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D. Ramadhani
"In general, it was assumed that the chromosome aberration induced by ionizing radiation is proportional to the chromosome size. From this viewpoint, the higher chromosome size, the more resistant to radiation. However, different opinions, in which chromosomes are particularly sensitive or resistant to radiation, are also still followed until now. Here in this research, we compared the chromosome sensitivity between chromosomes number 1, 2, and 4 using the FISH (fluorescence in situ hybridization) technique. From this research, we expect that the information obtained could show clearly whether a longer chromosome is more frequently involved in translocations and also more resistant to radiation than a shorter one. The type of chromosome aberration considered was limited only to translocation and we used one sample donor in order to avoid donor variability. The whole blood from a healthy female was irradiated with γ-rays with doses of 1, 3 and 5 Gy, respectively. Isolated lymphocytes from the whole blood were then cultured for 48 hours. After the culture process was completed, preparations of harvest and metaphase chromosomes were carried out. Chromosomes 1, 2, and 4 were stained with different fluorochromes. The translocation of each chromosome at each dose point was subsequently evaluated from 50 images obtained from an automated metaphase finder and capturing system. An additional analysis was performed to identify which chromosome arm was more frequently involved in translocation. Further analyses were also conducted with the aim of determining which chromosome band had a higher frequency of radiation-induced breakage. The experimental results showed that chromosome number 4 was more frequently involved in translocations compared to chromosomes 1 and 2 at 5 Gy. In contrast, at doses of 1 and 3 Gy translocations involving chromosomes number 1 and 2 were more numerous compared to the ones involving chromosome 4. However, if the number of translocation was accumulated for all the doses applied, the chromosome number 4 was the chromosome most frequently involved in translocations. Breakpoint analysis revealed that in chromosome 1, chromosome 2, and chromosome 4, the highest chromosome bands as break position were in band q32, p13, and q21, respectively. It can be concluded that chromosome 4 is more sensitive to radiation in all doses point, despite having less DNA content than chromosomes 1 and 2. Thus, it was showed that our research cannot support the general assumption about chromosome aberration induced by radiation being proportional to DNA content."
Center for Informatics and Nuclear Strategic Zone Utilization, 2016
607 AIJ 42:2 (2016)
Artikel Jurnal  Universitas Indonesia Library
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Anastasia Putri
"Chronic myeloid leukemia (CML) is a clonal haemopoietic stem cell disorders with reciprocal translocation in chromosome 9 (ch9) and 22 (ch22) which cause the fusion of Break cluster region-Abelson murine leukemia (BCR-ABL) oncogene. This fusion will activate tyrosine kinase. Imatinib mesylate is the first tyrosine kinase inhibitor (TKI), which could change the prognosis of CML patients. However, there is a resistance to TKI’s, and based on transcriptomic study, increase expression of gen signal transducer and activator of transcription (STAT) 5A and runt-related transcription factor 3 (RUNX3) can cause resistance to TKI’s. The STAT5 protein, which in normal myeloid cells being activated by cytokine, in CML patients was activated even without cytokines. STAT5 refer to STAT5A and STAT5B, however they have might have different role in hematopoietic stem cells or in CML cells. This review summarizes the role of STAT5 in tyrosine kinase inhibitor resistance in CML patients.

Leukemia myeloid kronis (CML) adalah kelainan sel punca hemopoietik klonal dengan translokasi resiprokal dalam kromosom 9 (ch9) dan 22 (ch22) yang menyebabkan fusi cluster Break-Abelson murine leukemia (BCR-ABL) onkogen. Penggabungan ini akan mengaktifkan tirosin kinase. Imatinib mesylate adalah inhibitor tirosin kinase (TKI) pertama yang dapat mengubah prognosis pasien CML. Namun, ada penolakan terhadap TKI, dan berdasarkan studi transkriptomik, peningkatan ekspresi transduser sinyal gen dan aktivator transkripsi (STAT) 5A dan faktor transkripsi terkait runt (RUNX3) dapat menyebabkan resistansi terhadap TKI. Protein STAT5, yang dalam sel-sel myeloid normal diaktifkan oleh sitokin, pada pasien CML diaktifkan bahkan tanpa sitokin. STAT5 merujuk pada STAT5A dan STAT5B, namun mereka mungkin memiliki peran yang berbeda dalam sel induk hematopoietik atau dalam sel CML. Ulasan ini merangkum peran STAT5 dalam resistensi inhibitor tirosin kinase pada pasien CML."
Jakarta: University of Indonesia. Faculty of Medicine, 2019
610 UI-IJIM 51:4 (2019)
Artikel Jurnal  Universitas Indonesia Library