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A comprehensive temporal proteome and phosphoproteome dataset of Y1 adrenocortical cells under FGF2 stimulation and SOS inhibition
Montoni, F.; Hanada, T.; Doi, K.; Wailemann, R. A. M.; Adachi, J.; Reis, M. d. S.; Natsume-Kitatani, Y.
KRAS amplification and SOS-mediated activation sustain ERK output in Y1 cells, and SOS is not solely responsible for KRAS activation, implicating a wider GEF and GAP landscape.
Moderate contradiction
2 prior failuresTwo documented clinical failures match this mechanism, or a single Phase 3 failure is on record.
Abstract excerpt
The Y1 mouse adrenocortical tumor cell line is a classic model for cancer studies and ACTH mediated steroidogenesis. The KRAS gene amplification and SOS mediated activation sustain elevated ERK levels, which drive the tumor phenotype of this cell line. Recent research revealed that SOS is not solely responsible for KRAS activation in Y1 cells, indicating a more complex regulatory landscape of GEFs and GAPs. This motivated a time resolved proteome and TMT phosphoproteome over a 0 to 30 minute time course under FGF2 stimulation or combined with SOS inhibitor.
Matching Claidex post-mortems
2 of 2 indexed- Jun 3, 2026BGB-53038, a pan-KRAS inhibitor, shelved at Phase 1 as BeOne pivots to a degraderBGB-53038SponsorMRS 22
- Sep 8, 2026Sotorasib versus consolidation durvalumab in ctDNA-positive stage III KRAS G12C lung cancer: a trial whose eligible population was defined out of existenceSotorasib (AMG 510)EnrollmentMRS 33
This is an automated contradiction flag, not an editorial judgment on the preprint's quality. Flags identify where the preclinical literature and the clinical failure record diverge.

