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Your search keyword '"Platelet doubling"' showing total 2 results
Start Over Descriptor "Platelet doubling" Topic acute myeloid leukemia
2 results on '"Platelet doubling"'

1. Impact of clinical features, cytogenetics, genetic mutations, and methylation dynamics of CDKN2B and DLC-1 promoters on treatment response to azacitidine.

Author

Martín, Iván, Navarro, Blanca, Serrano, Alicia, Villamón, Eva, Calabuig, Marisa, Solano, Carlos, Chaves, Felipe Javier, Yagüe, Nuria, Orts, Maribel, Amat, Paula, Fuentes, Azahara, Seda, Enrique, García, Francisca, Hernández-Boluda, Juan Carlos, and Tormo, Mar

Subjects
*ACUTE myeloid leukemia, *CYTOGENETICS, *MYELODYSPLASTIC syndromes, *METHYLATION, *CHROMOSOME abnormalities, *DNA metabolism, *PROTEIN metabolism, *PROTEINS, *CHROMOSOMES, *RESEARCH, *DNA, *GENETIC mutation, *CLINICAL trials, *RESEARCH methodology, *PROGNOSIS, *EVALUATION research, *MEDICAL cooperation, *AZACITIDINE, *DNA methylation, *COMPARATIVE studies, *GENES, *RESEARCH funding
Abstract

Azacitidine (AZA) is a DNA hypomethylation agent administered in myeloid neoplasms; however, there is still a lack of established predictors of response. We studied 113 patients with myelodysplastic syndromes (n = 85) or acute myeloid leukemia (n = 28) who received AZA to assess the predictive value on response of clinical features, cytogenetics, and molecular markers. Overall, 46 patients (41%) responded to AZA. Platelet doubling after the first AZA cycle was associated with a better response (68% vs. 32% responders, P = 0.041). Co-occurrence of chromosome 7 abnormalities and 17p deletion was associated with a worse response (P = 0.039). Pre-treatment genetic mutations were detected in 98 patients (87%) and methylation of CDKN2B and DLC-1 promoters were detected in 50 (44%) and 37 patients (33%), respectively. Patients with SF3B1 mutations showed a better response to AZA (68% vs. 35% responders, P = 0.008). In contrast, subjects with mutations in transcription factors (RUNX1, SETBP1, NPM1) showed a worse response (20% vs. 47% responders, P = 0.014). DLC-1 methylation pre-treatment was associated with poor clinical features and its reduction post-treatment resulted in a better response to AZA in MDS patients (P = 0.037). In conclusion, we have identified several predictors of response to AZA that could help select the best candidates for this treatment. [ABSTRACT FROM AUTHOR]

Published
2020
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2. Impact of clinical features, cytogenetics, genetic mutations, and methylation dynamics of CDKN2B and DLC-1 promoters on treatment response to azacitidine

Author

Enrique Seda, Francisca García, Iván Martín, M. Orts, Eva Villamón, Marisa Calabuig, Nuria Yagüe, Azahara Fuentes, Paula Amat, Carlos Solano, Juan Carlos Hernández-Boluda, Mar Tormo, Blanca Navarro, Alicia Serrano, and Felipe J. Chaves

Subjects
Oncology, Male, medicine.medical_specialty, NPM1, Myeloid, Azacitidine, Myelodysplastic syndromes, Gene mutation, Disease-Free Survival, 03 medical and health sciences, 0302 clinical medicine, Internal medicine, medicine, Humans, Promoter Regions, Genetic, Aged, Cyclin-Dependent Kinase Inhibitor p15, Chromosome 7 (human), Aged, 80 and over, Hematology, Acute myeloid leukemia, business.industry, Tumor Suppressor Proteins, GTPase-Activating Proteins, Myeloid leukemia, General Medicine, DNA, Neoplasm, DNA Methylation, Middle Aged, Platelet doubling, medicine.disease, Promoter methylation, Survival Rate, Leukemia, Myeloid, Acute, medicine.anatomical_structure, 030220 oncology & carcinogenesis, Myelodysplastic Syndromes, Gene mutations, Female, Chromosome Deletion, business, Nucleophosmin, Chromosomes, Human, Pair 7, 030215 immunology, medicine.drug
Abstract

Azacitidine (AZA) is a DNA hypomethylation agent administered in myeloid neoplasms; however, there is still a lack of established predictors of response. We studied 113 patients with myelodysplastic syndromes (n = 85) or acute myeloid leukemia (n = 28) who received AZA to assess the predictive value on response of clinical features, cytogenetics, and molecular markers. Overall, 46 patients (41%) responded to AZA. Platelet doubling after the first AZA cycle was associated with a better response (68% vs. 32% responders, P = 0.041). Co-occurrence of chromosome 7 abnormalities and 17p deletion was associated with a worse response (P = 0.039). Pre-treatment genetic mutations were detected in 98 patients (87%) and methylation of CDKN2B and DLC-1 promoters were detected in 50 (44%) and 37 patients (33%), respectively. Patients with SF3B1 mutations showed a better response to AZA (68% vs. 35% responders, P = 0.008). In contrast, subjects with mutations in transcription factors (RUNX1, SETBP1, NPM1) showed a worse response (20% vs. 47% responders, P = 0.014). DLC-1 methylation pre-treatment was associated with poor clinical features and its reduction post-treatment resulted in a better response to AZA in MDS patients (P = 0.037). In conclusion, we have identified several predictors of response to AZA that could help select the best candidates for this treatment.

Published
2020

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