immunofixation, without apparent bone marrow involvement. After a chemotherapy induction with VTD and autologous peripheral bone marrow transplant, she obtained an apparent complete remission for two years, when in 2012, routinary blood tests showed normal serum basic analyses but an excess of κmonoclonal free light chains (this parameter was not available at time of diagnosis) One month later, the patient developed an aggressive and diffuse clinical bone relapse and, due to the young age, she was treated with second line chemotherapy and allogeneic bone marrow transplant. There are studies showing that a cytoplasmic M-protein can be identified in nearly 85% of patients initially classified as NSMM. A lot of these patients, even in absence of measurable disease as presently defined, may be monitored by free light chain assay, able to reveal small amounts of monoclonal proteins. The availability of a more sensitive technique for the detection of monoclonal components in biological fluids is quite important, because it may help to make an earlier diagnosis and may represent another parameter of measurable disease, useful to monitor the patients for the optimal drug treatment
A therapy resistant myelodysplastic syndrome characterized by the presence of the rare reciprocal translocation t(3;12)(q26.2;p13)
Novel monoclonal antibodies: A really specific therapy for light chain amyloidosis
Light chain amyloidosis is a rare disease caused by clonal plasma cells in the bone marrow generating an excessive amount of immunoglobulin light chains. These chains misfold and produce insoluble fibrils that deposit in various organs, including the heart, kidneys, liver, nervous system, and digestive tract. Life expectancy and symptoms during the course of the disease vary depending on which and how many organs are affected. Targeted plasma cell therapy has significantly advanced the clinical management of amyloidosis, with ongoing progress. However, current clinical studies are investigating innovative targets, drug combinations and treatment strategies to improve therapeutic outcomes by minimizing adverse effects and refining patient prognosis in these challenging hematological conditions. In this paper, we review the state of the art regarding the use of anti-amyloid antibodies, as a revolutionary and innovative approach in the current scenario of amyloid treatment
Association of PIM gene translocation and TELAML1 rearrangement., LEUKEMIA RESEARCH,vol. Leuk Res. 2007 Dec;31(12):1761-2
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