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Correction: Cellular and Molecular Life Sciences (2022) 80:6 https://doi.org/10.1007/s00018-022-04634-2
In the published article reference 41 was missed in the third paragraph, under discussion section in the page 15, and the below mentioned reference has been incorrectly processed, and the error in the below references has been now updated.
Previously, we have reported that aberrant activation of the MET receptor modulates the cellular response to IR by rewiring key DNA damage response (DDR)-related phosphorylations in some tumor cell lines featuring MET activation [41]. Assuming that a MET–DDR interface underlies MET dependency, here we monitored 116 DDR- and RTK signalling-associated phosphosites in a panel of MET-positive, MET-responsive as well as non-responsive tumor models following targeted MET inhibition. This analysis revealed 14 METi-modulated phosphorylation events that were present solely in MET-addicted models, thus representing ‘MET-asa-driver’ footprints.
The original article has been updated.
References
Weinstein IB (2002) Cancer. Addiction to oncogenes—the Achilles heal of cancer. Science 297:63–64
Zagorac I et al (2018) In vivo phosphoproteomics reveals kinase activity profiles that predict treatment outcome in triple-negative breast cancer. Nat Commun 9:3501
Lange V, Picotti P, Domon B, Aebersold R (2008) Selected reaction monitoring for quantitative proteomics: a tutorial. Mol Syst Biol 4:222
Minari R et al (2021) Afatinib therapy in case of EGFR G724S emergence as resistance mechanism to osimertinib. Anticancer Drugs 32:758–762
Bardelli A et al (2013) Amplification of the MET receptor drives resistance to anti-EGFR therapies in colorectal cancer. Cancer Discov 3:658–673
Huang S, Peter Rodemann H, Harari PM (2016) Molecular targeting of growth factor receptor signaling in radiation oncology. Recent Results Cancer Res 198:45–87
Glück AA et al (2018) Identification of a MET-eIF4G1 translational regulation axis that controls HIF-1α levels under hypoxia. Oncogene 37:4181–4196
Wang Z et al (2022) Proteomic and phosphoproteomic analyses reveal the oncogenic role of PTK7-NDRG1 axis in non-small-cell lung cancer cell resistance to AZD9291. ACS Chem Biol 17:2849–2862
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Orlando, E., Medo, M., Bensimon, A. et al. Correction: An oncogene addiction phosphorylation signature and its derived scores inform tumor responsiveness to targeted therapies. Cell. Mol. Life Sci. 80, 85 (2023). https://doi.org/10.1007/s00018-023-04725-8
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DOI: https://doi.org/10.1007/s00018-023-04725-8