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Cancers
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Chronic Myeloid Leukemia
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Chronic Myeloid Leukemia

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Cancer Pathophysiology".

Deadline for manuscript submissions: closed (30 November 2020) | Viewed by 19866

Special Issue Editors

Dr. Gabriel Etienne

E-Mail Website
Guest Editor
Département d'Hématologie, Institut Bergonié, Bordeaux, France
Interests: chronic myeloid leukemia; tyrosine kinase inhibitors (TKI); BCR-ABL fusion protein
Dr. Marc Delord

E-Mail Website
Guest Editor
Biostatistique, Institut Universitaire d'Hématologie, Université Paris Diderot, Paris 75010, France
Interests: Epidemiology of Chronic Myeloid Leukemia (CML); Cancer Epidemiology

Special Issue Information

Dear Colleagues,

Twenty years ago, who could have imagined that a small oral molecule designed to target the deregulated tyrosine kinase activity of the BCR-ABL fusion protein would have transformed the prognosis of chronic myeloid leukemia (CML), a fatal disease in the absence of allogeneic hematopoietic stem cell transplantation?

Over the past 20 years the therapeutic arsenal has seen continual enrichment with second- and third-generation tyrosine kinase inhibitors (TKIs) and significant progress in molecular biology has enabled the quantitative assessment of minimal molecular residual disease, both deeply changing the course of the disease with an expected survival close to the healthy population and, in some selected patients, a prolonged treatment-free remission.

However, several unmet needs remain. Understanding the underlying mechanisms of disease progression, persistence, and/or resistance in TKIs, together with the evaluation of the benefit–risk equation of TKIs as a long-term issue at the individual level (i.e., personalized medicine) are some of these needs.

This series of articles is presented by an international team of experts in the field of CML and will contribute to this unbelievable medical history.

Dr. Gabriel Etienne
Dr. Marc Delord
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cancers is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • chronic myeloid leukemia (CML)
  • tyrosine kinase inhibitors (TKI)
  • BCR-ABL fusion protein

Published Papers (4 papers)

