Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 4 complete abstracts (732 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
A tyrosine kinase inhibitor and antineoplastic agent that inhibits the bcr-abl kinase created by chromosome rearrangements in chronic myeloid leukemia and acute lymphoblastic leukemia, as well as PDG-derived tyrosine kinases that are overexpressed in gastrointestinal stromal tumors.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Mesylate, Imatinib; Imatinib Methanesulfonate; Methanesulfonate, Imatinib; CGP 57148; CGP-57148; CGP57148; CGP57148B; STI571.
Where it fits in the MeSH classification
- Broader topics
- Benzamides; Piperazines; Pyrimidines
Related concepts
- Antineoplastic Agent
- Bcr-Abl
- Chronic Myeloid Leukemia
- Acute Lymphoblastic Leukemia
Research landscape
PubMed indexes 12,338 records tagged with the MeSH heading “Imatinib Mesylate” (counts retrieved 2026-10-31). 2,145 of them (17.4%) were published from 2020 onward, and the busiest period so far is 2010-2019 with 5,397 records.
Reviews account for 1,913 records (15.5%) and meta-analyses for 70. Randomized controlled trials number 299 (2.4%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 0 |
| 2000-2009 | 4,926 |
| 2010-2019 | 5,397 |
| 2020 onward | 2,145 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 1,913 | 15.5% |
| Meta-analyses | 70 | 0.6% |
| Randomized controlled trials | 299 | 2.4% |
Method: PubMed query "Imatinib Mesylate"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-31.
Reading the evidence in drugs and chemicals
Studies of a chemical or drug can answer very different questions: what it is and how it behaves in cells and animals, how the body handles it, and whether it changes outcomes in people. Laboratory and animal findings often do not carry over to patients, and observational studies of exposures are confounded by who uses a substance and why. Nothing on this page is a recommendation to use, avoid, start or stop any substance or medicine; talk to a qualified clinician or pharmacist about your own situation. Check the dose, the species, the comparison group and whether a patient-relevant outcome was measured.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| European LeukemiaNet 2020 recommendations for treating chronic myeloid leukemia | 2020 | Review article Design not recorded in structured metadata | 1,100 | cc by PMID 32127639 · DOI · PMC7214240 |
| The management of metastatic GIST: current standard and investigational therapeutics | 2021 | Review article Design not recorded in structured metadata | 195 | cc by PMID 33402214 · DOI · PMC7786896 |
| The c-Myc-regulated lncRNA NEAT1 and paraspeckles modulate imatinib-induced apoptosis in CML cells | 2018 | Research article Design not recorded in structured metadata | 106 | cc by PMID 30153828 · DOI · PMC6114538 |
| Transcriptional readthrough precedes alternative splicing programs triggered in CML cells by imatinib | 2026 | Research article Design not recorded in structured metadata | 6 | cc by PMID 41860998 · DOI · PMC13004010 |
European LeukemiaNet 2020 recommendations for treating chronic myeloid leukemia [1]
Abstract reading summary — source excerpts
- Opening excerpt
- The therapeutic landscape of chronic myeloid leukemia (CML) has profoundly changed over the past 7 years.
- Closing excerpt
- Treatment discontinuation may be considered in patients with durable DMR with the goal of achieving TFR.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (199 words)
The therapeutic landscape of chronic myeloid leukemia (CML) has profoundly changed over the past 7 years. Most patients with chronic phase (CP) now have a normal life expectancy. Another goal is achieving a stable deep molecular response (DMR) and discontinuing medication for treatment-free remission (TFR). The European LeukemiaNet convened an expert panel to critically evaluate and update the evidence to achieve these goals since its previous recommendations. First-line treatment is a tyrosine kinase inhibitor (TKI; imatinib brand or generic, dasatinib, nilotinib, and bosutinib are available first-line). Generic imatinib is the cost-effective initial treatment in CP. Various contraindications and side-effects of all TKIs should be considered. Patient risk status at diagnosis should be assessed with the new EUTOS long-term survival (ELTS)-score. Monitoring of response should be done by quantitative polymerase chain reaction whenever possible. A change of treatment is recommended when intolerance cannot be ameliorated or when molecular milestones are not reached. Greater than 10% BCR-ABL1 at 3 months indicates treatment failure when confirmed. Allogeneic transplantation continues to be a therapeutic option particularly for advanced phase CML. TKI treatment should be withheld during pregnancy. Treatment discontinuation may be considered in patients with durable DMR with the goal of achieving TFR.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 32127639 · DOI · PMC7214240
The management of metastatic GIST: current standard and investigational therapeutics [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Gastrointestinal stromal tumor (GIST) is the most common mesenchymal tumor of the gastrointestinal tract.
