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http://www.webmedcentral.com/images/Header_Logo.giftext/html2010-11-13T17:29:21+01:00http://www.webmedcentral.com/Dr. Radoslav GreksakLong-term Supression Of Bone Marrow With Prolonged Pancytopenia After Ibritumomab Tiuxetan In Jehovah\'s Witness Patient With Relapsed Follicular Non-hodgkin\'s Lymphoma
http://www.webmedcentral.com/article_view/1150
A 39-year old female Jehovah’s Witness patient presented with a relapse of B-cell follicular non-Hodgkin’s lymphoma.We had to avoid administration of any blood components as part of the treatment due to the conflict with the patient’s religious beliefs. Instead of administering a high-dose chemotherapy followed by autologous peripheral blood stem cell transplantation we identified radioimmunotherapy with ibritumomab tiuxetan as the best therapeutic option in the circumstances. The treatment with ibritumomab tiuxetan led to severe and long-term inhibition of bone marrow with prolonged pancytopenia, extreme low count of hemoglobin level, platelets and neutrophils. During the entire post-treatment period the patient has refused to receive red blood cells, plasma or platelet transfusions. The patient has spent 11 months in cytopenia without life-threatening bleeding or organ failure and until now the patient is surviving in a complete remission with normal blood cell counts.text/html2011-03-31T18:52:50+01:00http://www.webmedcentral.com/Dr. Mohamed MesmoudiSecondary Non Hodgkinian Lymphoma in a Patient Treated for Hodgkin Disease: A Case Report with Comprehensive Literature Review
http://www.webmedcentral.com/article_view/1819
The introduction of the intensive radiotherapy and chemotherapy has transformed the prognosis of Hodgkin disease and the long-term complications of the therapy became more frequent,?furthermore the carcinogenic effect of the used therapeutical agents leading to a high incidence of second malignancies was clearly demonstrated. We present here a case of a patient treated for Hodgkin disease who developed 15 years later a secondary non Hodgkin lymphoma. The objective of this presentation is to describe this rare metachronous association of two malignancies and to discuss the etiological links.text/html2012-07-03T16:43:00+01:00http://www.webmedcentral.com/Dr. Sasmita BiswalNovel Agents In CML Therapy: Tyrosine Kinase Inhibitors and Beyond
http://www.webmedcentral.com/article_view/3540
Treatment of Chronic myeloid leukemia represents one of cancer’s success stories. Deregulated tyrosine kinase activity of the BCR-ABL fusion protein has been established as the causative molecular event in CML. The drug Imatinib has revolutionized the treatment of CML and has become the gold standard of care in CML for it is a highly targeted BCR-ABL tyrosine kinase inhibitor (TKI) that induces complete hematologic response and sustained complete cytogenetic response in more than 80% of patients. Despite of such impressive response rates achieved with imatinib, some patients in the advanced stage of CML frequently obtain less modest responses. It may be due to resistance to the wonder drug imatinib, which in turn results in failure of treatment, even after large dose escalation. This has led to the development of novel treatment strategies which are currently being investigated in newly diagnosed CML and include upfront treatment with the next-generation tyrosine kinase inhibitors, such as dasatinib, nilotinib, or bosutinib, which also target the BCR-ABL but with increased in vitro potency as compared to imatinib, and possibly with a reduced potential for resistance. Such newer agents and combination approaches can improve treatment responses as compared with standard imatinib treatment. In addition, many other protein kinases implicated in signaling transduction downstream BCR-ABL also play critical roles in the pathogenesis of CML, thereby representing potential therapeutic targets as revealed from several clinical studies. While in many other cases, the CML cells develop mutations, which is a change in the amino acid sequence of the BCR-ABL oncogene, the most dangerous amongst them is the T315I mutation, which makes them resistant to the current targeted therapies (imatinib, dasatinib, and nilotinib). Newer drugs that work against T315I mutant cells are now being tested. Ponatinib, is one such pan-BCR-ABL inhibitor, which has shown ongoing strong efficacy in its continuing Phase 1 trial in treatment of the T315I mutation CML, as well as all other known mutations. Still other novel drugs in the pipeline, the farnesyl transferase inhibitors, such as lonafarnib and tipifarnib, seem to have some activity against CML and patients may respond favourably when such drugs are combined with imatinib. With many such novel drugs under development and many more in the pipe line, some of such drugs which are in various phases of clinical trials are being discussed.text/html2013-08-07T12:21:55+01:00http://www.webmedcentral.com/Prof. Heidrun KarlicEpigenetically active drugs target metabolic gene-regulation in leukemic cells
http://www.webmedcentral.com/article_view/4342
Background: Up-regulation of energy metabolism is a key feature of proliferating cells from cancers and leukemias. Thus, targeting of metabolic pathways represents a therapeutic challenge involving both dietary and drug-mediated strategies. The aim of this study was to evaluate the impact of the DNA-methyltransferase-inhibitor 5-desoxy-2-azacytidine (Decitabine, DAC) and the histone-deacetylase-inhibitor suberoyl anilide hydroxamic acid (SAHA, Vorinostat) on malignancy-associated metabolic pathways.
Methods: HL60 promyelocytic cells and KG1 myeloblastic leukemia cells were treated with DAC or SAHA for 3 days. RNA was isolated and gene expression was analyzed using Affymetrix human gene 1.0 arrays in comparison with published databases from normal CD34 positive hematopoietic progenitors. Pathvisio software tool was used for comparative quantification of gene-expression patterns from metabolic pathways based on established data banks such as KEGG and Wikipathways.
Results: A comparison of both leukemia cell lines to normal CD34+ cells indicated malignancy-associated stimulation of energy metabolism. Global evaluation on pathways demonstrated a significant drug-mediated downregulation of the intra-mitochondrial pathways, namely the tri-carbonic acid cycle and beta oxidation and to a lesser extent also cytoplasmic glycolysis.
Conclusion: The observation that the KG1 cell line reacted more sensitive to demethylating drugs than the HL60 cell line, where drug treatment selected for survival of differentiated cells, may support application of DAC and SAHA to leukemias with an undifferentiated phenotype but also with the potential to induce differentiation. Efficient targeting of intra-mitochondrial pathways appears to be associated with multiple pro-apoptotic activities of these drugs.