Basal Cell Carcinoma

Among them, STAT3 and GUCA1A emerged as key mediator hubs, each mediating multiple protein pathways (with the highest mediation proportion reaching 15.2%). This study reveals the causal associations between certain UKB pQTLs, BD pQTLs, and BCC, and identifies six BD pQTLs that mediate the effect of UKB pQTLs on BCC through STAT3 and GUCA1A as core mediator proteins, providing new genetic evidence for the precise stratification and targeted intervention of BCC.

An ensemble classifier combining logistic regression and random forest on pre-to-post expression deltas achieved an area under the receiver operating characteristic curve (AUC) of 0.812 (95% CI: 0.694-0.930; 5-fold cross-validated AUC = 0.806) for adaptive resistance prediction across n = 59 patients with available response annotations. These findings establish a consistent transcriptional signature of compensatory checkpoint upregulation during ICB therapy and provide a data-driven framework for early identification of adaptive resistance that warrants external prospective validation.

P2, N=70, Suspended, Thomas Jefferson University | Recruiting --> Suspended

Our findings support previous reports on the immune-privileged status of BCC. Contrary to the literature, we could not confirm PD-L1 expression on BCC cells, but rather on the intra- and peritumoral immune cells. Given these results and the literature suggesting a tendency of higher immunoreactivity compared to other BCC subtypes, basosquamous BCC might be a better target for anti-PD-1 therapy as opposed to other subtypes.

Collectively, this study systematically elucidates the toxicological mechanism by which DEHP promotes skin cancer development through subtype-specific pathways regulated by 11 key targets, clarifying its direct binding patterns with core targets and downstream pathway disruption characteristics. This not only fills a research gap in the molecular mechanisms of DEHP-induced skin carcinogenesis but also provides novel biomarkers for environmental exposure prevention and targeted interventions against skin cancer.

EN1 is a highly sensitive marker for AdCC and has prognostic value. MYB is a useful complementary marker, particularly when polymorphous adenocarcinoma is a consideration.

P1, N=25, Recruiting, University of California, Irvine

P2, N=798, Active, not recruiting, National Cancer Institute (NCI) | Trial primary completion date: May 2027 --> May 2026

P2, N=180, Recruiting, Philogen S.p.A. | Not yet recruiting --> Recruiting | Initiation date: Feb 2026 --> Jun 2026

P2, N=21, Active, not recruiting, Gruppo Oncologico del Nord-Ovest | Recruiting --> Active, not recruiting | Trial completion date: Jan 2026 --> Dec 2026

P2, N=18, Active, not recruiting, Case Comprehensive Cancer Center | Recruiting --> Active, not recruiting | N=28 --> 18

P=N/A, N=60, Recruiting, Roswell Park Cancer Institute | Trial completion date: Dec 2026 --> Jun 2027 | Trial primary completion date: Dec 2026 --> Jun 2027