1,721,092 research outputs found
Pegylated liposomal doxorubicin in combination with dexamethasone and bortezomib (VMD) or lenalidomide (RMD) in multiple myeloma pretreated patients
No full textBortezomib and liposomal doxorubicin are highly effective in obtaining the best possible response before autologous transplant for multiple myeloma
No full textFludarabine, Bortezomib, Myocet and rituximab chemotherapy in relapsed and refractory mantle cell lymphoma
No full textAbstract
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
No full textFree light chains are needed for the follow up of multiple myeloma
No full textNonsecretory 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)
No full textNovel monoclonal antibodies: A really specific therapy for light chain amyloidosis
No full textLight 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
No full textFolic acid fortification and cancer risk
No full textRoger Bayston and colleagues1 state that, to the best of our knowledge, folic acid does not reduce colorectal cancer risk but neither does it increase it. Although the question surrounding this type of cancer is still debated, we want to underline the possibility that folic acid fortification could have many more beneficial effects than merely those on neural tube defects.
Lack of maternal folate supplementation has been associated with an increased risk of childhood leukaemia, possibly resulting from DNA hypomethylation and strand breakage.2 Susceptibility to some types of cancer has been linked to the methylation level of the gene encoding cyclin-dependent kinase inhibitor 2A (CDKN2A), and there seems to be an interesting association between folate concentrations and consequent hypermethylation of such genes.3
Decreased dietary folate has also been associated with epigenetic silencing of CDKN2A in solid tumours, and this relation has been shown to be modified by the MTHFR genotype, suggesting a mechanism of action of folate deficiency in cancer.4
The folate pathways that maintain cell homoeostasis and genomic integrity during cellular division could represent an essential step in our understanding of the biology of cancers. Additional experimental and clinical observations could help clarify the role of folate concentrations and methylation of genes such as CDKN2A in the homoeostasis of normal and malignant blood cells.
To avoid the risk of colon cancer, perhaps a genetic analysis of patients could be done to identify individuals with the MTHFR 677TT genotype, which could be the only condition in which high concentrations of folate might promote colon cancer development.5
We declare that we have no conflict of interest
Beyond BCMA, why GPRC5D could be the right way: treatment strategies with immunotherapy at relapse after anti-BCMA agents
No full textMultiple Myeloma remains incurable, and there is a need for therapies with novel mechanisms of action. Recently, B cell maturation antigen targeted therapy has demonstrated deep and durable responses in a largely treated population. However, the relapse rate of myeloma patients after anti-BCMA treatment strategies is increasing worldwide, and one of the most challenging issues for them is to choose the best therapy sequencing. After anti-BCMA treatment, retreatment with anti-BCMA drugs remains an option, but new targets are emerging strongly. One of them is G protein-coupled receptor, class C group 5 member D (GPRC5D), that due to the very promising data from the use of chimeric antigen receptor T-cells (CAR-T) and bispecific antibodies (BsAb) seems to be the ideal candidate in the relay of myeloma treatment at relapse. In this literature review, we discuss data from treatment with the new drugs at relapse after anti-BCMA therapies, observing an undeniable benefit from the use of drugs directed against GPRC5D
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