Objective: The genetic hallmark of CML is known as the appearance of t(9;22)(q34.1;q11.2) (BCR-ABL1) which is present in more than 95% of cases. Here, we demonstrated practical laboratory tools for monitoring of BCR-ABL1 transcripts in chronic myeloid leukemia patients undergoing TK inhibitor therapy. Methods: Real time quantitative PCR and direct sequencing were performed for monitoring of BCR-ABL1 transcripts in 245 treated CML. Results: At month 3 after first time point of monitoring, we found that 89% (218/245), 2% (5/245), and 9% (22/245) of patients are determined as optimal, warning, and failure response, respectively. The responses to TKI were slightly decreased at months 6 as following 73% optimal (180/245), 18% warning (43/245), and 9% failure response (22/245). Additionally, responses to TKI were gradually decreased at month 12 after first time point of monitoring as following 65% optimal (160/245), 13% warning (31/245), and 22% failure (54/245). We could detect 20% (49/245) of patients positive for BCR-ABL1 TKD mutations. Interestingly, one third (17 of 49) of TKD mutated cases were positive for compound/polyclonal mutation patterns. While major molecular response were observed in the majority of patients without TKD mutation, resistant to TKI were detected in patients with T315I mutation (n = 9; % mean IS = 8.1510, % median IS = 9.7000), compound/polyclonal mutations with T315I (n = 9; % mean IS = 13.0779, % median IS = 5.404), and other TKD mutations (n = 14; % mean IS = 8.1416, % median IS = 1.060), respectively. Conlusion: These practical laboratory techniques provided a more comprehensive understanding of CML progression during drug therapy and could be of benefit in earlier prognosis.

Background: Epithelial ovarian cancer (EOC) is often challenging to diagnose, even though histological examination. microRNA (miRNA or miRNA) is bound to the target messenger RNA (mRNA) and causing the mRNA molecules are silenced. The identification of miRNA expression-based EOC subtypes is considered a critical means of prognostication. So far, the studies on EOC subtypes have not been well characterized. Objective: This study aimed to confirm the existence of miRNAs in EOC and to assess their potential as clinical biomarkers for EOC. Methods: We sampled 25 ovarian tumor tissues from patients with human ovarian tumors (17 malignant; 12 serous EOC, five non-serous EOC, and eight benign ovarian tumors). miRNA microarray detection was performed to identify EOC miRNAs. Real-time PCR was adapted for the validation of differentially expressed miRNAs detected by microarray analysis was related to hybridization intensity. Results: The results confirmed that miRNAs exist in EOC, relative expression of EOC miRNAs demonstrated that upregulation of miR-483-5p, and downregulation of miR-127-3p, and miR-532-5p were significantly expressed in the malignant group than in the benign group at p ' 0.05. Besides, miR-483-5p could also distinguish EOC subtypes between serous EOC and non-serous EOC, with a p ' 0.05. Conclusion: A comprehensive miRNA expression profiling can help to refine subtype classification in EOC, opening new opportunities for identifying clinically applicable markers for improved stratification and diagnostics of ovarian tumors.

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