Title

Targeting the cdk6 dependence of ph+ acute lymphoblastic leukemia

Authors

Patrizia Porazzi, Thomas Jefferson UniversityFollow
Marco De Dominici, University of Colorado Anschutz Medical Campus
Joseph Salvino, The Wistar Institute,
Bruno Calabretta, Thomas Jefferson UniversityFollow

Document Type

Article

Publication Date

9-1-2021

Comments

This article is the author’s final published version in Genes, Volume 12, Issue 9, September 2021, Article number 1355.

The published version is available at https://doi.org/10.3390/genes12091355.

Copyright © Porazzi et al.

Publication made possible in part by support from the Jefferson Open Access Fund

Abstract

Ph+ ALL is a poor-prognosis leukemia subtype driven by the BCR-ABL1 oncogene, either the p190-or the p210-BCR/ABL isoform in a 70:30 ratio. Tyrosine Kinase inhibitors (TKIs) are the drugs of choice in the therapy of Ph+ ALL. In combination with standard chemotherapy, TKIs have markedly improved the outcome of Ph+ ALL, in particular if this treatment is followed by bone marrow transplantation. However, resistance to TKIs develops with high frequency, causing leukemia relapse that results in

Recommended Citation

Porazzi, Patrizia; De Dominici, Marco; Salvino, Joseph; and Calabretta, Bruno, "Targeting the cdk6 dependence of ph+ acute lymphoblastic leukemia" (2021). Department of Cancer Biology Faculty Papers. Paper 184.
https://jdc.jefferson.edu/cbfp/184

Creative Commons License

This work is licensed under a Creative Commons Attribution 4.0 License.

Language

English