CIBICI   14215
CENTRO DE INVESTIGACION EN BIOQUIMICA CLINICA E INMUNOLOGIA
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
Increased expression of autophagy protein LC3 in patients with progressing Chronic Lymphocytic Leukemia
Autor/es:
DANIELA SOLEDAD ARROYO; MANZONE RODRIGUEZ, CLARISA; NATALIA SOLEDAD BÁEZ; CECILIA MARÍA RODRÍGUEZ; PABLO IRIBARREN
Reunión:
Congreso; Reunión Anual de Sociedades de Biociencias 2020; 2020
Institución organizadora:
Sociedad Argentina de Inmunología (SAI), Sociedad Argentina de Investigación Clínica (SAIC) y la Sociedad Argentina de Fisiología (SAFIS)
Resumen:
Increased expression of autophagy protein LC3 in patients with progressing Chronic Lymphocytic Leukemia Daniela S. Arroyo 1,2,3, Cecilia M. Rodríguez 1,2, Natalia S. Báez 1,2,3, Clarisa Manzone Rodríguez 5, Pablo Iribarren 2,5. 1 Laboratorio de Oncohematología, Hospital Nacional de Clínicas, UNC. 2 Dpto. Bioquímica Clínica, Facultad de Ciencias Químicas, UNC. 3 CONICET, 4 IMEX-CONICET-Academia Nacional de Medicina, Buenos Aires. 5 Centro de Investigación en Bioquímica Clínica e Inmunología (CIBICI-CONICET), Córdoba. Chronic lymphocytic leukemia (CLL) is the most common type of adult leukemia in the western hemisphere. It is characterized by a clonal proliferation of a population of CD5+ B lymphocytes that accumulate in the secondary lymphoid tissues, bone marrow, and blood. Some CLL patients remain free of symptoms for decades, whereas others rapidly become symptomatic or develop high-risk disease. Studying autophagy, which may modulate key protein expression and cell survival, may be important to the search for novel prognostic factors and molecules. Here, we applied flow cytometry technology to simultaneously detect autophagy protein LC3B with classical phenotypical markers used for the identification of tumoral CLL B cell clones. We found that two patients with progressing CLL showed increased expression of the autophagy protein LC3B, in addition to positive expression of CD38 and ZAP70 and unmutated status of IGHV. Our data suggest that activation of autophagy flux may correlate with CLL progression even before Ibrutinib treatment. Key words: Chronic Lymphocytic Leukemia, autophagy, LC3, progressing, cancer. Innate immune receptors, autophagy, cell death, Chronic Lymphocytic Leukemia