ArticleAmerican journal of cancer research2018
Multiple mechanisms involved in a low concentration of FL118 enhancement of AMR-MeOAc to induce pancreatic cancer cell apoptosis and growth inhibition.
Article in American journal of cancer research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
8 citing papers in PubMed, 9 citations in OpenAlex.
- Cracking the code of cancer immunotherapy resistance: emerging roles of pyroptosis and necroptosis.Journal of experimental & clinical cancer research : CR · 2025Review
- Structure-Activity Relationship of FL118 Platform Position 7 Versus Position 9-Derived Compounds and Their Mechanism of Action and Antitumor Activity.Journal of medicinal chemistry · 2023Article
- Preparation of a camptothecin analog FLQY2 self-micelle solid dispersion with improved solubility and bioavailability.Journal of nanobiotechnology · 2022Article
- MUC1-C dictates neuroendocrine lineage specification in pancreatic ductal adenocarcinomas.Carcinogenesis · 2022Article
- Article
- Design, Synthesis, and In Vitro/In Vivo Anti-Cancer Activities of Novel (20International journal of molecular sciences · 2020Article
- Review
- Cancer therapeutics using survivin BIRC5 as a target: what can we do after over two decades of study?Journal of experimental & clinical cancer research : CR · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Activating mutations in GTPase protein KRAS occurs in approximately 90% of pancreatic cancers. Mutated KRAS lead to constitutive activation of RAF/MEK/ERK and PI3K/Akt pathways in pancreatic cancer. There is currently no effective KRAS-targeted therapeutics available in the clinic for treating this subset of cancer. In this study we demonstrate that combination of a plant-isolated triterpenoid compound AMR-MeOAc with a low concentration of an antiapoptotic protein inhibitor, FL118 exhibited synergistic cytotoxic activity against pancreatic cancer cells with either mutant KRAS (HPAF-II, KRAS
Indexed as
Identifiers
30555743PMC6291652W2983108327What OpenQuestion 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 OpenQuestion graph.