Cholangiocarcinoma

P2, N=40, Recruiting, Institut für Klinische Krebsforschung IKF GmbH at Krankenhaus Nordwest

We report a case illustrating how the investigation of a proliferation of double-negative αβ T lymphocytes led to the diagnosis of cholangiocarcinoma. Although a direct link between the two cannot be proven, we hypothesize that tumor antigenic stimulation selected a T lymphocyte clone.

Our in vivo data demonstrate that SLU7 is a promising, versatile target for possibly diverse cancers. Its multimodal mechanism offers potential to overcome tumor heterogeneity, reverse immune tolerance, and enhance immunotherapy efficacy.

SDHB positivity may indicate favorable tumor biology, but further studies are needed to validate its prognostic value. Surgical resection remains curative for localized PHL.

Prior molecular studies have focused mainly on the DNAJB1-PRKACA fusion gene, which is pathognomonic for FLC, but no reliable circulating biomarker has been established for FLC diagnosis or disease monitoring...Routine measurement of serum PCT could facilitate earlier recognition of FLC and also provide a non-invasive tool to track treatment response. Future research should validate these findings prospectively, explore the biological mechanisms underlying CALCA overexpression in FLC, and assess whether PCT-guided monitoring can predict prognosis, improve patient outcomes or clinical trial design in this rare malignancy.

Consistently, expression of IL-15 resulted in blockade of tumor progression in the TKP CCA model. These findings highlight the importance of oncogenic Kras in CCA tumor maintenance and underscore KRAS inhibition as a potential therapeutic approach for CCA.

UESL should be included in the differential diagnosis of atypical liver masses, even in elderly patients. Early surgical resection offers the best chance for survival, though outcomes remain dismal in advanced age due to rapid recurrence and metastasis. Heightened awareness of this entity is crucial to mitigate diagnostic delays.

Increased stiffness promotes chemoresistance, with gemcitabine IC50 rising from 0.139 to 0.282 µm and cisplatin from 2.49 to 4.23 µm, alongside epithelial-mesenchymal transition (EMT), as evidenced by a 64% reduction in E-cadherin and a 6.35 fold increase in MMP2 expression. These changes contribute to a pre-metastatic niche, as confirmed by a 4.11 fold increase in invasive cell counts in PET membrane invasion assays. This dynamic stiffness-tunable platform provides a robust in vitro model for studying stiffness-driven invasion and pre-metastatic niche formation in ICC and offers a valuable tool for personalized screening of anti-fibrotic and chemosensitizing therapies.

These effects were mediated by EMT phenotype switching through the activation of the Jag2/Notch1/Hes5 pathway. Our findings enhance the understanding of the novel mechanisms driving ICC progression and metastasis, suggesting that SVEP1 is a potential biomarker for ICC diagnosis.

Together, these data identify FXR as an immune checkpoint and support repurposing UDCA for ICC immunotherapy.