gemcitabine

OC patients with low CRS score had a lower half maximal inhibitory concentration value of some drugs (Gemcitabine, Tamoxifen, and Nilotinib, etc) and lower score of some cancer-related hallmarks (Notch signaling, hypoxia, and glycolysis, etc). The current study developed an optimal CRS in OC, which acted as an indicator for the prognosis, stratifying risk and guiding treatment for OC patients.

Notably, PDAC-X2 cells demonstrated resistance to multiple drugs, including gemcitabine, paclitaxel, 5-fluorouracil and oxaliplatin. In conclusion, PDAC-X2 presents an invaluable preclinical model. Its utility lies in facilitating the study of drug resistance mechanisms and the exploration of alternative therapeutic approaches aimed at enhancing the prognosis of this tumour type.

P2, N=40, Recruiting, Sun Yat-Sen Memorial Hospital of Sun Yat-Sen University | Not yet recruiting --> Recruiting

P3, N=448, Recruiting, Mural Oncology, Inc | Active, not recruiting --> Recruiting | Trial completion date: Dec 2026 --> May 2027 | Trial primary completion date: Dec 2025 --> May 2026

The results of this follow-up analysis continue to support the promise of combined gemcitabine/ATRi therapy in platinum resistant ovarian cancer, an active area of investigation with several ongoing clinical trials.

Among the high-risk patients, our study identified 12 candidate drugs and verified gemcitabine as the most significant one that could target our signature and be effective in treating LUAD...According to the findings of this study, the use of mRLncSig has the potential to aid in forecasting the prognosis of LUAD and could serve as a potential target for immunotherapy. Moreover, our signature may assist in identifying targets and therapeutic agents more effectively.

P2/3, N=260, Recruiting, Merck Sharp & Dohme LLC | N=420 --> 260 | Trial completion date: Dec 2025 --> Jun 2027 | Trial primary completion date: Dec 2025 --> Jun 2027

P2, N=71, Recruiting, Memorial Sloan Kettering Cancer Center

P1, N=282, Recruiting, Amgen | Not yet recruiting --> Recruiting

The detection of K17 in 10% or greater of PDAC cells identified patients with shortest survival. Among patients with low K17 PDACs, 5-FU-based treatment was more likely than gemcitabine-based therapies to extend survival.

Tumor-agnostic carrier-cocktails significantly enhance the therapeutic efficacy of existing alpha-particle radionuclide-antibody treatments.

The addition of durvalumab to a gemcitabine plus cisplatin regimen has significantly improved overall survival in the phase 3 TOPAZ-1 trial and is currently recommended as a standard first-line treatment. The phase 3 ABC-06 and phase 2b NIFTY trials have shown the benefit of second-line fluoropyrimidine plus oxaliplatin, and fluoropyrimidine plus nanoliposomal irinotecan, respectively...However, most patients eventually show resistance to the treatment, and tumor progression occurs within a year. Indeed, there should be further efforts to improve the outcomes of patients with advanced IHCCA.

P2, N=71, Active, not recruiting, Do-Youn Oh | Recruiting --> Active, not recruiting | Trial completion date: Nov 2021 --> Dec 2024 | Trial primary completion date: Nov 2021 --> Dec 2024

P1/2, N=80, Recruiting, Prestige Biopharma Limited

P2, N=200, Recruiting, Seoul National University Hospital | Trial completion date: Dec 2024 --> Dec 2025 | Trial primary completion date: Dec 2023 --> Dec 2024

P2, N=33, Not yet recruiting, Francesco De Cobelli

P2, N=393, Active, not recruiting, Astellas Pharma Global Development, Inc. | Recruiting --> Active, not recruiting

P2, N=77, Active, not recruiting, Seoul National University Hospital | Trial completion date: Dec 2024 --> Dec 2025 | Trial primary completion date: Dec 2023 --> Dec 2024

P2, N=31, Active, not recruiting, Seoul National University Hospital | Trial completion date: Dec 2023 --> Dec 2024

The IC50 of cells to gemcitabine was determined using the CCK8 assay...Simultaneously, EGLN2-mediated degradation of HIF-1α was reduced. This ultimately led to elevated HIF-1α-mediated downstream gene expression, promoting increased glucose uptake and glycolysis, and ultimately resulting in heightened chemotherapy resistance and malignancy.

