ArticleJournal of cancer science and clinical therapeutics2022
A new era: tumor microenvironment in chemoresistance of pancreatic cancer.
Article in Journal of cancer science and clinical therapeutics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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.
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Who cites it
5 citing papers in PubMed, 9 citations in OpenAlex.
- Immune-driven stromal inflammation in pancreatic cancer within a microfluidic platform.Biofabrication · 2026Article
- Mitochondria-targeted metformin analogs activate the ER stress-unfolded protein response pathway to drive apoptosis in pancreatic cancer.Cell death & disease · 2026Article
- Ferroptosis-Based Nanotherapy for Pancreatic Ductal Adenocarcinoma Through Glutathione Depletion and Iron Accumulation.International journal of nanomedicine · 2026Review
- The xenobiotic transporterFrontiers in pharmacology · 2024Article
- The Role of Adipokines in Pancreatic Cancer.Frontiers in oncology · 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
3 authors at 2 institutions in 1 country.
Funding
Abstract
Pancreatic ductal adenocarcinoma (PDAC) is a solid malignant tumor with an extremely poor prognosis. Gemcitabine (GEM)-based chemotherapy remains one of the most important treatment choices for PDAC. However, either as monotherapy or as a part of the combination chemotherapy, GEM achieved only limited success in improving the survival of patients with advanced PDAC, primarily due to GEM resistance. PDAC is characterized by an extensive desmoplasia in the tumor microenvironment (TME). Increasing evidence indicates that this fibrotic TME not only actively participates in the tumor growth and spread of PDAC but also contributes to the induction of GEM resistance. Here we review the current advances of how TME components are involved in the induction of GEM resistance.
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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.