Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0023473 (chronic myeloid leukemia)
 18,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The results of the Pediatric Bone Marrow Transplant Program at The King Faisal Specialist Hospital and Research Center (KFSH & RC) from June 1993 to October 1995 were reviewed for a preliminary report on the outcome of children undergoing bone marrow transplantation (BMT) particularly in relation to mortality and morbidity. A total of 64 bone marrow transplants were performed on 60 patients during this period of time. The study patients included 28 with acute leukemia, 10 with severe combined immune deficiency, five with chronic myeloid leukemia, four with Fanconi's anemia and 13 others with miscellaneous disorders. The average hospitalization period was six weeks per patient. Forty three of these patients (72%) were alive and disease-free after a median follow-up of 14 months (range 1-27 months). Eight patients died from transplant-related toxicity within 100 days of BMT. One patient died of chronic graft versus host disease (GVHD) of the liver. Eight patients with acute leukemia relapsed within one year after BMT. Further details regarding the preparative regimens, toxicity of BMT, GVHD and disease-free survival are reviewed in this report.
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PMID:Bone marrow transplantation in children: the king faisal specialist hospital experience. 1841 40

Chronic myeloid leukemia (CML) patients who do not achieve landmark responses following treatment with imatinib mesylate (IM) are considered IM-resistant. Although IM-resistance can be due to BCR-ABL kinase domain (KD) mutations, many IM-resistant patients do not have detectable BCR-ABL KD mutations. MicroRNAs (miRNAs) are short non-coding RNAs that control gene expression. To investigate the role of miRNAs in IM-resistance, we recruited 8 chronic phase CML patients with IM-resistance who tested negative for BCR-ABL KD mutations and 2 healthy normal controls. Using miRNA sequencing, we identified 54 differentially expressed miRNAs; 43 of them downregulated. The 3 most differentially downregulated miRNAs were miR-146a-5p, miR-99b-5p and miR-151a-5p. Using real-time quantitative reverse transcriptase-polymerase chain reaction, the expression patterns of the 3 miRNAs were validated on the same cohort of 8 patients in addition to 3 other IM-resistant CML patients. In-silico analysis showed that the predicted gene targets are ATRIP, ATR, WDR48, RAD51C and FANCA genes which are involved in the Fanconi Anemia/BRCA pathway. This pathway regulates DNA damage response (DDR) and influences disease response to chemotherapy. Thus it is conceivable that DDR constitutes a key component in IM-resistance. Further research is needed to elucidate miRNA modulation of the predicted gene targets.
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PMID:MicroRNAs that affect the Fanconi Anemia/BRCA pathway are downregulated in imatinib-resistant chronic myeloid leukemia patients without detectable BCR-ABL kinase domain mutations. 2854 7


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