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کاربرد نوع شرط:
- جایگاه : پژوهشی
- مجله: Asian Pacific Journal of Cancer Prevention
- نوع مقاله: Journal Article
- کلمات کلیدی: Chronic myeloid leukemia,BCR-ABL1 mRNA,BCR-ABL1 TKD mutations
- چکیده:
- چکیده انگلیسی: 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.
- انتشار مقاله: 18-11-1398
- نویسندگان: Nittaya Limsuwanachot,Adcharee Kongruang,Budsaba Rerkamnuaychoke,Roongrudee Singdong,Pimjai Niparuck,Saengsuree Jootar,Teerapong Siriboonpiputtana
- مشاهده
- جایگاه : پژوهشی
- مجله: Asian Pacific Journal of Cancer Prevention
- نوع مقاله: Journal Article
- کلمات کلیدی: Myelodysplastic syndrome,RNA splicing machinery,SF3B1 mutation
- چکیده:
- چکیده انگلیسی: Genetic mutations in genes encoding critical component of RNA splicing machinery including SF3B1 are frequently
identified and recognized as the pathogenesis in the development of myelodysplatic syndrome (MDS). In this study,
PCR sequencings specific for SF3B1 exon 13, 14, 15, and 16 were performed to analyse genomic DNA isolated from
bone marrow samples of 72 newly diagnosed MDS patients. We found that 10 of 72 (14%) patients harbor SF3B1
missense mutations including E622D (1/72), R625C/G (2/72), H662Q (1/72), K666T (1/72), K700E (4/72) and G740E
(1/72), respectively. Mutations were predominantly located on exon 14 and 15 of SF3B1 coding sequence. Interestingly,
patients with SF3B1 mutations exhibited higher platelet counts (195×109/L VS. 140×109/L, p-value = 0.025) as well as
lower hemoglobin levels (81 g/L VS. 92 g/L, p-value = 0.009) and associated with ring sideroblast phenotype (p-value
< 0.001) when compared with patients without the SF3B1 mutation. In summary, we reported the frequency of SF3B1
mutations in Thai patients with different subtypes of MDS. SF3B1 mutations were predominantly occurred in MDS-RS
and considered as favourable prognosis value. This study further highlighted the clinical important of SF3B1 mutations
analysis for the classification of MDS.- انتشار مقاله: 30-08-1396
- نویسندگان: Punchita Rujirachaivej,Teerapong Siriboonpiputtana,Budsaba Rerkamnuaychoke,Suthada Magmuang,Takol Chareonsirisuthigul,Paisarn Boonsakan,Sawang Petvises,Tanasan Sirirat,Pimjai Niparuck,Suporn Chuncharunee
- مشاهده