MUC19 (Mucin 19, Oligomeric)

Finally, we identified the intrinsic tandem repeats in MUC19 to be its functional domain, which promotes cell survival and cell cycle through activating mechanistic target of rapamycin (mTOR) signaling in EBV-positive cells...In this study, we revealed that EBV induced the duplicated copy number variants of the MUC19 gene and enhanced its expression, which further promotes cell survival and cell cycle via mTOR signaling. Overall, this study maps the genomic perturbations induced by EBV primary infection and offers new insights into the critical role of MUC19 in EBV latency.

The independent prognostic factors identified in this study provide a theoretical basis for individualized prognosis judgment in OCCC and HGSC. The SMGs and TMB levels may serve as valuable indicators for prognosis and evaluating targeted therapy or immunother-apy efficacy. Druggable genes such as NOTCH1 and RYR3 offer promising therapeutic tar-gets, while stage-specific pathway enrichments reveal potential intervention strategies. Further validation in larger cohorts is needed to confirm these findings. Our study advances the under-standing of molecular heterogeneity in ovarian cancer and lays the groundwork for personal-ized treatment strategies, ultimately improving patient outcomes.

Interestingly, the personalized-treatment targetable alterations, such as microsatellite instability and mismatch repair or homologous recombination deficiencies did not differ between the primary tumors and paired metastases or between the metastases from different secondary sites and had no prognostic value. The results suggest a potential prognostic role of KRAS mutations, mutation load, and CNVs in PDAC patients after metastasectomy and encourage further molecular profiling for personalized treatment of PDAC patients with different metastasis localization.

The identification of these specific genomic alterations in transformed SCLC contributes to a better understanding of the mechanisms driving this transformation. This knowledge may guide future predicting the transformation of SCLC and the development of personalized treatment strategies for these patients.

APT does not appear to have a specific molecular signature but shares genomic alterations with both PA and PC. The incidence of CDC73 mutations is low, and it remains unclear whether these mutations are associated with a higher risk of recurrence. Our study confirms that PI3 K/AKT/mTOR and Wnt signaling represents the pivotal pathways in parathyroid tumorigenesis and also revealed mutations in key epigenetic modifier genes (BCOR, KDM2A, MBD4, and EZH2) involved in chromatin remodeling, DNA, and histone methylation.

NEAT1 or MUC19 overexpression disrupted their protective role of silencing METTL3 in AECs, thereby increasing apoptosis and inflammatory injury. In conclusion, this is the first study to suggest that METTL3 aggravates SP-induced cell damage via the NEAT1/CTCF/MUC19 axis.

Our study revealed that PGR, PTPRD, RELN, MUC19, LRP1B, and FAT3 mutation could serve as predictive biomarkers. Our systematic nomograms demonstrate significant potential in predicting the prognosis for NSCLC patients with sensitivity to different ICI treatment strategies.

Alterations in Mucin family genes are common in ccRCC. HVN is associated with worse prognosis and may predict decreased benefit from anti-angiogenic TKIs.

The detailed characterization including molecular, morphological, and drug-sensitivity profiling makes these models valuable pre-clinical tools for drug development applications and research on precision cancer therapy. The pleomorphic model additionally enables research on a functional and cell-based level of this rare NCSLC subentity.

The role of trefoil factor-1 with respect to metastasis of estrogen receptor-positive breast cancer also merits further investigation. In addition, mucin 19 has emerged as an unexplored target for treatment of breast cancer.

We characterized the genomic heterogeneity among different tumors. We offered novel clues to the clonal evolution between MPLC and their lymphatic metastases, thus advancing the treatment strategies and preventions of MPLC with LNM.

The MUC family seems to have an influence on the development of ALL in the Amerindian population and especially MUC19 and MUC3A are shown as possible hotspots. In addition, the 11 new variants found point to the need to have their clinical impact analyzed.