ReviewCancers2020
Molecular Bases of Mechanisms Accounting for Drug Resistance in Gastric Adenocarcinoma.
Review in Cancers, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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
31 citing papers in PubMed, 60 citations in OpenAlex.
- Mechanisms of chemoresistance in gastric cancer: interplay between microRNAs and the tumor microenvironment.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Review
- Ferroptosis as a Therapeutic Vulnerability to Overcome Chemoresistance in Gastric Cancer.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Linolenic Acid Inhibits Cancer Stemness and Induces Apoptosis by Regulating Nrf2 Expression in Gastric Cancer Cells.Current issues in molecular biology · 2025Article
- Prediction of Patient Drug Response via 3D Bioprinted Gastric Cancer Model Utilized Patient-Derived Tissue Laden Tissue-Specific Bioink.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Carbon-ion radiotherapy induces ferroptosis and M1 macrophage polarization to inhibit the development of gastric cancer by downregulating DHODH.Frontiers in medicine · 2025Article
- Preclinical evaluation of fenretinide against primary and metastatic intestinal type‑gastric cancer.Oncology letters · 2024Article
- PPIC-labeled CAFs: Key players in neoadjuvant chemotherapy resistance for gastric cancer.Translational oncology · 2024Article
- Emerging roles of circular RNAs in tumorigenesis, progression, and treatment of gastric cancer.Journal of translational medicine · 2024Review
- The ceramide synthase (CERS/LASS) family: Functions involved in cancer progression.Cellular oncology (Dordrecht, Netherlands) · 2023Review
- The critical role of circular RNAs in drug resistance in gastrointestinal cancers.Medical oncology (Northwood, London, England) · 2023Review
- Article
- Evaluation of Drug Resistance in the Tamoxifen-treated MKN-45 Gastric Cancer Cell Line via the Epithelial-mesenchymal Transition Signaling Pathway.International journal of molecular and cellular medicine · 2023Article
- The hypoxia-inducible factor-1α in stemness and resistance to chemotherapy in gastric cancer: Future directions for therapeutic targeting.Frontiers in cell and developmental biology · 2023Review
- Silence of URI in gastric cancer cells promotes cisplatin-induced DNA damage and apoptosis.American journal of cancer research · 2023Article
- IL-15 armoring enhances the antitumor efficacy of claudin 18.2-targeting CAR-T cells in syngeneic mouse tumor models.Frontiers in immunology · 2023Article
- Eriodictyol Suppresses Gastric Cancer Cells via Inhibition of PI3K/AKT Pathway.Pharmaceuticals (Basel, Switzerland) · 2022Article
- Identification of 8-gene risk prediction signature associated withJournal of gastrointestinal oncology · 2022Article
- Expression of Chemoresistance-Associated ABC Proteins in Hepatobiliary, Pancreatic and Gastrointestinal Cancers.Cancers · 2022Review
- Article
- Copy number alterations and epithelial‑mesenchymal transition genes in diffuse and intestinal gastric cancers in Mexican patients.Molecular medicine reports · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 1 institution in 1 country.
Funding
Abstract
Gastric adenocarcinoma (GAC) is the most common histological type of gastric cancer, the fifth according to the frequency and the third among the deadliest cancers. GAC high mortality is due to a combination of factors, such as silent evolution, late clinical presentation, underlying genetic heterogeneity, and effective mechanisms of chemoresistance (MOCs) that make the available antitumor drugs scarcely useful. MOCs include reduced drug uptake (MOC-1a), enhanced drug efflux (MOC-1b), low proportion of active agents in tumor cells due to impaired pro-drug activation or active drug inactivation (MOC-2), changes in molecular targets sensitive to anticancer drugs (MOC-3), enhanced ability of cancer cells to repair drug-induced DNA damage (MOC-4), decreased function of pro-apoptotic factors versus up-regulation of anti-apoptotic genes (MOC-5), changes in tumor cell microenvironment altering the response to anticancer agents (MOC-6), and phenotypic transformations, including epithelial-mesenchymal transition (EMT) and the appearance of stemness characteristics (MOC-7). This review summarizes updated information regarding the molecular bases accounting for these mechanisms and their impact on the lack of clinical response to the pharmacological treatment currently used in GAC. This knowledge is required to identify novel biomarkers to predict treatment failure and druggable targets, and to develop sensitizing strategies to overcome drug refractoriness in GAC.
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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.