ReviewDiscover oncology2025
Mechanistic insights and therapeutic strategies for targeting autophagy in pancreatic ductal adenocarcinoma.
Review in Discover oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
7 citing papers in PubMed.
- Dual targeting of SLC6A14 and autophagy/macropinocytosis enhances therapeutic efficacy in pancreatic ductal adenocarcinoma.The Biochemical journal · 2026Article
- CREB-SEC61G feedback loop sustains enhanced autophagy and boosts proliferation in PDAC.Cell death & disease · 2026Article
- Cytoskeleton reorganization induced by a novel K6-K14 keratin fusion promotes cancer stemness and cellular plasticity via cGAS-STING selection.Oncogenesis · 2026Article
- Tumor Microenvironment: Insights from Multiparametric MRI in Pancreatic Ductal Adenocarcinoma.Cancers · 2026Article
- Demystifying anti-inflammatory therapeutic strategies against pancreatitis and concomitant diseases: a 2025 perspective.Theranostics · 2026Review
- Increasing autophagy activity suppressesAmerican journal of cancer research · 2026Article
- Calliviminone A fromPlants (Basel, Switzerland) · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
Pancreatic ductal adenocarcinoma (PDAC) is characterised by early metastasis and resistance to anti-cancer therapy, leading to an overall poor prognosis. Macroautophagy (hereinafter referred to as autophagy) is a conserved cellular homeostasis mechanism that degrades various cargoes (e.g., proteins, organelles, and pathogens) mainly playing a role in promoting survival under environmental stress. Autophagy is an essential defense mechanism against PDAC initiation, acting on multiple levels to maintain cellular and tissue homeostasis. However, autophagy is also intimately involved in the molecular mechanisms driving PDAC progression, facilitating the adaptation of cancer cells to the tumor microenvironment's harsh conditions. In this review, we examine the complex role of autophagy in PDAC and assess the potential of modulating autophagy as a therapeutic strategy. By reviewing current research and clinical trials, we seek to elucidate how targeting autophagy can disrupt PDAC tumor survival mechanisms, enhance the efficacy of existing treatments, and ultimately improve patient outcomes.
Indexed as
Identifiers
What Socratic holds
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 Socratic graph.