Chronic myeloid leukemia

Multidrug resistance gene (MDR1) polymorphisms may not be directly associated with response to imatinib in chronic myeloid leukemia

J. L. Wang, Liu, H. J., Li, F., Yang, W. Y., Wang, J. M., Tan, S. F., and Wang, Q., Multidrug resistance gene (MDR1) polymorphisms may not be directly associated with response to imatinib in chronic myeloid leukemia, vol. 14, pp. 14967-14978, 2015.

Our study aimed to investigate the association between multidrug resistance (MDR1) gene polymorphisms and the response to imatinib (IM) in chronic myeloid leukemia (CML). An electronic databases in PubMed, Cochrane Library, Wanfang, China National Knowledge Infrastructure, and VIP were searched using combinations of keywords relating to MDR1 polymorphisms and the response to IM in CML. Studies retrieved from database searches were screened using stringent inclusion and exclusion criteria.

Inhibition of human chronic myelogenous leukemia K562 cell growth following combination treatment with resveratrol and imatinib mesylate

X. J. Wang and Li, Y. H., Inhibition of human chronic myelogenous leukemia K562 cell growth following combination treatment with resveratrol and imatinib mesylate, vol. 14, pp. 6413-6418, 2015.

To investigate the effect of treatment with resveratrol combined with imatinib mesylate on human chronic myelogenous leukemia K562 cell growth inhibition and apoptosis, in vitro cultured human chronic myelogenous leukemia K562 cells were incubated with different concentrations of resveratrol and imatinib mesylate when the cells were in the logarithmic phase. Next, the cell growth inhibition was evaluated using the MTT assay and cellular morphology observation. Apoptosis was determined using Annexin V fluorescein isothiocyanate/propidium iodide double staining.

Discovery of somatic mutations in the progression of chronic myeloid leukemia by whole-exome sequencing

Y. Huang, Zheng, J., Hu, J. D., Wu, Y. A., Zheng, X. Y., Liu, T. B., and Chen, F. L., Discovery of somatic mutations in the progression of chronic myeloid leukemia by whole-exome sequencing, vol. 13, pp. 945-953, 2014.

We performed whole-exome sequencing in samples representing accelerated phase (AP) and blastic crisis (BC) in a subject with chronic myeloid leukemia (CML). A total of 12.74 Gb clean data were generated, achieving a mean depth coverage of 64.45 and 69.53 for AP and BC samples, respectively, of the target region. A total of 148 somatic variants were detected, including 76 insertions and deletions (indels), 64 single-nucleotide variations (SNV), and 8 structural variations (SV).

Study on the treatment of the p15 gene combined with Bcr-abl-specific siRNA and STI571 for chronic myeloid leukemia

W. Wang, Du, Y., Li, N. - N., Lv, F. - F., and Lin, G. - Q., Study on the treatment of the p15 gene combined with Bcr-abl-specific siRNA and STI571 for chronic myeloid leukemia, vol. 13, pp. 4089-4101, 2014.

The aim of this study was to investigate the effect of the p15 gene combined with Bcr-abl-specific siRNA and STI571 on the proliferation, cell cycle and apoptosis of K562 chronic myeloid leukemia cells. Using the gene sequence results, we amplified the p15 gene from normal peripheral blood by RT-PCR, and constructed a p15-pcDNA3.1 vector. The K562 cell line with G418 resistance was screened, synthesized and transfected for bcr-abl gene fusion point for 21-nt siRNA.

Philadelphia-negative chromosomal evolution during treatment for chronic myeloid leukemia

H. - H. Hsiao, Liu, Y. - C., Lee, C. - P., Chang, C. - S., and Lin, S. - F., Philadelphia-negative chromosomal evolution during treatment for chronic myeloid leukemia, vol. 11, pp. 317-321, 2012.

