BRAF mutation

Benign struma ovarii do not harbor BRAF alterations. DICER1 and POLD1 variants need further investigation in this tumor pathology.

RAS or MEK inhibition co-targeting is effective against this resistance mechanism. This study provides preclinical rationale for clinical testing of exarafenib in BRAF Class II/III cancers and unveils RAS-mediated ARAF-KSR1 complex formation as a resistance mechanism and rational co-therapy strategies.

P4, N=13, Completed, University Hospital, Rouen | Recruiting --> Completed | N=40 --> 13

This study provides a comprehensive genomic overview of AM, highlighting recurrent alterations in the MAPK and cell cycle pathways, and potential demographic-specific molecular signatures. These findings support the need for expanded molecular profiling to improve prognostic accuracy and identify targets for future therapy.

Persons who have a more pro-inflammatory lifestyle may have an increased recurrence risk (IRR 1.21, 95% CI 0.97-1.52), which was most pronounced for persons with MSS and KRAS or PIK3CA wildtype tumours (IRR 1.31, 95% CI 0.90-1.90 and IRR 1.30, 95% CI 0.98-1.71, respectively). Our results suggest that associations between the LIS and recurrence might differ based on molecular tumour characteristics.

Between mCRC diagnosis and death or withdrawal, patients were frequently exposed to fluoropyrimidine (99.0%), irinotecan (96.2%), oxaliplatin (88.4%), anti-vascular endothelial growth factor (78.7%) and anti-epidermal growth factor receptor (40.1%). PROMETCO provided information on real-world prescribing patterns and efficacy. OS from mCRC diagnosis and PFS from 3L and beyond were similar to previous long-term follow-up data from clinical trials.

This meta-analysis shows that KRAS, NRAS, and BRAF mutations are important for adverse prognostic markers in colorectal cancer, linked to reduced overall survival. Routine molecular testing for these mutations is vital to enable personalized treatment, improve patient stratification, and enhance clinical outcomes in colorectal cancer management.

As FLCN and SDH are not currently included in the current guidelines for EO-CRC, PVs/LPVs in these genes may be underestimated. To better understand their significance, we recommend including their assessment in all patients with EO-CRC.

Treatment included surgery and systemic therapies (nivolumab and ipilimumab, followed later by tovorafenib). The patient's clinical course was marked by aggressive local progression and therapeutic challenges. This case highlights the rarity of such presentations and the need for further research into the clinicopathological and molecular features of infantile melanoma arising in congenital melanocytic nevus (CMN).

P2, N=20, Active, not recruiting, Melanoma Institute Australia | Trial completion date: Jan 2036 --> Oct 2035

Multiplex immunofluorescence staining demonstrated that BCL-xL inhibition effectively triggered apoptosis in heterogeneous PDX tumor slice models, including models harboring oncogenic BRAF mutations. Our findings suggest that cetuximab-resistant CRC retains apoptotic competence, and that BCL-xL inhibition serves as a robust alternative therapeutic strategy that is largely independent of the tumor mutational profile.

P1/2, N=24, Not yet recruiting, University of Chicago