LRP1B (LDL Receptor Related Protein 1B)

A multifactorial cause is suspected. Chronic gingivostomatitis, immunosuppression, and/or viral infection may be associated with FOSCC in young cats.

The integrated analysis of longitudinal WES data from primary tumors and matched PDXs enabled the identification of a core set of conserved, potentially deleterious mutations. The four prioritized mutations (PTPRK, PIK3CB, LRP1B, and IGF2R) provide new insights into the genetic landscape of gastric cancer and represent promising candidates for the development of targeted therapeutic strategies.

Mutations in BAP1, CHEK2, and DICER1 are independently associated with poorer prognosis in UM, while SF3B1 defines a distinct histologic subgroup. Routine mutational profiling by targeted NGS may aid in risk stratification and follow-up of UM patients.

The model is robust and effectively reflects NSCLC heterogeneity while predicting prognosis. RORA promotes the expression of ZNF490 to inhibit NUDFs and oxidative phosphorylation.

In conclusion, a subset of CKD-/ESRD-associated iCCAs in Taiwan shows molecular and chemical evidence of AA exposure. However, the modest correlation between AA adducts and SBS22a signatures and the paucity of T>A transversions in driver genes suggests that AA acts as a contributory rather than causal factor, possibly synergizing with aging and liver disease-related mutagenic processes.

HAS and non-hepatoid AFPGC exhibit a high degree of similarity at both the genomic and transcriptomic levels.

Comprehensive molecular profiling in a MTB setting reveals distinct and therapeutically relevant mutational patterns across urologic cancers. These data support the integration of MTBs into clinical workflows and highlight the potential of co-mutational signatures to guide personalized treatment strategies.

Altogether, these findings were insufficient to establish a diagnosis of pcGDTCL. We review the clinical, histopathologic, and molecular sequencing data pertaining to our rare patient as well as the recent literature on indolent CD30+LPD with gamma-delta T-cells.

NSCLC with co-expression of Thyroid Transcription Factor-1 and p40 is a rare and diagnostically challenging subtype, most frequently observed in older male patients with a history of smoking and predominantly arising in peripheral lung regions. The morphological, immunophenotypic and molecular features of these tumors suggest that they may originate from stem-like basal cells with dual-lineage differentiation. Literature review identified high-frequency alterations in TP53, FGFR1, CDKN2A, EGFR, KRAS, MYC, NF1 and AKT1. Next-generation sequencing-based genomic profiling facilitate the diagnosis and treatment of such cases.

HAD/ACED demonstrated higher TP53 mutation accumulation and TP53-related cancer stemness gene overexpression, including LIN28B, IGF2BP1, and HMGA2. Therefore, TP53 and these cancer stemness genes might be involved in the occurrence of HAD/ACED.

Notably, the mutational landscape of LRP1B exhibits marked tissue specificity and molecular subtype heterogeneity, which may influence the efficacy of immunotherapy, targeted therapies, and cytotoxic chemotherapy. In this review, we provide a comprehensive overview of the mutation patterns, mechanistic functions, immunological roles, and therapeutic predictive value of LRP1B across various cancer types, with the aim of supporting its development as a biomarker and therapeutic target in precision oncology.

We successfully established a PDX model of gallbladder adenosquamous carcinoma, with KRAS (G12V) identified as a potential initiating mutation, and the probable tumor-initiating cell is derived from an EpCAM-positive putative cancer stem cell. Sequential analysis revealed the emergence of resistant clones and adaptive selection of chromatin remodelers in the PDX model.