Chromosome evolution is one of the major mechanisms of disease progression and resistance in chronic myeloid leukemia (CML) patients. However, the clinical significance of chromosomal evolution in the Philadelphia (Ph)-negative clone during therapy is not fully understood. We evaluated 94 CML patients in the chronic phase of CML during treatment of the disease. Six of them had Ph-negative chromosome abnormalities during treatment.

Association between methylene tetrahydrofolate reductase and glutathione S-transferase M1 gene polymorphisms and chronic myeloid leukemia in a Brazilian population

G. S. Lordelo, Miranda-Vilela, A. L., Akimoto, A. K., Alves, P. C. Z., Hiragi, C. O., Nonino, A., Daldegan, M. B., Klautau-Guimarães, M. N., and Grisolia, C. K., Association between methylene tetrahydrofolate reductase and glutathione S-transferase M1 gene polymorphisms and chronic myeloid leukemia in a Brazilian population, vol. 11, pp. 1013-1026, 2012.

Chronic myeloid leukemia is a hematopoietic stem cell disorder that causes uncontrolled proliferation of white blood cells. Although the clinical and biological aspects are well documented, little is known about individual susceptibility to this disease. We conducted a case-control study analyzing the prevalence of the polymorphisms MTHFR C677T, MTHFR A1298C, del{GSTM1}, del{GSTT1}, and haptoglobin in 105 patients with chronic myeloid leukemia (CML) and 273 healthy controls, using PCR-based methods.

Analysis of BCR/ABL transcripts in healthy individuals

J. A. Boquett, Alves, J. R. P., and de Oliveira, C. E. C., Analysis of BCR/ABL transcripts in healthy individuals, vol. 12, pp. 4967-4971, 2013.

The chimeric oncogene BCR/ABL, which is the product of reciprocal translocation between chromosomes 9 and 22, is a known molecular marker of chronic myeloid leukemia (CML), and is related to the major factors involved in leukemogenesis. Some previous studies have also reported the presence of this oncogene in peripheral blood cells of healthy individuals. In this study, we investigated the presence of BCR/ABL transcripts in peripheral blood of individuals aged 40 years or more without symptoms of CML.

Response to treatment with imatinib mesylate in previously treated chronic-phase chronic myeloid leukemia patients in a hospital in Brazil

C. A. P. Silveira, Daldegan, M. B., and Ferrari, I., Response to treatment with imatinib mesylate in previously treated chronic-phase chronic myeloid leukemia patients in a hospital in Brazil, vol. 10, pp. 2038-2048, 2011.

We analyzed the results of treatment with imatinib mesylate in 70 patients with chronic-phase chronic myeloid leukemia who had previously been treated (with second-line or higher imatinib), many of them in a late chronic phase. The median follow-up period was 60.5 months (range 3-100 months). Our objective was to assess the efficacy and safety of treatment. The mean dose was 400 mg per day. The hematologic response rate was 92.1% at six months, while the cumulative rates of major and complete cytogenetic responses were 73.6 and 66.3%, respectively.

Differential molecular response of the transcripts B2A2 and B3A2 to imatinib mesylate in chronic myeloid leukemia

J. Alexandre de Lemos, de Oliveira, C. Martins, Scerni, A. Carolina C., Bentes, A. Q., Beltrão, A. Cristina, Bentes, I. Regina G., Azevedo, T. Cristina, and Maradei-Pereira, L. Maria Cunh, Differential molecular response of the transcripts B2A2 and B3A2 to imatinib mesylate in chronic myeloid leukemia, vol. 4, pp. 803-811, 2005.

Chronic myeloid leukemia (CML) originates from the hematopoietic stem cell and is characterized by the reciprocal translocation t(9;22)(q34;q11), which results in the BCR-ABL fusion gene on chromosome 22q-, also known as the Philadelphia chromosome. This chimeric gene codes for a cytoplasmic protein with constitutive tyrosine-kinase activity, responsible for cellular transformation and leukemogenesis in CML.

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