Journal
Cell communication and signaling
Publication Date
12-16-2025
Volume
24
Issue
1
First Page
61
Document Type
Open Access Publication
DOI
10.1186/s12964-025-02568-3
Rights and Permissions
He, F., Lin, S., Gao, B. et al. A proteogenomic gene signature defines prognostic subgroups highlighting PI3K/AKT/mTOR signaling pathway as a therapeutic vulnerability in myeloid malignancies. Cell Commun Signal 24, 61 (2026). https://doi.org/10.1186/s12964-025-02568-3 This article is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License, which permits any non-commercial use, sharing, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if you modified the licensed material. You do not have permission under this licence to share adapted material derived from this article or parts of it. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by-nc-nd/4.0/.
Recommended Citation
He, Fan; Lin, Shuyang; Gao, Bei; Ramesh, Varun; Kim, Alexander B; Kong, Tim; Fisher, Daniel A C; Letson, Christopher T; Brakhane, Molly; Fulbright, Mary; Yu, Yanbo; Sardiello, Marco; Di Paola, Jorge; Sykes, Stephen M; and Oh, Stephen T, "A proteogenomic gene signature defines prognostic subgroups highlighting PI3K/AKT/mTOR signaling pathway as a therapeutic vulnerability in myeloid malignancies." Cell communication and signaling. 24, 1. 61 (2025).
https://digitalcommons.wustl.edu/oa_4/6713
Department
ICTS (Institute of Clinical and Translational Sciences)
Additional Links
Supplemental material is available for this article at publisher site.