P1, N=60, Recruiting, UroGen Pharma Ltd. | Trial completion date: Dec 2024 --> Dec 2025 | Trial primary completion date: Dec 2024 --> Dec 2025

P1, N=260, Recruiting, ADC Therapeutics S.A. | N=196 --> 260

P1, N=48, Recruiting, Patrick Dillon, MD | Trial completion date: Jan 2025 --> Jan 2026 | Trial primary completion date: Aug 2024 --> Aug 2025

We established MIA-GEM cells, a PDAC cell line resistant to gemcitabine (GEM), a first-line anticancer drug, using the human PDAC cell line-MIA-PaCa-2...Elevated MAST4 expression correlated with a poorer prognosis in PDAC. Consequently, nuclear MAST4 emerges as a potential marker for GEM resistance and poor prognosis, representing a novel therapeutic target for PDAC.

Sensitivity of tumor cells to gemcitabine was evaluated...We concluded that MSLN could induce chemoresistance by enhancing migration, invasion, EMT and cancer stem cell traits of pancreatic cancer cells. Targeting MSLN could represent a promising therapeutic strategy for reversing EMT and chemoresistance in pancreatic cancer cells.

P1/2, N=117, Not yet recruiting, Fudan University

P3, N=263, Not yet recruiting, Boehringer Ingelheim

P3, N=424, Recruiting, Sun Yat-sen University | Not yet recruiting --> Recruiting

P3, N=780, Recruiting, Merck Sharp & Dohme LLC | Not yet recruiting --> Recruiting

P3, N=100, Active, not recruiting, Milton S. Hershey Medical Center | Trial completion date: Apr 2024 --> Dec 2024 | Trial primary completion date: Apr 2024 --> Dec 2024 | Recruiting --> Active, not recruiting

P1, N=500, Recruiting, Shanghai Jiao Tong University School of Medicine | Trial completion date: Dec 2025 --> Dec 2027 | Trial primary completion date: Dec 2024 --> Dec 2026

Immunotumoroid response to ICIs (nivolumab, pembrolizumab, and durvalumab) and chemotherapy (cisplatin, gemcitabine, and paclitaxel) was monitored in real-time with Cytotox Red staining in an Incucyte device, and the immunotumoroid response was compared to retrospective clinical drug responses. This model could enable valuable insights into the complex interactions between cancer cells, the immune system, and the microenvironment. This is a feasibility study on a small number of cases, and additional studies with larger case numbers are required including correlation with clinical response.

P1/2, N=12, Active, not recruiting, National Cancer Institute (NCI) | N=106 --> 12 | Trial completion date: Aug 2024 --> Apr 2025 | Trial primary completion date: Aug 2024 --> Mar 2024

P2/3, N=600, Recruiting, Sutro Biopharma, Inc. | Phase classification: P2 --> P2/3 | N=140 --> 600

P3, N=1, Terminated, Suzhou Suncadia Biopharmaceuticals Co., Ltd. | N=104 --> 1 | Not yet recruiting --> Terminated; Sponsor R & D Strategy Adjustment]

Nucleoside analogs such as gemcitabine (GEM; dFdC) and cytarabine (Ara-C) require nucleoside transporters to enter cells, and deficiency in equilibrative nucleoside transporter 1 (ENT1) can lead to resistance to these drugs. In A549 cells treatment with Ara-C, CP-4055 and EA-4126 decreased the p-P38/P38 after 6 hr. The findings suggest that both parent drugs, prodrugs, and the EA chain influence cell survival and signaling pathways.

We found that Trametinib has a lower IC50 than Gemcitabine in PDAC cell lines. The study shows Trametinib has a critical inhibitory effect on PDAC. Besides, the combination of Trametinib with Palbociclib can inhibit the proliferation of PDAC-resistant cells.

P3, N=186, Recruiting, Genelux Corporation | Trial primary completion date: Aug 2024 --> Aug 2025

P3, N=210, Not yet recruiting, Sun Yat-Sen Memorial Hospital of Sun Yat-Sen University

P2, N=60, Not yet recruiting, Zhejiang Cancer Hospital

P1/2, N=116, Recruiting, Cantargia AB | Phase classification: P1b/2 --> P1/2

PDAC cells were treated with DEX, and the cell proliferation, migration, invasion, and chemosensitivity to gemcitabine (GEM) were evaluated. Our results thus demonstrated that DEX treatment changed PDAC cells' functions, resulting in decreased cell proliferation, increased cell migration and invasion, and decreased sensitivity to GEM. The molecular mechanisms of these changes involve ECM1 and KRT6A, whose expressions are induced by DEX.