- Closing excerpt
- It examines the standard treatment options available but also explores the novel treatment approaches in the setting of imatinib refractory GIST.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (177 words)
Gastrointestinal stromal tumor (GIST) is the most common mesenchymal tumor of the gastrointestinal tract. The majority of GISTs harbor gain of function mutations in either KIT or PDGFRα. Determination of the GIST molecular subtype upon diagnosis is important because this information informs therapeutic decisions in both the adjuvant and metastatic setting. The management of GIST was revolutionized by the introduction of imatinib, a KIT inhibitor, which has become the standard first line treatment for metastatic GIST. However, despite a clinical benefit rate of 80%, the majority of patients with GIST experience disease progression after 2-3 years of imatinib therapy. Second and third line options include sunitinib and regorafenib, respectively, and yield low response rates and limited clinical benefit. There have been recent FDA approvals for GIST including ripretinib in the fourth-line setting and avapritinib for PDGFRA exon 18-mutant GIST. This article aims to review the optimal treatment approach for the management of patients with advanced GIST. It examines the standard treatment options available but also explores the novel treatment approaches in the setting of imatinib refractory GIST.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 33402214 · DOI · PMC7786896
The c-Myc-regulated lncRNA NEAT1 and paraspeckles modulate imatinib-induced apoptosis in CML cells [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Chronic myeloid leukemia (CML) is a clonal disease characterized by the presence of the constitutively active tyrosine kinase BCR-ABL oncoprotein.
- Closing excerpt
- Collectively, these results assign a biological function to the NEAT1 lncRNA in CML apoptosis and may lead to fuller understanding of the molecular events leading to CML.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (201 words)
Chronic myeloid leukemia (CML) is a clonal disease characterized by the presence of the constitutively active tyrosine kinase BCR-ABL oncoprotein. Although BCR-ABL is crucially important for pathogenesis and treatment response, it is thought that some additional factors might be involved in the regulation of these processes. Aberrant expression of long noncoding RNAs (lncRNAs) has recently been identified to be involved in various diseases including cancer, suggesting that lncRNAs may play a role in BCR-ABL-mediated CML. In this study, we found that nuclear-enriched abundant transcript 1 (NEAT1), a lncRNA essential for the formation of nuclear body paraspeckles, is significantly repressed in primary CML cells. NEAT1 expression could be restored by inhibiting BCR-ABL expression or its kinase activity in K562 cells. We also demonstrated that NEAT1 is regulated by c-Myc. Knockdown of NEAT1 could promote imatinib (IM)-induced apoptosis, and we demonstrated that the NEAT1-binding paraspeckle protein splicing factor proline/glutamine-rich (SFPQ) is required for NEAT1-mediated apoptosis in K562 cells. RNA-seq analysis revealed that SFPQ regulates cell growth and death pathway-related genes, confirming its function in IM-induced apoptosis. Collectively, these results assign a biological function to the NEAT1 lncRNA in CML apoptosis and may lead to fuller understanding of the molecular events leading to CML.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 30153828 · DOI · PMC6114538
Transcriptional readthrough precedes alternative splicing programs triggered in CML cells by imatinib [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Cellular stresses regulate transcriptional readthrough, whereby RNA polymerase II elongates past a gene's polyadenylation cleavage site without RNA cleavage.
