gemcitabine

P1, N=260, Active, not recruiting, ADC Therapeutics S.A. | Recruiting --> Active, not recruiting

The expression of chemoresistance genes has been detected, including KLF4 (doxorubicin and ifosfamide), ULK1, LUM, GPNMB, and CAVIN1 (doxorubicin), and AHNAK2 (gemcitabine) in tumor cells and ETS1 (gemcitabine) in TME. This study provides the first description of the single-cell transcriptome of UPS with resistance to two lines of chemotherapy, showcasing the gene expression in subpopulations of tumor cells and TME, which may be potential markers for personalized cancer therapy.

Additionally, only pathological Pn-ASVs interacted with heat shock protein 70-1a (HSP70-1a), leading to significant rescue of gemcitabine-induced PDAC apoptosis. In silico analysis revealed that the presence or absence of exon 21 changes the tertiary structure of Pn and the binding sites for HSP70-1a. Altogether, Pn-ASVs with exon 21 secreted from CAFs play a key role in supporting tumor growth by interacting with cancer cell-derived HSP70-1a, indicating that Pn-ASVs with exon 21 might be a potential therapeutic and diagnostic target in PDAC patients with rich stroma.

SIRT1 influences apoptosis and chemoresistance through hypoxia, enhancing glycolytic metabolism and HIF-1α signaling, which sustain tumor survival against drugs like gemcitabine...This review meticulously explores the nuanced involvement of sirtuins in pancreatic cancer, elucidating their contributions to tumorigenesis and suppression through mechanisms such as metabolic reprogramming, the maintenance of genomic integrity and epigenetic modulation. Furthermore, it emphasizes the urgent need for the development of targeted therapeutic interventions aimed at precisely modulating sirtuin activity, thereby enhancing therapeutic efficacy and optimizing patient outcomes in the context of pancreatic malignancies.

IHC stratification of primary tumors by HMGA2 and GATA6 status in pancreatic cancer is associated with differential outcomes, survival following chemotherapy, and tumor microenvironments. As a nuclear marker for basal disease, HMGA2 complements GATA6 to identify disease subtypes in PDAC.

We found that UMKO1 possesses a gene for the long form of cytidine deaminase, which can inactivate the standard PDAC chemotherapeutic agent gemcitabine...We found that while none of the bacterial supernatants changed the abundance of CD8 T cells, granzyme B positive CD8 T cells were the lowest in tumor explants exposed to UMKO1 , and not other isolated Klebsiella species or the non-pathogenic laboratory strain E. coli K12 . In summary, the isolated collection of bacteria and fungi from this study are a valuable toolbox to study the impact of microbiota on pancreatic cancer.

In conclusion, POU4F1 upregulation promoted GEM resistance in lung cancer cells by promoting autophagy through increasing METTL3-mediated TWF1 m6A modification. The online version contains supplementary material available at 10.1007/s13205-024-04161-w.

P2, N=78, Recruiting, Akeso | Not yet recruiting --> Recruiting | N=60 --> 78 | Trial completion date: Jun 2025 --> Dec 2025 | Trial primary completion date: Dec 2024 --> Jun 2025

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

P1/2, N=30, Not yet recruiting, Lisata Therapeutics, Inc. | Trial completion date: Jun 2027 --> Sep 2027 | Initiation date: Dec 2024 --> Mar 2025 | Trial primary completion date: Jun 2027 --> Sep 2027

The ability of MLTS to predict patient outcomes and its association with key genomic and cellular features underscore its potential as a target for personalized therapy. Future research may focus on integrating MLTS with additional molecular signatures to enhance its clinical application in precision oncology.

Two hundred sixty-six patients were randomly assigned 2:1 to olaparib tablets (300 mg twice daily; n = 178) or physician's choice of single-agent nonplatinum chemotherapy (pegylated liposomal doxorubicin, paclitaxel, gemcitabine, or topotecan; n = 88). BRCA reversion mutations might have contributed to this finding. No patient randomly assigned to olaparib with a BRCA reversion mutation detected at baseline (6 of 170 [3.5%]) achieved an objective tumor response.

P1, N=230, Active, not recruiting, Merck Sharp & Dohme LLC | Trial completion date: Feb 2025 --> Jun 2025 | Trial primary completion date: Feb 2025 --> Jun 2025

P3, N=254, Active, not recruiting, Sichuan Kelun Pharmaceutical Research Institute Co., Ltd. | Trial completion date: Dec 2024 --> Mar 2025

P1/2, N=543, Active, not recruiting, Genmab | Recruiting --> Active, not recruiting

P1, N=4, Recruiting, Roberto Vargas | Trial completion date: Jun 2025 --> Dec 2025 | Trial primary completion date: Dec 2024 --> Jun 2025

P2, N=401, Active, not recruiting, AstraZeneca | Trial completion date: Sep 2024 --> Sep 2025

Our case report strengthens the evidence that crizotinib may be a viable treatment option for patients with ICC with a c-MET tyrosine kinase fusion, necessitating additional clinical investigation.

Concurrently, drug sensitivity analyses demonstrated that high KCNA1 expression promoted gemcitabine resistance in patients, while KCNA1 knockdown increased sensitivity to gemcitabine. In conclusion, we developed a novel UPS-based prognostic model for THCA, identified key gene KCNA1, and assessed immunotherapy and drug sensitivity, revealing new therapeutic targets.

