ArticleOncology reports2022
Genome‑wide expression and methylation analyses reveal aberrant cell adhesion signaling in tyrosine kinase inhibitor‑resistant CML cells.
Article in Oncology reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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.
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- Targeting Integrin α2 to Overcome Imatinib Resistance in Chronic Myeloid Leukemia Cells.Biomolecules · 2025Article
- Molecular mechanism and biological pathway of high-expressed RAD51 in regulating cell adhesion and potentially affecting oral squamous cell carcinoma.Discover oncology · 2025Article
- The role of the lysine histone methylase KMT2D in chronic myeloid leukemia.Frontiers in pharmacology · 2025Article
- Association of fibronectin 1 deregulation with tyrosine kinase inhibitor resistance in chronic myeloid leukemia.Frontiers in cell and developmental biology · 2025Article
- Clinical significance of upregulated Rho GTPase activating protein 12 causing resistance to tyrosine kinase inhibitors in hepatocellular carcinoma.World journal of gastrointestinal oncology · 2024Article
- BTK acts as a modulator of the response to imatinib in chronic myeloid leukemia.Oncology letters · 2024Article
- Clinical applications of abnormal DNA methylation in chronic myeloid leukemia.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2024Article
- Clonal evolution in tyrosine kinase inhibitor-resistance: lessons fromFrontiers in oncology · 2023Article
- Regulation and Function of CCL2 and N-Myc in Retinoic Acid-treated Neuroblastoma Cells.Cancer genomics & proteomicsArticle
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although chronic myeloid leukemia (CML) can be effectively treated using BCR‑ABL1 kinase inhibitors, resistance due to kinase alterations or to BCR‑ABL1 independent mechanisms remain a therapeutic challenge. For the latter, the underlying mechanisms are widely discussed; for instance, gene expression changes, epigenetic factors and alternative signaling pathway activation. In the present study,
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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.