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Containing Chemotherapy (containing + chemotherapy)
Selected AbstractsModulation of antigen expression in B-cell precursor acute lymphoblastic leukemia during induction therapy is partly transient: Evidence for a drug-induced regulatory phenomenon.CYTOMETRY, Issue 3 2010Results of the AIEOP-BFM-ALL-FLOW-MRD-Study Group Abstract Background: Changes of antigen expression on residual blast cells of acute lymphoblastic leukemia (ALL) occur during induction treatment. Many markers used for phenotyping and minimal residual disease (MRD) monitoring are affected. Glucocorticoid (GC)-induced expression modulation has been causally suspected, however, subclone selection may also cause the phenomenon. Methods: We investigated this by following the phenotypic evolution of leukemic cells with flow cytometry from diagnosis to four time points during and after GC containing chemotherapy in the 20 (of 360 consecutive) B-cell precursor patients with ALL who had persistent MRD throughout. Results: The early expression changes of CD10 and CD34 were reversible after stop of GC containing chemotherapy. Modulation of CD20 and CD45 occurred mostly during the GC phase, whereas CD11a also changed later on. Blast cells at diagnosis falling into gates designed according to "shifted" phenotypes from follow-up did not form clusters and were frequently less numerous than later on. Conclusions: Our data support the idea that drug-induced modulation rather than selection causes the phenomenon. The good message for MRD assessment is that modulation is transient in at least two (CD10 and CD34) of the five prominent antigens investigated and reverts to initial aberrant patterns after stop of GC therapy, whereas CD20 expression gains new aberrations exploitable for MRD detection. © 2010 Clinical Cytometry Society [source] Treatment of refractory fludarabine induced autoimmune haemolytic with the anti-cd20 monoclonal antibody rituximabINTERNATIONAL JOURNAL OF LABORATORY HEMATOLOGY, Issue 1 2006R. SWORDS Summary A patient with cold-type autoimmune haemolytic anaemia for 8 years developed progressive B cell chronic lymphocytic leukaemia (CLL). Despite the risk of fludarabine induced exacerbation of haemolysis, he was given aggressive anti-CLL therapy with six courses of FCR (fludarabine 25 mg/m2 D1,3, cyclophosphamide 250 mg/m2 D2,4 and rituximab 375 mg/m2 D1) every 4 weeks. This resulted in a marked acute increase in haemolysis shortly after completing each course of fludarabine. However, haemolysis had settled to its baseline level by the time of subsequent courses of FCR. FCR resulted in complete clinical remission of CLL but residual haemolysis persisted. The patient was then given four weekly infusions of single agent rituximab, resulting in ongoing remission of haemolysis. In this patient, rituximab appears to have controlled fludarabine induced exacerbation of autoimmune haemolysis. In addition, subsequent single agent rituximab therapy resulted in prolonged remission of cold-type autioimmune haemolytic anaemia. It remains to be seen if the addition of rituximab will allow other patients with a positive direct Coomb's test and/or autoimmune haemolysis to receive fludarabine containing chemotherapy without undue risk of life-threatening haemolytic anaemia. [source] Fatal peripheral neuropathy following FLA chemotherapyINTERNATIONAL JOURNAL OF LABORATORY HEMATOLOGY, Issue 4 2004W. L. Osborne Summary We discuss a case with significant progressive peripheral neurological deterioration following administration of both fludarabine and cytarabine as part of the FLA (fludarabine and cytarabine) regime. Of particular interest is that toxicity only occurred during the second course of FLA and sixth course of Ara-C containing chemotherapy. At this point, a new antifungal agent had been commenced, suggesting a possible drug interaction enhancing the risk of known neurological toxicity with this regime. [source] Absence of large intragenic rearrangements in the DPYD gene in a large cohort of colorectal cancer patients treated with 5-FU-based chemotherapyBRITISH JOURNAL OF CLINICAL PHARMACOLOGY, Issue 2 2010Laia Paré WHAT IS ALREADY KNOWN ABOUT THIS SUBJECT , Dihydropyrimidine dehydrogenase (DPD) is the enzyme responsible for the elimination of approximately 80% of the administered dose of 5-fluorouracil (5-FU). , Mutations in the DPD-coding gene have been shown to increase the risk of severe toxicity in 5-FU treated