Abstract
Laura A. Estrada-Abreo1,2, Leonor Rodríguez-Cruz2, Yanelly Garfias-Gómez1, Janeth E. Araujo-Cardenas1, Gabriela Antonio-Andrés3, Alfonso R. Salgado-Aguayo4, Darío Orozco-Ruiz5, José Refugio Torres-Nava5, Juan D. Díaz-Valencia1, Sara Huerta-Yépez3 and Genaro Patiño-López1
1 Immunology and Proteomics Laboratory, Hospital Infantil de México Federico Gómez, México City, México
2 Cell Biology and Flow Cytometry Laboratory, Department of Health Sciences, Universidad Autónoma Metropolitana, Iztapalapa, México
3 Oncologic Diseases Research Unit, Hospital Infantil de México Federico Gómez, México City, México
4 Laboratory of Research on Rheumatic Diseases, National Institute of Respiratory Diseases, Ismael Cosío Villegas, México City, México
5 Oncology Service, Hospital Infantil Moctezuma, México City, México
Correspondence to:
Genaro Patiño-López, | email: | gpatino@himfg.edu.mx |
Keywords: Myosin 1g; acute lymphoblastic leukemia; high risk; biomarker; pediatric
Received: March 13, 2021 Accepted: August 13, 2021 Published: September 14, 2021
ABSTRACT
Acute Lymphoblastic Leukemia (ALL) is the most frequent cancer in pediatric population. Although the treatment has improved and almost 85% of the children are cured about 20% suffer relapse, therefore finding molecules that participate in the pathogenesis of the disease for the identification of relapse and patients at risk is an urgent unmet need. Class I myosins are molecular motors involved in membrane tension, endocytosis, phagocytosis and cell migration and recently they have been shown important for development and aggressiveness of diverse cancer types, however Myo1g an hematopoietic specific myosin has not been studied in cancer so far. We evaluated the expression of Myo1g by qRT-PCR, Immunocytochemistry and Immunofluorescence in a cohort of 133 ALL patients and correlated the expression at diagnosis and after treatment with clinical features and treatment outcomes. We found high expression levels of Myo1g in Peripheral Blood Mononuclear Cells (PBMCs) from patients with ALL at diagnosis and those levels decreased after complete remission; furthermore, we found an increase in Myo1g expression on patients with 9:22 translocation and those who relapse. This study show that Myo1g is over expressed in ALL and that may participate in the pathogenesis of the disease specially in high-risk patients.