P2, N=0, Withdrawn, Sun Yat-sen University | N=37 --> 0 | Recruiting --> Withdrawn

P2, N=35, Completed, HonorHealth Research Institute | Active, not recruiting --> Completed | N=10 --> 35 | Trial completion date: Dec 2023 --> Mar 2024

P1, N=101, Recruiting, Institut Curie | Trial completion date: Dec 2024 --> Dec 2025 | Trial primary completion date: Dec 2024 --> Jul 2025

P2, N=57, Recruiting, Zhejiang Provincial People's Hospital

A tendence toward a better OS was found for BRCAness patients which did not reach the statistical significance. On the other hand, BRCAness patients showed significantly higher PFS compared to no BRCAness patients This real-world analysis largely confirmed the TOPAZ-1 findings, supporting gemcitabine, cisplatin, and durvalumab as a first-line standard of care for patients with advanced BTC.

The patient was treated with pemigatinib (a selective FGFR inhibitor) in combination with Gemcitabine and Cisplatin at our hospital. To the best of our knowledge, this is the first reported rare case of unresectable cHCC-CCA with FGFR2-PRDM16 fusion in a child successfully treated with a combination of pemigatinib and chemotherapy as a first-line regimen. This treatment combination may be effective and safe for patients with unresectable cHCC-CCAs.

Patients with LAPCCA frequently tolerate induction gemcitabine-cisplatin, leading to a 26% resection rate with 40 months overall survival. These findings support routine re-staging after three to six cycles of palliative treatment, and lay the groundwork for future prospective trials in this patient group.

Furthermore, Mn (II) activates the cGAS-STING pathway, increasing susceptibility to ROS-induced DNA double-strand breaks, promoting macrophage maturation, inhibiting M2 polarization, and enhancing the cytotoxic function of T lymphocytes against tumor cells. In summary, this combination of chemotherapy and immunotherapy presents a promising strategy for the treatment of breast cancer.

P=N/A, N=27, Not yet recruiting, University of Saskatchewan | Trial completion date: Mar 2026 --> Dec 2026 | Trial primary completion date: Mar 2026 --> Dec 2026

P2, N=70, Recruiting, Tianjin Medical University Cancer Institute and Hospital

We reviewed cfDNA results from a local prospective solid tumour cohort (PREDiCT-l) and two randomized trials: CCTG CO.26 (durvalumab + tremelimumab [D+T] or best supportive care in metastatic colorectal cancer) and CCTG PA.7 (gemcitabine and nab-paclitaxel +/- D+T in metastatic pancreatic adenocarcinoma). CHIP is common in patients with solid tumours. Although not appearing to impact rates of adverse events, CHIP may impact outcomes from immunotherapy or chemotherapy.

Conversely, decreased apoptosis and gemcitabine sensitivity along with accelerated cell proliferation ability were observed in PSMD2-overexpressing PANC-1 cells...Importantly, MK-2206 largely reversed the oncogenic functions of PSMD2 on the growth and proliferation of PANC-1 cells...We identified that PSMD2 acted as a tumor-promoting protein in pancreatic cancer through the activation of the AKT/mTOR pathway. The overexpression of PSMD2 may be a potential biomarker that predicts the response of pancreatic cancer patients to AKT inhibitor treatments.

However, the GX regimen should be considered in patients who cannot tolerate hematological toxicity. ClinicalTrials.gov identifier: NCT02207335.

Hormonal or endocrine therapy includes selective estrogen receptor modulators (SERMs) such as raloxifene, tamoxifen and toremifene, selective estrogen-receptor degraders (SERDs) including elacestrant and fulvestrant, and aromatase inhibitors such as anastrozole, letrozole, and exemestane...These agents include taxanes (docetaxel, nab-paclitaxel, and paclitaxel), anthracyclines (doxorubicin, epirubicin), anti-metabolites (capecitabine, gemcitabine, fluorouracil, methotrexate), alkylating agents (carboplatin, cisplatin, and cyclophosphamide), and drugs that target microtubules (eribulin, ixabepilone, ado-trastuzumab emtansine). Patients with ER-positive tumors are treated with 5-10 years of endocrine therapy and chemotherapy. For patients with metastatic breast cancer, standard first-line and follow-up therapy options include targeted approaches such as CDK4/6 inhibitors, PI3K inhibitors, PARP inhibitors, and anti-PDL1 immunotherapy, depending on the tumor type and molecular profile.

P2/3, N=60, Not yet recruiting, SUNHO（China）BioPharmaceutical CO., Ltd.

P3, N=537, Active, not recruiting, Children's Oncology Group | Trial completion date: Jun 2026 --> Dec 2026 | Trial primary completion date: Jun 2026 --> Dec 2026

P2, N=46, Recruiting, Wake Forest University Health Sciences | Suspended --> Recruiting

P=N/A, N=300, Recruiting, Second Affiliated Hospital, School of Medicine, Zhejiang University

P2, N=20, Recruiting, ImmunityBio, Inc. | Not yet recruiting --> Recruiting

P2, N=30, Recruiting, Tianjin Medical University Cancer Institute and Hospital | Not yet recruiting --> Recruiting

P2, N=41, Recruiting, Zhujiang Hospital | Trial completion date: Apr 2025 --> Apr 2027 | Trial primary completion date: Oct 2023 --> Oct 2026

P1/2, N=30, Recruiting, Lisata Therapeutics, Inc. | Not yet recruiting --> Recruiting

P2, N=194, Active, not recruiting, Trishula Therapeutics, Inc. | Recruiting --> Active, not recruiting