- Closing excerpt
- Thus, imatinib can provoke a cascade of early changes to transcription and splicing fidelity that may lead to longer-term adjustments in gene expression, cancer cell differentiation, and the development of therapy resistance.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (155 words)
Cellular stresses regulate transcriptional readthrough, whereby RNA polymerase II elongates past a gene's polyadenylation cleavage site without RNA cleavage. Readthrough has been reported in several cancer types. Here, we use long-read sequencing of nascent RNA to quantify transcriptional readthrough in chronic myeloid leukemia (CML) cells and characterize early responses to the targeted therapeutic, imatinib. We show that the amount, length, and gene specificity of readthrough increase within 1 hour, before gene expression and alternative splicing alterations emerge. Notably, imatinib-dependent messenger RNA (mRNA) isoform changes involved "readthrough chimeras," in which exons from an upstream gene are alternatively spliced to exons in a downstream gene. Altered mRNA isoforms and chimera levels were detected in imatinib-resistant K562 cells as well as cells of patients with CML. Thus, imatinib can provoke a cascade of early changes to transcription and splicing fidelity that may lead to longer-term adjustments in gene expression, cancer cell differentiation, and the development of therapy resistance.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41860998 · DOI · PMC13004010
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Kinase drug discovery 20 years after imatinib: progress and future directions [5]
- Research article Therapeutic drug monitoring of imatinib, nilotinib, and dasatinib for patients with chronic myeloid leukemia [6]
- Research article Immunological off-target effects of imatinib [7]
- Research article Imatinib Treatment for Locally Advanced or Metastatic Dermatofibrosarcoma Protuberans: A Systematic Review [8]
- Research article Treatment-free remission with first- and second-generation tyrosine kinase inhibitors [9]
- Research article Imatinib discontinuation in chronic myeloid leukaemia patients with undetectable BCR-ABL transcript level: A systematic review and a meta-analysis [10]
References
- Hochhaus A, Baccarani M, Silver RT, Schiffer C, Apperley JF, Cervantes F, et al.. European LeukemiaNet 2020 recommendations for treating chronic myeloid leukemia. . 2020. PMID 32127639 · DOI · PMC7214240
- Kelly CM, Gutierrez Sainz L, Chi P. The management of metastatic GIST: current standard and investigational therapeutics. . 2021. PMID 33402214 · DOI · PMC7786896
- Zeng C, Liu S, Lu S, Yu X, Lai J, Wu Y, et al.. The c-Myc-regulated lncRNA NEAT1 and paraspeckles modulate imatinib-induced apoptosis in CML cells. . 2018. PMID 30153828 · DOI · PMC6114538
- Podszywałow-Bartnicka P, Shine M, Lin J, Neugebauer KM. Transcriptional readthrough precedes alternative splicing programs triggered in CML cells by imatinib. . 2026. PMID 41860998 · DOI · PMC13004010
- Cohen P, Cross D, Jänne PA. Kinase drug discovery 20 years after imatinib: progress and future directions. Nat Rev Drug Discov. 2021. PMID 34002056 · DOI · PMC8127496
- Miura M. Therapeutic drug monitoring of imatinib, nilotinib, and dasatinib for patients with chronic myeloid leukemia. Biol Pharm Bull. 2015. PMID 25947908 · DOI
- Zitvogel L, Rusakiewicz S, Routy B, Ayyoub M, Kroemer G. Immunological off-target effects of imatinib. Nat Rev Clin Oncol. 2016. PMID 27030078 · DOI
- Navarrete-Dechent C, Mori S, Barker CA, Dickson MA, Nehal KS. Imatinib Treatment for Locally Advanced or Metastatic Dermatofibrosarcoma Protuberans: A Systematic Review. JAMA Dermatol. 2019. PMID 30601909 · DOI · PMC8909640
- Cortes J, Rea D, Lipton JH. Treatment-free remission with first- and second-generation tyrosine kinase inhibitors. Am J Hematol. 2019. PMID 30394563 · DOI · PMC6587857
- Campiotti L, Suter MB, Guasti L, Piazza R, Gambacorti-Passerini C, Grandi AM, et al.. Imatinib discontinuation in chronic myeloid leukaemia patients with undetectable BCR-ABL transcript level: A systematic review and a meta-analysis. Eur J Cancer. 2017. PMID 28365527 · DOI
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-31.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.