Evidence map›Paper›PMID 38424138›Full record

ArticleLeukemia2024

Long-term outcomes after upfront second-generation tyrosine kinase inhibitors for chronic myeloid leukemia: managing intolerance and resistance.

Simone Claudiani, Farhan Chughtai, Afzal Khan, Chloe Hayden, Fiona Fernando, Jamshid Khorashad, Victoria Orovboni, Glenda Scandura, Andrew Innes, Jane F Apperley and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Leukemia, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
9.1field-weighted citation impact, top 2% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

15 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 2 institutions in 1 country.

Simone ClaudianiCentre for Haematology, Department of Immunology and Inflammation, Faculty of Medicine, Imperial College London, London, UK. s.claudiani@imperial.ac.uk.ORCID 0000-0003-3686-7610
Farhan ChughtaiCentre for Haematology, Department of Immunology and Inflammation, Faculty of Medicine, Imperial College London, London, UK.ORCID 0009-0005-0456-3358
Afzal KhanCentre for Haematology, Department of Immunology and Inflammation, Faculty of Medicine, Imperial College London, London, UK.
Chloe HaydenImperial Molecular Pathology, Hammersmith Hospital, Imperial College Healthcare NHS Trust, London, UK.
Fiona FernandoCentre for Haematology, Department of Immunology and Inflammation, Faculty of Medicine, Imperial College London, London, UK.
Jamshid KhorashadCentre for Haematology, Department of Immunology and Inflammation, Faculty of Medicine, Imperial College London, London, UK.ORCID 0000-0002-6961-7311
Victoria OrovboniImperial Molecular Pathology, Hammersmith Hospital, Imperial College Healthcare NHS Trust, London, UK.
Glenda ScanduraCentre for Haematology, Department of Immunology and Inflammation, Faculty of Medicine, Imperial College London, London, UK.
Andrew InnesCentre for Haematology, Department of Immunology and Inflammation, Faculty of Medicine, Imperial College London, London, UK.ORCID 0000-0003-0918-8882
Jane F ApperleyCentre for Haematology, Department of Immunology and Inflammation, Faculty of Medicine, Imperial College London, London, UK.ORCID 0000-0002-1710-1794
Dragana MilojkovicCentre for Haematology, Department of Immunology and Inflammation, Faculty of Medicine, Imperial College London, London, UK.
Imperial College Healthcare NHS Trust · GBImperial College London · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Second-generation tyrosine kinase inhibitors (2GTKI) are more effective in inducing rapid molecular responses than imatinib when used first-line in patients with chronic myeloid leukemia in chronic phase (CML-CP). However, failure of first line-2GTKI (1L-2GTKI) still occurs and there is no consensus regarding subsequent management. We retrospectively analyzed the outcome of 106 CML-CP patients treated with 1L-2GTKI and with a median follow-up of 91 months. 45 patients (42.4%) switched to an alternative TKI, 28 for intolerance (26.4%) and 17 (16%) for resistance. Most patients who remained on 1L-2GTKI achieved deep molecular responses (DMR) and 15 (14.1%) are in treatment-free remission (TFR). Intolerant patients also obtained DMR, although most required multiple TKI changes and were slower to respond, particularly if treated with 2L-imatinib. Inferior outcomes were observed in resistant patients, who failed alternative 2L-2GTKI and required 3/4GTKI and/or allogeneic hematopoietic stem cell transplant (alloSCT). 7yr-OS was significantly lower for these individuals (66.1%) than for intolerant patients and those who remained on 1L-2GTKI (100% and 97.9%, respectively; p = 0.001). It is apparent that failure of 1L-2GTKI is a challenging problem in modern CML therapy. Intolerance can be effectively managed by switching to an alternative 2GTKI, but resistance requires early consideration of 3/4GTKI.

Indexed as

Leukemia, Myelogenous, Chronic, BCR-ABL PositiveTyrosine Kinase InhibitorsDasatinibFusion Proteins, bcr-ablHumansImatinib MesylateProtein Kinase InhibitorsRetrospective StudiesDasatinibFusion Proteins, bcr-ablImatinib MesylateProtein Kinase InhibitorsTyrosine Kinase Inhibitors

Identifiers

PMID38424138
PMCPMC10997507
OpenAlexW4392282973

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.