Extension usage examples:
Here's how our browser extension sees the article:
Article summary:
1. N6-methyladenosine (m6A) modification is associated with imatinib resistance in gastrointestinal stromal tumor (GIST).
2. METTL3, a methyltransferase, is responsible for the increased m6A modification levels in imatinib-resistant GIST cells and tissues.
3. The m6A-mediated MRP1 reduces IM concentration inside cells, resulting in drug resistance, by stimulating MRP1 mRNA translation via binding with YTHDF1 and eEF-1.
Article analysis:
The article “N6-methyladenosine modification regulates imatinib resistance of gastrointestinal stromal tumor by enhancing the expression of multidrug transporter MRP1” is a well-written and comprehensive review of the role of N6-methyladenosine (m6A) modification in imatinib resistance of gastrointestinal stromal tumor (GIST). The authors provide evidence to support their claims that m6A modification levels are elevated in imatinib-resistant GIST cells and tissues, and that methyltransferase METTL3 is one of the main proteins responsible for this aberrant modification. They also discuss how increased METTL3 levels contribute to imatinib resistance and worse progression-free survival of GIST patients.
The article is generally reliable and trustworthy as it provides evidence from clinical studies to support its claims. The authors have used data from 35 patients who underwent radical resection for GIST at the First Affiliated Hospital of Nanjing Medical University China between February 2015 and February 2019, as well as 18 patients whose disease progressed even though they were regularly taking imatinib. Furthermore, they have used various methods such as RT-qPCR, m6A sequencing (m6A-seq), m6A RNA immunoprecipitation (RIP)-qPCR, determination of intracellular imatinib concentration, mRNA stability assay, protein stability assay, subcellular fractionation, RIP-RT-qPCR, polysome profiling and LC-MS/MS to validate their findings.
However, there are some potential biases that should be noted when considering the trustworthiness of this article. Firstly, the sample size used in this study was relatively small compared to other studies on similar topics; thus it may not be representative enough to draw general conclusions about the role of m6A modification in GIST drug resistance. Secondly, while