Abstract

Research in Medical & Engineering Sciences Glycogen Synthase Kinase-3β(GSK-3β ) is a Critical Factor in Intracellular Signaling Pathways in Acute Lymphoblastic Leukemia Cristian Fabian Layton Tovar* Autonomous University of Mexico State, Mexico *Corresponding author: Cristian Fabian Layton Tovar, General Agustín Olachea 1401, Ocho Cedros, Toluca, México, CP 50170 Submission: November 11, 2017; Published: December 19, 2017 DOI: 10.31031/RMES.2017.03.000552 ISSN : 2576-8816Volume3 Issue1

Highlights

  • Acute lymphoblastic leukemia (ALL) development is associated with deregulation in different points of the molecular signaling pathways associated with the hematopoiesis process

  • The use of kinase inhibitors of BCR/ABL gene as a molecular target in patients positive to the Philadelphia chromosome (Ph + ALL) is available, this occurs with a prevalence of 5% in children and 30 % in adults. [2,3] or ErbB, a promoter of survival signaling and cell proliferation expressed in B-cell lymphoblast [4,5]

  • Glycogen synthase kinase-3β (GSK-3β) has been identified as an important regulator of nuclear factor kappa B (NF-kB) transcriptional activity, these effects should regulate the apoptosis in leukemic cells

Read more

Summary

Introduction

ALL development is associated with deregulation in different points of the molecular signaling pathways associated with the hematopoiesis process. The translocations induced an aberrant expression of the enzymes that regulate the intracellular signaling process [1]. JAK mutations and CRLF2 over expression in patients with refractory leukemia have been identified and treatment with JAK inhibitors has shown favorable results.

Results
Conclusion
Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.