KRAS mutation

P2, N=124, Active, not recruiting, SWOG Cancer Research Network | Trial completion date: Mar 2026 --> Dec 2026 | Trial primary completion date: Mar 2026 --> Dec 2026

Our work defines a chemotherapy-resistant and metastasis-enriched malignant epithelial subpopulation in PDAC that drives disease progression through an immune-cold niche. We identify RARRES1 as a pivotal regulator of this process, contributing to both therapy resistance and immune exclusion, and propose it as a novel pan-cancer prognostic biomarker. These findings reveal a targetable cellular mechanism underlying poor treatment response in PDAC.

These findings suggest that nonampullary duodenal neoplasms of gastric phenotype can be reclassified as "gastric-type adenomas" based on excellent prognosis and common genetic alterations, albeit a wide spectrum of morphology and gastric phenotypic expression. MDM2 amplification may contribute to histologic progression.

P2, N=60, Not yet recruiting, Gustave Roussy, Cancer Campus, Grand Paris

P1/2, N=5, Completed, National Cancer Institute (NCI) | N=70 --> 5 | Recruiting --> Completed

Cutaneous metastases from colorectal cancer show heterogeneous and sometimes rare presentations, including herpetiform and pseudotumoral patterns. Vulvar involvement is exceptionally uncommon therefore prompt recognition and histopathological confirmation are essential in patients with persistent or atypical lesions to avoid misdiagnosis and allow timely management.

Pathological subtypes of CCA exhibit distinct clinical outcomes and molecular characteristics. Classification based on pathological subtype provides a useful framework for understanding the clinical and molecular heterogeneity of CCA.

They thereafter achieved excellent clinical outcomes, including complete and partial responses, with sustained benefits. The POSEIDON regimen may represent a potent therapeutic option for this rare patient population with multiple negative prognostic factors.

This work elucidates a previously unrecognized paracrine circuit linking neural plasticity with epithelial reprogramming through ganglioside signaling, providing mechanistic insights into microenvironmental regulation of early pancreatic carcinogenesis. Our findings position neuronal-ADM interactions and glycosphingolipid metabolism as promising therapeutic targets for intercepting PDAC development at premalignant stages.

Recurrence risk among patients with R0N0 pCCA was heterogeneous. The proposed risk score stratified patients into markedly different risk categories relative to recurrence, which may help guide utilization of adjuvant therapy as well as surveillance in the postoperative setting.

P1/2, N=51, Recruiting, Arvinas Inc. | N=14 --> 51

P1, N=17, Terminated, AstraZeneca | Phase classification: P1/2 --> P1