patients. , The IVS14+1G>A is the most common DPYD mutation. WHAT THIS STUDY ADDS , The intragenic rearrangements of DPYD using multiplex ligation-dependent probe amplification (MLPA) were studied for the first time in a large series of 234 colorectal cancer patients treated with 5-FU-containing chemotherapy. , No deletions or duplications of one or more DPYD exons were detected. The presence of the IVS14+1G>A mutation was also excluded. , These data show that neither the large genomic rearrangements in the DPYD gene nor the IVS14+1G>A mutation are responsible for the serious toxicity associated with a 5-FU containing regimen in this cohort of Spanish patients. AIMS To study the relationship between the toxicity associated with a 5-FU-based therapy and the presence of (i) the large intragenic rearrangements in the DPYD gene and (ii) the IVS14+1G>A mutation. METHODS We used the multiplex ligation-dependent probe amplification technique (MLPA) to study genomic DNA from 234 colorectal cancer patients treated with 5-FU-based chemotherapy. RESULTS We did not detect any deletion/duplication in the DPYD gene. The presence of the IVS14+1G>A mutation was also excluded. CONCLUSIONS Neither the large genomic rearrangements in the DPYD gene nor the IVS14+1G>A mutation play a significant role in the development of serious toxicity associated with a 5-FU containing regimen. [source] Mantle Cell Lymphoma in the Ocular RegionACTA OPHTHALMOLOGICA, Issue 2008S HEEGAARD Purpose To characterize the clinicopathological features of mantle cell lymphoma (MCL) in the ocular region. Methods All lymphoid lesions were retrieved searching the Danish Ocular Lymphoma Database 1980-2007. Specimens were collected from Danish pathology departments and re-evaluated with a panel of monoclonal antibodies. For all patients with confirmed MCL the complete clinical files were collected and reviewed. Results Twenty-one patients with MCL were identified comprising nine percent (21/230) of all lymphomas in the ocular region. There were 18 male and three female patients with an age range from 60 to 90 years (median 75 years). Ocular region MCL as first presenting symptom included 67% of the patients. Of these, 71% had bilateral involvement and all had lymphoma in more than one site within the ocular region. The orbit (71%) and eyelids (64%) were the most commonly affected sites. At the time of diagnosis 93% of the patients were in Ann Arbor stage III/IV, with bone marrow involvement (79%) and B-symptoms (50%). Median overall survival (OS) was 30 months and the five-year OS rate was 21%. Patients receiving anti-CD20 (Rituximab)-containing chemotherapy had a significant better 5-year OS rate (80 %) (p < 0,027) than patients in treatment regimes without Rituximab (5-year OS rate, 29%). Conclusion MCL presenting in the ocular region has a male predominance and affects elderly patients. The orbit and eyelids were frequently involved. Patients with ocular region MCL as first presenting symptom had a high proportion of bilateral affection. Patients had advanced stage disease at diagnosis, multiple relapses and a low 5-year OS rate similar to systemic MCL. Treatment with Rituximab-containing chemotherapy improved survival significantly. [source] Early prediction of anthracycline induced cardiotoxicityACTA PAEDIATRICA, Issue 4 2007Bedirhan Erkus Abstract Aim: The purpose of this study is to evaluate echocardiographically determined cardiac functions with serum levels of brain natriuretic peptide (BNP), cardiac troponin I (cTnI) and total antioxidant status (TAOS) in childhood leukemia treated with chemotherapeutics containing anthracyclines. Methods: A study group of 29 patients who have been followed for acute lymphoblastic leukemia (ALL) and administered a treatment protocol containing chemotherapy of anthracyclines were included in the analysis. Levels of BNP, cTnI and TAOS were studied in serum samples of the patients. Results: We demonstrated that as the drug dosage increased, systolic ejection fraction (EF) and shortening fraction (FS) values decreased (EF r2= 0.2327, FS r2= 0.251). On the other hand, increased dosage of anthracycline therapy was associated with significant raise in plasma BNP levels (r2= 0.246) and significant decrease in serum TAOS levels (r2= 0.317) without any change in serum cTnI levels. Conclusion: Our study suggest that serum TAOS and BNP levels may be useful as an early and sensitive indicator of anthracycline induced cardiotoxicity. [source] | ||||||||||