ArticleCancer cell2014
Structure, function, and resistance in chronic myeloid leukemia.
Article in Cancer cell, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
7 citing papers in PubMed.
- Ponatinib as first-line treatment for patients with chronic myeloid leukaemia in chronic phase: a phase 2 study.The Lancet. Haematology · 2015Trial
- Mechanisms underlying therapeutic resistance of tyrosine kinase inhibitors in chronic myeloid leukemia.International journal of biological sciences · 2024Review
- Resistance to Tyrosine Kinase Inhibitors in Chronic Myeloid Leukemia-From Molecular Mechanisms to Clinical Relevance.Cancers · 2021Review
- Molecular Mechanisms of Resistance to Tyrosine Kinase Inhibitors.Current hematologic malignancy reports · 2019Review
- Cobll1 is linked to drug resistance and blastic transformation in chronic myeloid leukemia.Leukemia · 2017Article
- The Cancer Drug Dasatinib Increases PGC-1α in Adipose Tissue but Has Adverse Effects on Glucose Tolerance in Obese Mice.Endocrinology · 2016Article
- Polypharmacology in Precision Oncology: Current Applications and Future Prospects.Current pharmaceutical design · 2016Review
Corrections and comments
- Comment on
Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic myeloid leukemia (CML) is effectively treated by tyrosine kinase inhibitors (TKIs). Rarely, CML cases develop TKI resistance through acquisition of compound mutations. In this issue of Cancer Cell, Zabriskie and colleagues study how structural changes caused by compound mutations cause clinically relevant changes in TKI sensitivity.
Indexed as
Identifiers
25203318What 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.