KRT17 (Keratin 17)

Our study uncovers layer-specific molecular landscapes in tongue OLP and identifies KRT17 as a candidate implicated in immune-epithelial crosstalk, providing novel insights into pathogenesis and a potential direction for future therapeutic exploration.

Our study demonstrates that KRT17 marks a distinct transcriptional signature in a subpopulation of epithelial cells within histologically low-grade IPMN. This population of cells likely represents a transitional state of histologically low-grade epithelial cells undergoing progression to a higher grade of dysplasia and thus may represent a higher risk of progression to carcinoma.

CDKN2A and PCTH1 mutations, frequently detected in melanoma and basal cell carcinoma, respectively, were detected in the second case. The presence of 2 components with distinct immunoprofile yet with some common genetic aberration suggests that basomelanocytic tumors may arise from a common progenitor.

To study resistance mechanisms, we developed the organoid drug resistance assay (ODR-test) with patient-derived organoids from our ovarian cancer biobank and identified sustained phenotypic reprogramming and cellular plasticity of organoids under carboplatin pressure as a conserved mechanism irrespective of the basal resistance level. Additionally, we found that KRT17 expression status (K-score) is a significant negative prognostic histopathological biomarker in a large cohort (N = 384) of patients with advanced HGSOC. In organoids, increased KRT17 levels enhanced sensitivity to PI3K/Akt inhibitors alpelisib and afuresertib, highlighting the potential of KRT17 as a stratification biomarker for targeted therapies.

Focusing on TCP1, a chaperonin subunit upregulated in high-risk tumors, we demonstrate that TCP1 knockdown in breast cancer cell lines substantially impairs cell migration (~50% reduction in wound closure) and invasion (P < 0.01). These findings reveal functionally distinct malignant cell states within breast cancer and identify TCP1 as a promising therapeutic target to disrupt aggressive, stem-like tumor cell programs, ultimately guiding more personalized treatment strategies.

UPK2 marks a distinct subset of CRCs with poor prognosis, epithelial-mesenchymal transition, micropapillary growth, and squamous differentiation. These findings may affect the development of targeted therapies in precision medicine.

Given its cancer-specific overexpression, multifaceted role in malignancy (including resistance), and promising preclinical evidence that targeting KRT17 can reverse resistance, KRT17 emerges as a significant diagnostic/prognostic biomarker and a compelling therapeutic target. This review critically synthesizes evidence for KRT17's role in drug resistance and evaluates its potential for overcoming this major barrier to successful cancer treatment.

In the seven illustrative cases presented, URO17® aided clinical decision-making as part of routine diagnostic and surveillance workflows. The test's integration with existing cytology processes supports its potential role as a noninvasive adjunct for evaluating patients with suspected or recurrent urothelial carcinoma.

In conclusion, m6A RNA modification may contribute to SKCM metastasis by regulating the expression of CDH3, KRT17, PKP1 and CRABP2, as well as modulating the tumor immune microenvironment. These findings offer novel insights into the metastatic mechanisms of SKCM and identify potential biomarkers for its diagnosis, prognosis and targeted immunotherapy.

We also found that MmuPV1 E7 potentiates this signaling through increased sensitivity to epidermal growth factor stimulation. Our collective data show that MmuPV1 E7 promotes several phenotypes associated with "high-risk" HPV infection and cancers.

Consistently, immunofluorescence analysis of pyruvate carboxylase (PC), keratin 17 (KRT17), and KMT5C substantiated distinct expression patterns in tumor boundary and center lesions. This study initially presents the spatial proteomic heterogeneity landscape in RB with ONI and uncovers its molecular reprogramming.