Comparison of microRNA Expression Profile in Patients Newly Diagnosed with Chronic Myeloid Leukemia and Treated by Allogeneic Hematopoietic Stem Cell Transplantation
Ontology highlight
ABSTRACT: Expression profile of 14 newly diagnosed patients with Chronic Myeloid Leukemia and 14 Philadelphia chromosome negative patients after allo haematopoietc stem cell transplantation. We tested 754 microRNAs by reverse transcription quantitative polymerase chain reaction (RT-qPCR) array for each patient.
Project description:Expression profile of 14 Chronic Myeloid Leukemia Philadelphia chromossome negative patients after allo haematopoietc stem cell transplantation and Chronic Myeloid Leukemia treated with imatinib mesylate. We tested 754 microRNAs by reverse transcription quantitative polymerase chain reaction (RT-qPCR) array for each patient.
Project description:Acute Myeloid Leukemia (AML) is a heterogenous disease characterized by immature blasts at different maturation stage. We used single cell sequencing technique to analyze newly diagnosed AML patients.
Project description:Lymphoid committed CD34+lin-CD10+CD24- progenitors undergo a rebound at month 3 after allogeneic hematopoietic stem cell transplantation (allo-HSCT) in the absence of acute graft-versus-host disease (aGVHD). Here, we analyzed transcriptional programs of cell-sorted circulating lymphoid committed progenitors and CD34+Lin-CD10- non lymphoid progenitors in 11 allo-HSCT patients having (n=5) or not developed (n=6) grade 2 or 3 aGVHD and in 7 age-matched healthy donors. Major deregulated pathways included protein synthesis, energy production, cell cycle regulation and cytoskeleton organization. Notably, genes from protein biogenesis, translation machinery and cell cycle (CDK6) were over-expressed in progenitors from patients in the absence of aGVHD compared with healthy donors and patients affected by aGVHD. Expression of many genes from the mitochondrial oxidative phosphorylation metabolic pathway leading to ATP production were more specifically increased in lymphoid committed progenitors in absence of aGVHD. This was also the case for genes involved in cell mobilization such as those regulating Rho GTPases activity. In all, we show that circulating lymphoid committed progenitors undergo profound changes in metabolism favoring cell proliferation, energy production and cell mobilization after allo-HSCT in humans. These mechanisms are abolished in case of aGVHD or its treatment, indicating a persistent cell-intrinsic defect after exit from bone marrow.
Project description:The aim of this study is to assess the Fecal Microbiota Transplantation (FMT) efficacy in the prevention of allogeneic hematopoietic stem cell transplantation (allo-HSCT) complications and particularly Graft versus Host Disease (GvHD).
The hypothesis of this study is that allogeneic FMT may improve outcomes of these patients.
Project description:We recently defined a gene expression-based signature of high-risk multiple myeloma; this predictive signature was developed with and independently validated for newly diagnosed patients treated with high dose therapy and stem cell rescue. Here we use Phase 3 clinical trial data to show that this signature also predicts short survival in relapsed disease treated with single agent bortezomib or high dose dexamethasone. In addition, a survival signature derived with relapsed myeloma samples identified newly diagnosed patients with short survival. Taken together these data suggest that a similar biology underlies poor outcome in both newly diagnosed and relapsed myeloma and provide strong evidence that the high-risk signature is a powerful tool to identify patients who are candidates for new therapeutic regimens. Keywords: Model validation
Project description:We recently defined a gene expression-based signature of high-risk multiple myeloma; this predictive signature was developed with and independently validated for newly diagnosed patients treated with high dose therapy and stem cell rescue. Here we use Phase 3 clinical trial data to show that this signature also predicts short survival in relapsed disease treated with single agent bortezomib or high dose dexamethasone. In addition, a survival signature derived with relapsed myeloma samples identified newly diagnosed patients with short survival. Taken together these data suggest that a similar biology underlies poor outcome in both newly diagnosed and relapsed myeloma and provide strong evidence that the high-risk signature is a powerful tool to identify patients who are candidates for new therapeutic regimens. Keywords: Model validation See above (Series_summary)
Project description:The aim of this study was to gain insight into the potential mechanism of resistance to arsenic trioxide and to identify genes that are modulated in the malignant promyelocytes at the time of relapse in APL patients. We analyzed the gene expression profile by the whole genome microarray of primary promyelocytes obtained from 8 newly diagnosed and 8 at relapse patients. Agilent one-color experiment,Organism: Human ,Agilent Whole Genome Human 4x44k (AMADID: 014850) , Labeling kit: Agilent Quick-Amp labeling Kit (p/n5190-0442) newly diagnosed versus relapse acute promyelocytic leukemia
Project description:Prostate cancer (PCa) is the most common malignant tumour, with high incidence rates and heterogeneity in men around the world. It is becoming an increasing burden on the health care system due to lack of tests for precise detection of disease, risk assessment and response to treatments. We used SWATH-MS as a discovery proteomics tool to identify markers in the serum of newly diagnosed PCa patients and healthy controls to facilitate the improved diagnosis. Furthermore, identification and expression of proteins was also determined in patients undergone radiotherapy and prostatectomy for monitoring of the clinical response to respective treatment options. Thus, this study provides the basis for a proteomic signature to improve diagnostics of patients with localised prostate cancer.
Project description:The aim of this study was to gain insight into the potential mechanism of resistance to arsenic trioxide and to identify genes that are modulated in the malignant promyelocytes at the time of relapse in APL patients. We analyzed the gene expression profile by the whole genome microarray of primary promyelocytes obtained from 8 newly diagnosed and 8 at relapse patients.