COL17A1 (Collagen Type XVII Alpha 1 Chain)

COL17A1 was overexpressed in several cancers but underexpressed in melanoma, without strong correlation to tumor-infiltrating immune cells. Although the incidence of ICI-induced BP significantly differed on the basis of cancer type, COL17A1 mutations or dysregulation do not appear to drive this phenomenon, suggesting alternative immune mechanisms.

SLC27A2 mRNA expression was elevated in tumor tissues relative to adjacent noncancerous tissues, whereas the mRNA expression levels of the other four genes were decreased. This study reveals the important role of PTMs in BC prognosis and provides new perspectives for the prognostic assessment of BC patients as well as personalized treatment.

We confirmed that the INHBA/TP63 axis played a key role in mediating the regulation of COL17A1+ tumor cells by POSTN+ fibroblasts. Our findings provide new insights into the characteristics of the tumor microenvironment and the crosstalk between tumor and fibroblasts, offering valuable multiomics data resources for elucidating tumor progression mechanisms.

This study establishes a visceral pain model centered on pancreatic parenchymal nociception rather than secondary neural effects, and for the first time proposes an interconnected regulatory network linking epigenetic modifications, immune reprogramming, and neural plasticity, revealing dual pain pathogenesis mechanisms: (1) immune microenvironment reshaping that potentiates neuroinflammation, and (2) direct ion channel regulation enhancing neuronal excitability. These findings provide a mechanistic foundation for developing methylation-based prognostic biomarkers and multimodal analgesic therapeutic strategies targeting the immuno-neural nexus.

COL17A1, a collagen highly and specifically expressed in HNSCC, mediates in part Uchl5-mediated immune evasion. Our findings suggest an unappreciated role for UCHL5 in promoting EMT in HNSCC and highlight ECM modulation as a strategy to improve immunotherapy responses.

In vivo studies demonstrate that L1low cells correlate with increased collagen deposition, reduced sensitivity to gemcitabine, and heightened liver metastasis. By modulating collagen dynamics and enhancing drug delivery, Tranilast may improve treatment outcomes for patients with low L1CAM-expressing tumors. Understanding the mechanisms by which L1low cells contribute to collagen secretion and tumor aggressiveness is essential for developing effective interventions in pancreatic cancer.

This study provides evidence and explores the biological significance of BET1L, COL17A1, CFAP43, SH3PXD2A, TTC28, ZNRF3, SLK, AKR1C3, NRXN3, and RSPO3 as potential therapeutic targets for meningiomas, providing new insights into the development of targeted therapy for meningiomas.

PLOD3, COL17A1, FN1, and LAMB3 were identified as the key mutated genes in recurrent samples. These findings could provide a new perspective for understanding the tumorigenesis and recurrence mechanisms of ACP. A deeper exploration is needed to determine whether these key mutated genes promote ACP recurrence and drive the overproduction of keratin nodules in recurrent cases.

High-risk patients exhibited elevated tumor mutation burden (TMB), reduced NK/CD8+ T cell infiltration, and resistance to Erlotinib/Oxaliplatin but sensitivity to 5-Fluorouracil. UBASH3B's dual role in immune suppression and drug resistance highlights its potential for stratifying PC patients into tailored treatment groups. The findings underscore the importance of integrating machine learning with immune profiling to advance precision oncology for PC.

Especially CEACAM5, TMPRSS4, and AQP5 were identified as the most promising targets for distinguishing PDAC from healthy tissues and detecting lymph node metastasis during FGS. The development of probes targeting multiple markers, such as AQP5 with CEACAM5 and/or TMPRSS4, may help overcome interpatient variability and enhance detection across patients.

The mean age at diagnosis varied significantly among conditions, reflecting the diagnostic challenges and clinical variability of genodermatoses. This study emphasizes the critical role of WES and CES in diagnosing genodermatoses and understanding their molecular basis, which enhances diagnostic accuracy and supports personalized management strategies.

CAFs-derived COL17A1 promoted GEM resistance and tumorigenesis in PC by interacting with ACTN4, suggesting a new method for overcoming GEM resistance in PC.