ArticleFrontiers in pharmacology2023
Myelofibrosis at diagnosis is associated with the failure of treatment-free remission in CML patients.
Article in Frontiers in pharmacology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed, 5 citations in OpenAlex.
- Clinicopathological Features and Exploratory Outcome Associations of Bone Marrow Fibrosis in Newly Diagnosed Acute Lymphoblastic Leukemia: A Single-Center Retrospective Cohort Study.Cancer medicine · 2026Article
- A nomogram for predicting T315I-free survival in chronic phase chronic myeloid leukemia patients: a multicenter retrospective study.Scientific reports · 2025Article
- Telomere Length Is Associated With Adverse Atrial Remodeling in Patients With Atrial Fibrillation.Journal of the American Heart Association · 2025Article
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Authors and funding
15 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
The management of patients with chronic myeloid leukemia (CML) has been revolutionized by the introduction of tyrosine kinase inhibitors (TKIs), which induce deep molecular responses so that treatment can eventually be discontinued, leading to treatment-free remission (TFR) in a subset of patients. Unfortunately, leukemic stem cells (LSCs) often persist and a fraction of these can again expand in about half of patients that attempt TKI discontinuation. In this study, we show that presence of myelofibrosis (MF) at the time of diagnosis is a factor associating with TFR failure. Fibrotic transformation is governed by the action of several cytokines, and interestingly, some of them have also been described to support LSC persistence. At the cellular level, these could be produced by both malignant cells and by components of the bone marrow (BM) niche, including megakaryocytes (MKs) and mesenchymal stromal cells (MSCs). In our cohort of 57 patients, around 40% presented with MF at diagnosis and the number of blasts in the peripheral blood and BM was significantly elevated in patients with higher grade of MF. Employing a CML transgenic mouse model, we could observe higher levels of alpha-smooth muscle actin (α-SMA) in the BM when compared to control mice. Short-term treatment with the TKI nilotinib, efficiently reduced spleen weight and
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