CPA3 (Carboxypeptidase A3)

The identification of CA12, consistent with previous findings on its role in oncogenesis and estrogen regulation, highlights the therapeutic potential of targeting this pathway. Furthermore, the additional genes identified expand our understanding of metabolic alterations in response to estrogen signaling in breast cancer, thereby offering new avenues for mechanistic exploration and the development of potential therapeutic targets.

Immunophenotypic distribution of secretome granules indicates a decrease in the number of Tryptase-, Chymase- and CPA3-mast cells, which is inversely proportional to the pTNM stage of non-metastatic seminoma.

Silva C ECA exhibits a distinctive immune- and matrix-centric tumor-stroma axis based on proteome alterations observed. Tumor microenvironment-resolved proteomics identified Silva pattern-specific biomarkers and therapeutic vulnerabilities that warrant functional and clinical validation.

This study demonstrated active MC participation in the evolution of the FGF23+ PMT microenvironment. The findings may be applied in translational medicine to develop novel algorithms for personalised therapy in patients with FGF23-secreting tumours, offering an alternative when surgical removal of the tumour is not feasible.

Our approach also reduced the cost of HPV integration detection by 90% compared to WGS while also minimizing sequencing data volume. We believe that this method captures HPV integrations at significantly reduced costs and lesser sequencing data volume leading to better understanding of disease progression and monitoring cancer treatment.

This integrative eQTL and Mendelian randomization analysis provides evidence of a positive causal association between 14 key co-expressed genes and mesothelioma genetically. These disease critical genes are implicated in correlations with biological processes and infiltrated immune cells related to mesothelioma. Moreover, our study lays a theoretical foundation for further research into the mechanisms of mesothelioma and potential clinical applications.

We developed a powerful prognostic signature in LUAD that accurately predicts clinical outcomes and can guide immunotherapy and chemotherapy responses.

High-risk group showed low immune cell infiltration, high TIDE score, and worse prognosis, and the patients in this group exhibited a high drug sensitivity to Cisplatin, Erlotinib, Paclitaxel, Saracatini, and CGP_082996. GJB3, DKK1, CPA3, and KRT6A were all high- expressed in LUAD cells, and silencing GJB3 inhibited the migration and invasion of LUAD cells. A novel NMRG signature was developed, contributing to the prognostic evaluation and personalized treatment for LUAD patients.

In conclusion, this study revealed increased MC density in ccRCC. Although the proportion of activated MCs was not significantly altered in ccRCC tissues compared with normal tissues, this finding highlights a shift in the MC phenotype from CTSGhighMCs to more activated VEGFA+MCs, providing a potential therapeutic target for inhibiting ccRCC progression.

SOX4 and CPA3 can be considered as key proteins of FA, coumaric acid-4-O-glucoside and kaempferol-3-O-neohesperidin have been found to have therapeutic potency for FA.

Enhanced mast cell numbers, as well as activation and degranulation are a consequence of NACT exposure. Post-NACT mast cells displayed differing associations with survival outcomes that was dependent upon granule classification. Ultimately, mast cells represent a clinically relevant putative HGSOC immune target.

These data suggest that many of the miR-365 targets are expressed in the oral cancers screened, with the differential expression of UBR3, ZCCHC14, HOMEZ, and NUDT12, which may be correlated with chemoresistance among two specific oral cancer cell lines (SCC25, SCC9). These results suggest this differential expression may signal potential targets for patient treatment with tumors exhibiting miR-365 and chemotherapeutic resistance.