Gallbladder Cancer

Collectively, our results suggest that KLF5 regulates GBC cell proliferation, invasion, migration, angiogenesis, as well as apoptosis, via mediating PDGFA transcriptionally, which might provide a novel therapeutic strategy for treatment of human GBC.

P2, N=27, Active, not recruiting, Abramson Cancer Center at Penn Medicine | Trial completion date: Dec 2024 --> Dec 2026 | Trial primary completion date: Dec 2024 --> Dec 2026

P2, N=14, Active, not recruiting, Georgetown University | Trial completion date: Dec 2023 --> Dec 2024

P2, N=80, Recruiting, Lisata Therapeutics, Inc. | Trial completion date: Dec 2025 --> Mar 2026 | Trial primary completion date: Dec 2025 --> Mar 2026

P=N/A, N=261, Completed, University of Pittsburgh | Phase classification: P3 --> P=N/A

The adverse impact of KRAS mutations in BTC is driven by G12 alterations in patients with IHC regardless of resection status, which was not observed in GB or EHC. There are unique comutational partners in distinct BTC subsets. These differences have important clinical implications in the era of KRAS-targeted therapeutics.

Tissue validation showed bile 5,6-DHET positively correlated with tissue PCNA (proliferation), and caspase-3 linked to cancer development (r 2 >0.5, p < 0.05). In conclusion, the bile molecular landscape provides critical molecular understanding and outlines metabolomic indicator panels for early CAGB detection.

P2, N=100, Active, not recruiting, Boehringer Ingelheim | Recruiting --> Active, not recruiting

P2, N=110, Active, not recruiting, Tianjin Medical University Cancer Institute and Hospital

P=N/A, N=400, Recruiting, RenJi Hospital

Gallbladder follicular lymphoma is difficult to diagnose preoperatively, however, extra-regional lymph node swelling and relatively low apparent diffusion coefficients on magnetic resonance imaging can help its diagnosis.

P=N/A, N=30000, Active, not recruiting, University of Edinburgh | Trial completion date: Nov 2024 --> Jan 2025

EGFR and SMAD4 expression were found to be negatively correlated in GBC tissue samples. ERBB2 overexpression/amplification was observed in 30% of the GBC samples. We also found a low percentage of GBC samples to show KRAS codon 12 mutation in Indian GBC patient population, as had been previously documented in pancreatic cancers.

P3, N=114, Not yet recruiting, Rajiv Gandhi Cancer Institute & Research Center, India

The present review focuses on the latest progress regarding the role and mechanism of the cGAS/STING pathway in gastrointestinal cancer, and discusses treatment approaches and related applications based on the cGAS/STING signaling pathway. In order to improve the knowledge of the connection between the cGAS/STING pathway and gastrointestinal cancer, aid the diagnosis and treatment of gastrointestinal cancer, and lessen the burden on patients and society, the present review also discusses future research directions and existing challenges regarding cGAS/STING in the study of gastrointestinal cancer.

This case also demonstrates that benign conditions such as biliary obstruction, chronic inflammation, and xanthogranulomatous cholecystitis can cause significant elevations in CA19-9 levels. Therefore, careful differentiation and comprehensive evaluation are crucial for accurate diagnosis and appropriate management in such cases.

P3, N=452, Active, not recruiting, SWOG Cancer Research Network | Trial completion date: Oct 2024 --> Mar 2025

P1/2, N=40, Not yet recruiting, Mayo Clinic

Our study highlights the advantage of integrating small-RNA sequencing results from different types of samples and independent datasets, and the need for international research collaborations to identify and validate biomarkers for secondary prevention of rare tumours such as GBC. The function of miR-4533 and its interaction with SIPA1L2 in GBC development need to be further investigated.

Inhibition of LGALS1 reduced tumor growth and Treg prevalence in ICC mouse models. Overall, this study unveils T cell diversity across BTC subtypes at the single-cell and spatial level that could open paths for tailored immunotherapies.

There are currently very few reports related to this tumor worldwide, and protocols for diagnosis and treatment are limited. Therefore, we collected and analyzed clinical data from this patient, along with relevant literature, to create a comprehensive summary.

