In This Issue

Abstract

In This Issue| January 09 2023 In This Issue Author & Article Information Online Issn: 2159-8290 Print Issn: 2159-8274 ©2023 American Association for Cancer Research2023American Association for Cancer Research Cancer Discov (2023) 13 (1): 1–3. https://doi.org/10.1158/2159-8290.CD-13-1-ITI Related Content A commentary has been published: A Molecular Switch between Mammalian MLL Complexes Dictates Response to Menin–MLL Inhibition A commentary has been published: Disabling Uncompetitive Inhibition of Oncogenic IDH Mutations Drives Acquired Resistance A commentary has been published: Molecular Characterization of Acquired Resistance to KRASG12C–EGFR Inhibition in Colorectal Cancer View more A commentary has been published: A Small Molecule Reacts with the p53 Somatic Mutant Y220C to Rescue Wild-type Thermal Stability A commentary has been published: Human Papillomavirus 42 Drives Digital Papillary Adenocarcinoma and Elicits a Germ Cell–like Program Conserved in HPV-Positive Cancers A commentary has been published: Creating MHC-Restricted Neoantigens with Covalent Inhibitors That Can Be Targeted by Immune Therapy A commentary has been published: Osimertinib + Savolitinib to Overcome Acquired MET-Mediated Resistance in Epidermal Growth Factor Receptor–Mutated, MET-Amplified Non–Small Cell Lung Cancer: TATTON A commentary has been published: Cell Competition Shapes Metastatic Latency and Relapse A commentary has been published: Intraventricular B7-H3 CAR T Cells for Diffuse Intrinsic Pontine Glioma: Preliminary First-in-Human Bioactivity and Safety A commentary has been published: Identifying the Transcriptional Drivers of Metastasis Embedded within Localized Melanoma A commentary has been published: An Aged/Autoimmune B-cell Program Defines the Early Transformation of Extranodal Lymphomas View less Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Facebook Twitter LinkedIn MailTo Tools Icon Tools Get Permissions Cite Icon Cite Search Site Article Versions Icon Versions Version of Record January 9 2023 Citation In This Issue. Cancer Discov 1 January 2023; 13 (1): 1–3. https://doi.org/10.1158/2159-8290.CD-13-1-ITI Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest Search Advanced Search The combination of KRASG12C and EGFR inhibitors allows for the targeting of KRAS mutations in colorectal cancer, but acquired resistance limits the duration of response. Yaeger and colleagues characterized mechanisms of resistance to KRASG12C plus EGFR inhibitors and found that heterogenous resistance changes largely converge on reactivation of ERK signaling. Moreover, KRASG12C amplification is a recurrent resistance mechanism that is positively selected for with treatment. When treatment is stopped, the acquired KRASG12C amplification leads to oncogene-induced senescence due to supraphysiologic ERK signaling and high mTOR signaling, opening the potential for new therapeutic approaches targeting this senescence. See article, p. 41. The tumor suppressor/transcription factor p53 is the most frequently mutated and inactivated gene in cancer. The p53 Y220C mutation occurs in 1% of patients and results in a thermally unstable protein that unfolds at physiologic temperatures. In this study, Guiley and Shokat discovered compounds that covalently... You do not currently have access to this content.