ReviewCancer drug resistance (Alhambra, Calif.)2022
Targeting the complement system in pancreatic cancer drug resistance: a novel therapeutic approach.
Review in Cancer drug resistance (Alhambra, Calif.), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
17 citing papers in PubMed, 19 citations in OpenAlex.
- Proteomic Profiling of Extracellular Vesicle-Enriched Plasma Using Mag-Net for Biomarker Discovery in Pancreatic Ductal Adenocarcinoma.Journal of proteome research · 2026Article
- Recent advances and treatment strategies in liver metastasis of pancreatic neuroendocrine tumors.Cancer metastasis reviews · 2025Review
- Article
- Biodistribution of a Mucin 4-Selective Monoclonal Antibody: Defining a Potential Therapeutic Agent Against Pancreatic Cancer.International journal of molecular sciences · 2025Article
- Hypoxia Induces Extensive Protein and Proteolytic Remodeling of the Cell Surface in Pancreatic Adenocarcinoma (PDAC) Cell Lines.Journal of proteome research · 2025Article
- UPP1 and AHSA1 as emerging biomarkers and targets in pancreatic cancer: A proteomic approach.Biomolecules & biomedicine · 2025Article
- The multiverse of CD46 and oncologic interactions.The Journal of clinical investigation · 2025Review
- Improving drug repositioning with negative data labeling using large language models.Journal of cheminformatics · 2025Article
- Targeting Triple NK Cell Suppression Mechanisms: A Comprehensive Review of Biomarkers in Pancreatic Cancer Therapy.International journal of molecular sciences · 2025Review
- The complement C3a/C3aR pathway is associated with treatment resistance to gemcitabine-based neoadjuvant therapy in pancreatic cancer.Computational and structural biotechnology journal · 2024Article
- Innate and adaptive immune-directed tumour microenvironment in pancreatic ductal adenocarcinoma.Frontiers in immunology · 2024Review
- Revolutionizing Cancer Treatment: Unveiling New Frontiers by Targeting the (Un)Usual Suspects.Cancers · 2023Article
- Fluorinated andPharmaceutics · 2023Article
- Chronic effects of pulsed high intensity focused ultrasound aided delivery of gemcitabine in a mouse model of pancreatic cancer.Ultrasonics · 2023Article
- The immune response to a fungus in pancreatic cancer samples.bioRxiv : the preprint server for biology · 2023Article
- The inflammatory response of human pancreatic cancer samples compared to normal controls.PloS one · 2023Article
- Complement and Fungal Dysbiosis as Prognostic Markers and Potential Targets in PDAC Treatment.Current oncology (Toronto, Ont.) · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pancreatic cancer is ranked as the fourth leading cause of cancer-related mortality and is predicted to become the second leading cause of cancer-related death by 2030. The cause of this high mortality rate is due to pancreatic ductal adenocarcinoma's rapid progression and metastasis, and development of drug resistance. Today, cancer immunotherapy is becoming a strong candidate to not only treat various cancers but also to combat against chemoresistance. Studies have suggested that complement system pathways play an important role in cancer progression and chemoresistance, especially in pancreatic cancer. A recent report also suggested that several signaling pathways play an important role in causing chemoresistance in pancreatic cancer, major ones including nuclear factor kappa B, signal transducer and activator of transcription 3, c-mesenchymal-epithelial transition factor, and phosphoinositide-3-kinase/protein kinase B. In addition, it has also been proven that the complement system has a very active role in establishing the tumor microenvironment, which would aid in promoting tumorigenesis, progression, metastasis, and recurrence. Interestingly, it has been shown that the downstream products of the complement system directly upregulate inflammatory mediators, which in turn activate these chemo-resistant pathways. Therefore, targeting complement pathways could be an innovative approach to combat against pancreatic cancer drugs resistance. In this review, we have discussed the role of complement system pathways in pancreatic cancer drug resistance and a special focus on the complement as a therapeutic target in pancreatic cancer.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.