ArticleBiologics : targets & therapy2007
Imatinib-resistant chronic myeloid leukemia (CML): Current concepts on pathogenesis and new emerging pharmacologic approaches.
Article in Biologics : targets & therapy, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 32 citations in OpenAlex.
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- Mirk/Dyrk1B Kinase Inhibitors in Targeted Cancer Therapy.Pharmaceutics · 2024Review
- Survivin Small Molecules Inhibitors: Recent Advances and Challenges.Molecules (Basel, Switzerland) · 2023Review
- Integrated genomic sequencing in myeloid blast crisis chronic myeloid leukemia (MBC-CML), identified potentially important findings in the context of leukemogenesis model.Scientific reports · 2022Article
- Functionalized Lineage Tracing Can Enable the Development of Homogenization-Based Therapeutic Strategies in Cancer.Frontiers in immunology · 2022Article
- The Role of Vesicle Trafficking Defects in the Pathogenesis of Prion and Prion-Like Disorders.International journal of molecular sciences · 2020Review
- Deciphering the scalene association among type-2 diabetes mellitus, prostate cancer, and chronic myeloid leukemia via enrichment analysis of disease-gene network.Cancer medicine · 2019Article
- Characterization of cancer genomic heterogeneity by next-generation sequencing advances precision medicine in cancer treatment.Precision clinical medicine · 2018Review
- Using Genome Sequence to Enable the Design of Medicines and Chemical Probes.Chemical reviews · 2018Review
- AFLP-AFLP in silico-NGS approach reveals polymorphisms in repetitive elements in the malignant genome.PloS one · 2018Article
- Genetic Mutations and Epigenetic Modifications: Driving Cancer and Informing Precision Medicine.BioMed research international · 2017Review
- Anchor-based classification and type-C inhibitors for tyrosine kinases.Scientific reports · 2015Article
- Carbenoxolone induces apoptosis and inhibits survivin and survivin-ΔEx3 genes expression in human leukemia K562 cells.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2011Article
- Small interfering RNA against BCR-ABL transcripts sensitize mutated T315I cells to nilotinib.Haematologica · 2010Article
- Assessment of Dasatinib Versus Nilotinib as Upfront Therapy for Chronic Phase of Chronic Myeloid Leukemia in Qatar: A Cost-Effectiveness Analysis.Cancer control : journal of the Moffitt Cancer CenterArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic myeloid leukemia (CML) is a stem cell disease, in which the BCR/ABL oncoprotein is considered essential for abnormal growth and accumulation of neoplastic cells. During the past 10 years, the BCR/ABL tyrosine kinase inhibitor imatinib (STI571) has successfully been introduced in the treatment of the disease. However, intrinsic as well as acquired resistance against the drug have been described and have been recognized as an emerging problem and challenge in clinical practice, and a key issue in CML research. Most of the respective concepts focus on imatinib-resistant mutants of BCR/ABL that are detectable in a high proportion of cases. However, other factors also contribute to resistance against imatinib, including the genetic background, the biologic features of CML stem cells, gene amplifications, silencing of tumor suppressor genes, and various pharmacologic aspects. In this article, the mechanisms of resistance against imatinib and other BCR/ABL tyrosine kinase inhibitors in CML are discussed together with strategies to overcome and to prevent resistance with available drugs or with novel antileukemic approaches.
Indexed as
Identifiers
19707313PMC2721289W1221250553What 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.