Basal cell carcinoma (BCC) is the most common human cancer, yet molecular processes governing its development and varied clinical behavior remain poorly characterized. We performed an integrated genomic and transcriptional analysis of a large BCC cohort (n = 443) combining newly generated and publicly available whole genome, exome, methylation array and transcriptome data with corresponding clinical information. We observed wide variation in tumor mutational burden across BCC samples and a driver landscape dominated by PTCH1, TERT promoter, and TP53. Replication timing and TP53 status jointly determined activity of UV-induced mutational signatures (SBS7a/b), with TP53-mutant tumors accumulating more mutations in early-replicating regions due to impaired DNA damage response efficiency. BCC displayed remarkably low aneuploidy, except in rare metastatic cases. Mutation timing analysis indicated that TP53 inactivation generally precedes PTCH1 loss. Transcriptomic profiling identified LGR5⁺ hair-follicle stem cells as the most likely cell of origin, characterized by low MHC-I and high TGF-β expression. Integrative multi-omic clustering identified four distinct molecular subtypes of basal cell carcinoma, characterized by differences in histological presentation, immune infiltration patterns, Hedgehog signaling pathway activity, and mutational burden, thereby defining key molecular dimensions of BCC heterogeneity.