ReviewClinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico2026
Unravelling the pathogenesis and therapeutic approaches of pancreatic ductal adenocarcinoma.
Review in Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Fatty acids metabolic reprogramming and tumor microenvironment in pancreatic cancer: targeting pathways.Clinical and experimental medicine · 2026Review
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pancreatic ductal adenocarcinoma (PDAC) is one of the aggressive cancers having high metastasis, late progression and resistance to therapies. PDAC arises from the ductal epithelium of the pancreas. The tumour microenvironment plays a key role in metastasis. One of the reasons behind PDAC being so aggressive as a cancer is that it forms a dense stroma around the neoplastic epithelium, which contributes to further tumour progression, invasion, metastasis and drug resistance. The key components of PDAC include the extracellular matrix (ECM), cancer-associated fibroblasts (CAFs) and vasculature. The dense stroma in the ECM prevents drug penetration into cancer cells, making PDAC more challenging to treat. The oncogenic KRAS mutation is mainly responsible for the initiation, progression, immune evasion and further therapy resistance in this cancer. Despite having a low rate of survival, therapies available for this cancer are now emerging and developing rapidly. There are many more therapies now available for the treatment of PDAC, including immunotherapies, targeted gene therapies, stroma-targeting therapies and novel chemotherapies, which are much more promising in this cancer. This article focuses on the pathogenesis of PDAC and the various recent therapies used to treat it. It further discusses future perspectives in the treatment of this cancer, AI-driven therapies and challenges in this field.
Indexed as
Identifiers
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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.