Nature Communications (Sep 2022)
Oncogenic RAS commandeers amino acid sensing machinery to aberrantly activate mTORC1 in multiple myeloma
- Yandan Yang,
- Arnold Bolomsky,
- Thomas Oellerich,
- Ping Chen,
- Michele Ceribelli,
- Björn Häupl,
- George W. Wright,
- James D. Phelan,
- Da Wei Huang,
- James W. Lord,
- Callie K. Van Winkle,
- Xin Yu,
- Jan Wisniewski,
- James Q. Wang,
- Frances A. Tosto,
- Erin Beck,
- Kelli Wilson,
- Crystal McKnight,
- Jameson Travers,
- Carleen Klumpp-Thomas,
- Grace A. Smith,
- Stefania Pittaluga,
- Irina Maric,
- Dickran Kazandjian,
- Craig J. Thomas,
- Ryan M. Young
Affiliations
- Yandan Yang
- Lymphoid Malignancies Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health
- Arnold Bolomsky
- Lymphoid Malignancies Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health
- Thomas Oellerich
- Department of Medicine II, Heamatology/Oncology, Goethe University
- Ping Chen
- Lymphoid Malignancies Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health
- Michele Ceribelli
- Division of Preclinical Innovation, National Center for Advancing Translational Sciences, National Institutes of Health
- Björn Häupl
- Department of Medicine II, Heamatology/Oncology, Goethe University
- George W. Wright
- Biometric Research Branch, DCTD, National Cancer Institute, National Institutes of Health
- James D. Phelan
- Lymphoid Malignancies Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health
- Da Wei Huang
- Lymphoid Malignancies Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health
- James W. Lord
- Lymphoid Malignancies Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health
- Callie K. Van Winkle
- Lymphoid Malignancies Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health
- Xin Yu
- Lymphoid Malignancies Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health
- Jan Wisniewski
- Experimental Immunology Branch, National Cancer Institute, National Institutes of Health
- James Q. Wang
- Lymphoid Malignancies Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health
- Frances A. Tosto
- Division of Preclinical Innovation, National Center for Advancing Translational Sciences, National Institutes of Health
- Erin Beck
- Division of Preclinical Innovation, National Center for Advancing Translational Sciences, National Institutes of Health
- Kelli Wilson
- Division of Preclinical Innovation, National Center for Advancing Translational Sciences, National Institutes of Health
- Crystal McKnight
- Division of Preclinical Innovation, National Center for Advancing Translational Sciences, National Institutes of Health
- Jameson Travers
- Division of Preclinical Innovation, National Center for Advancing Translational Sciences, National Institutes of Health
- Carleen Klumpp-Thomas
- Division of Preclinical Innovation, National Center for Advancing Translational Sciences, National Institutes of Health
- Grace A. Smith
- Laboratory of Pathology, Center for Cancer Research, National Cancer Institute, National Institutes of Health
- Stefania Pittaluga
- Laboratory of Pathology, Center for Cancer Research, National Cancer Institute, National Institutes of Health
- Irina Maric
- Hematology Service, Department of Laboratory Medicine, National Institutes of Health Clinical Center
- Dickran Kazandjian
- Department of Medicine, University of Miami Health System
- Craig J. Thomas
- Lymphoid Malignancies Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health
- Ryan M. Young
- Lymphoid Malignancies Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health
- DOI
- https://doi.org/10.1038/s41467-022-33142-x
- Journal volume & issue
-
Vol. 13,
no. 1
pp. 1 – 19
Abstract
RAS mutations are commonly found in multiple myeloma (MM). Here, the authors show that oncogenic RAS mutations activate mTORC1 signalling in MM and combining mTORC1 and MEK/ERK inhibitors synergize to improve survival in preclinical models.