External validation using The Cancer Genome Atlas (TCGA) databases confirmed the expression of candidate genes, underscoring their potential as therapeutic targets. These findings provide valuable insights into the molecular heterogeneity and complexity of HBCs, opening new avenues for personalized therapeutic interventions.

This report supports the clinical benefit of anti-EGFR antibodies for EGFR-amplified biliary tract cancers and the importance of genomic analysis in personalized therapy and drug resistance research.

P1/2, N=101, Recruiting, National Cancer Institute (NCI) | Trial completion date: Dec 2024 --> Dec 2025 | Trial primary completion date: Dec 2024 --> Dec 2025

P2, N=603, Completed, Merck Sharp & Dohme LLC | Active, not recruiting --> Completed

P1, N=572, Recruiting, Seagen Inc. | N=430 --> 572 | Trial completion date: Jan 2027 --> Nov 2027 | Trial primary completion date: Jun 2025 --> Nov 2027

P3, N=68, Completed, Krankenhaus Nordwest | Recruiting --> Completed | N=300 --> 68

P=N/A, N=600, Completed, Shanghai Eastern Hepatobiliary Surgery Hospital; Shanghai Eastern Hepatobiliary Surgery Hospital

P=N/A, N=0, Recruiting, Affiliated Hospital of North Sichuan Medical College; Affiliated Hospital of North Sichuan Medical College

P=N/A, N=60, Not yet recruiting, Fifth Affiliated Hospital, Sun Yat-Sen University; Fifth Affiliated Hospital, Sun Yat-Sen University

P2, N=54, Not yet recruiting, The second hospital of Lanzhou University; The second hospital of Lanzhou University

P2, N=38, Not yet recruiting, Shanghai Eastern Hepatobiliary Surgery Hospital; Shanghai Eastern Hepatobiliary Surgery Hospital

P2, N=27, Not yet recruiting, West China Hospital of Sichuan University; West China Hospital of Sichuan University

They also confirmed that all the BCL-2 stained slides (with the exception of one reactive case) were negative for BCL-2 immunohistochemical stain. BCL-2 immunohistochemical stain is not a promising marker in the differentiation between reactive epithelium and dysplasia/carcinoma in the gallbladder.

Through the dynamical study of the model and its response to different perturbations, we report novel triple node combinations that can be targeted to efficiently reduce GBC growth. This network can be used as a generalized framework to investigate different crosstalk pathways linked with cancer progression.

Furthermore, SOX9/TCF7L2 double-high GBC preclinical models are found to be susceptible to SE-targeted CDK7 inhibition therapy in vitro and in vivo. Together, this study provides novel insights into the epigenetic mechanisms underlying the oncogenesis of a subset of GBCs with poorer prognosis and illustrates promising prognostic stratification and therapeutic strategies for treating those GBC patients in future clinical trials.

P3, N=148, Enrolling by invitation, Erasmus Medical Center

The present study revealed that TRIM47 contributes to the progression of GBC and is therefore an important biomarker for predicting the prognosis of GBC and for therapeutic intervention.

In conclusion, NSAID users were less likely to have gallbladder dysplasia, suggesting that NSAIDs might be beneficial for symptomatic gallstones patients. The inverse association between immune-related markers and dysplasia requires additional research, ideally in prospective studies with asymptomatic participants, to understand the role of the inflammatory response in the natural history of GBC and to address the biological effect of NSAIDs.

Upon reevaluation, the primary resected specimen was found to include approximately 10% of neuroendocrine tumor components. This case suggests that different FDG uptake between primary and metastatic cancer may necessitate differential diagnosis.

P=N/A, N=360, Recruiting, Cedars-Sinai Medical Center | Trial primary completion date: Jun 2025 --> Jan 2026

ERK and AKT signaling and their downstream target genes were regulated by CEACAM6 and thus the treatment with AKT inhibitor capivasertib or ERK inhibitor ulixertinib mitigated the CEACAM6-induced migration. These findings demonstrate that CEACAM6 is crucially involved in gallbladder cancer progression by promoting migration and inhibiting cell adhesion through ERK and AKT signaling providing specific options for treatment of CEACAM6-positive cancers.