Multimers of the HPV genome are generated in cervical tumors replicating as extrachromosomal episomes, which is associated with deletion and rearrangement of the HPV genome and provides a mechanism for oncogenesis without integration.

IGF2-Wnt signaling plays a key role in AT2-mediated alveolar repair after cigarette smoking–induced injury but also drives pathogenesis of pulmonary emphysema and cancer when hyperactivated.

DAB2IP is lost in early-stage tumors, which amplifies RAS signaling, triggers inflammatory mediators, and recruits macrophages in KRAS-mutant colon cancers.

Cross-talk with T_TEX CD8⁺ T cells mediated by the VEGFR2 axis induces aggressive properties in cancer stem cells to promote tumor progression.

YTHDF2 regulates RIG-I–mediated innate immune signaling to support bladder cancer progression, highlighting the functional importance of m⁶A modifications in bladder cancer and uncovering therapeutic opportunities to improve patient outcomes.

Metastatic cancer cells upregulate ANO1 to activate cell-intrinsic and -extrinsic mechanisms that alter cholesterol metabolism and stimulate fibroblasts, which can be targeted with ANO1 inhibitors to inhibit metastatic growth.

Sialylated cancer IgG activates c-Met-SOX2 signaling to promote stemness properties in cancer cells and can be targeted to suppress tumor growth.

The bifunctional mAb fusion design of BCA101 targets it to the tumor microenvironment where it inhibits EGFR and neutralizes TGFβ to induce immune activation and to suppress tumor growth.

Analysis of DNA methylation landscapes provides insights into the cell-of-origin of PanIN lesions, clarifies the role of PanIN lesions as metaplastic precursors to human PDAC, and suggests potential targets for chemoprevention.

Genomic analyses reveal that primary and relapse LBCL-IP originate from a common progenitor cell with a small set of genetic alterations, followed by extensive parallel diversification, elucidating the clonal evolution of LBCL-IP.