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Research

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11 pages, 12555 KiB  
Article
Genetic Screening for Potential New Targets in Chronic Myeloid Leukemia Based on Drosophila Transgenic for Human BCR-ABL1
by Marco Lo Iacono, Elisabetta Signorino, Jessica Petiti, Monica Pradotto, Chiara Calabrese, Cristina Panuzzo, Francesca Caciolli, Barbara Pergolizzi, Marco De Gobbi, Giovanna Rege-Cambrin, Carmen Fava, Claudia Giachino, Enrico Bracco, Giuseppe Saglio, Francesco Frassoni and Daniela Cilloni
Cancers 2021, 13(2), 293; https://doi.org/10.3390/cancers13020293 - 14 Jan 2021
Cited by 2 | Viewed by 2108
Abstract
Chronic myeloid leukemia is a myeloproliferative neoplasm characterized by the presence of the Philadelphia chromosome that originates from the reciprocal translocation t(9;22)(q34;q11.2) and encodes for the constitutively active tyrosine kinase protein BCR-ABL1 from the Breakpoint Cluster Region (BCR) sequence and the [...] Read more.
Chronic myeloid leukemia is a myeloproliferative neoplasm characterized by the presence of the Philadelphia chromosome that originates from the reciprocal translocation t(9;22)(q34;q11.2) and encodes for the constitutively active tyrosine kinase protein BCR-ABL1 from the Breakpoint Cluster Region (BCR) sequence and the Abelson (ABL1) gene. Despite BCR-ABL1 being one of the most studied oncogenic proteins, some molecular mechanisms remain enigmatic, and several of the proteins, acting either as positive or negative BCR-ABL1 regulators, are still unknown. The Drosophila melanogaster represents a powerful tool for genetic investigations and a promising model to study the BCR-ABL1 signaling pathway. To identify new components involved in BCR-ABL1 transforming activity, we conducted an extensive genetic screening using different Drosophila mutant strains carrying specific small deletions within the chromosomes 2 and 3 and the gmrGal4,UAS-BCR-ABL1 4M/TM3 transgenic Drosophila as the background. From the screening, we identified several putative candidate genes that may be involved either in sustaining chronic myeloid leukemia (CML) or in its progression. We also identified, for the first time, a tight connection between the BCR-ABL1 protein and Rab family members, and this correlation was also validated in CML patients. In conclusion, our data identified many genes that, by interacting with BCR-ABL1, regulate several important biological pathways and could promote disease onset and progression. Full article
(This article belongs to the Special Issue Chronic Myeloid Leukemia)
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17 pages, 954 KiB  
Article
Incidences of Deep Molecular Responses and Treatment-Free Remission in de Novo CP-CML Patients
by Gabriel Etienne, Stéphanie Dulucq, Fréderic Bauduer, Didier Adiko, François Lifermann, Corinne Dagada, Caroline Lenoir, Anna Schmitt, Emilie Klein, Samia Madene, Marie-Pierre Fort, Fontanet Bijou, Marius Moldovan, Beatrice Turcq, Fanny Robbesyn, Françoise Durrieu, Laura Versmée, Sandrine Katsahian, Carole Faberes, Axelle Lascaux and François-Xavier Mahonadd Show full author list remove Hide full author list
Cancers 2020, 12(9), 2521; https://doi.org/10.3390/cancers12092521 - 4 Sep 2020
Cited by 13 | Viewed by 3091
Abstract
Background: Tyrosine Kinase Inhibitors (TKIs) discontinuation in patients who had achieved a deep molecular response (DMR) offer now the opportunity of prolonged treatment-free remission (TFR). Patients and Methods: Aims of this study were to evaluate the proportion of de novo chronic-phase chronic myeloid [...] Read more.
Background: Tyrosine Kinase Inhibitors (TKIs) discontinuation in patients who had achieved a deep molecular response (DMR) offer now the opportunity of prolonged treatment-free remission (TFR). Patients and Methods: Aims of this study were to evaluate the proportion of de novo chronic-phase chronic myeloid leukemia (CP-CML) patients who achieved a sustained DMR and to identify predictive factors of DMR and molecular recurrence-free survival (MRFS) after TKI discontinuation. Results: Over a period of 10 years, 398 CP-CML patients treated with first-line TKIs were included. Median age at diagnosis was 61 years, 291 (73%) and 107 (27%) patients were treated with frontline imatinib (IMA) or second- or third-generation TKIs (2–3G TKI), respectively. With a median follow-up of seven years (range, 0.6 to 13.8 years), 182 (46%) patients achieved a sustained DMR at least 24 months. Gender, BCR-ABL1 transcript type, and Sokal and ELTS risk scores were significantly associated with a higher probability of sustained DMR while TKI first-line (IMA vs. 2–3G TKI) was not. We estimate that 28% of CML-CP would have been an optimal candidate for TKI discontinuation according to recent recommendations. Finally, 95 (24%) patients have entered in a TFR program. MRFS rates at 12 and 48 months were 55.1% (95% CI, 44.3% to 65.9%) and 46.9% (95% CI, 34.9% to 58.9%), respectively. In multivariate analyses, first-line 2–3G TKIs compared to IMA and TKI duration were the most significant factors of MRFS. Conclusions: Our results suggest that frontline TKIs have a significant impact on TFR in patients who fulfill the selection criteria for TKI discontinuation. Full article
(This article belongs to the Special Issue Chronic Myeloid Leukemia)
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Review

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22 pages, 6671 KiB  
Review
Definition, Epidemiology, Pathophysiology, and Essential Criteria for Diagnosis of Pediatric Chronic Myeloid Leukemia
by Meinolf Suttorp, Frédéric Millot, Stephanie Sembill, Hélène Deutsch and Markus Metzler
Cancers 2021, 13(4), 798; https://doi.org/10.3390/cancers13040798 - 14 Feb 2021
Cited by 20 | Viewed by 9241
Abstract
Depending on the analytical tool applied, the hallmarks of chronic myeloid leukemia (CML) are the Philadelphia Chromosome and the resulting mRNA fusion transcript BCR-ABL1. With an incidence of 1 per 1 million of children this malignancy is very rare in the first 20 [...] Read more.
Depending on the analytical tool applied, the hallmarks of chronic myeloid leukemia (CML) are the Philadelphia Chromosome and the resulting mRNA fusion transcript BCR-ABL1. With an incidence of 1 per 1 million of children this malignancy is very rare in the first 20 years of life. This article aims to; (i) define the disease based on the WHO nomenclature, the appropriate ICD 11 code and to unify the terminology, (ii) delineate features of epidemiology, etiology, and pathophysiology that are shared, but also differing between adult and pediatric patients with CML, (iii) give a short summary on the diseases to be considered as a differential diagnosis of pediatric CML, (iv) to describe the morphological, histopathological and immunophenotypical findings of CML in pediatric patients, (v) illustrate rare but classical complications resulting from rheological problems observed at diagnosis, (vi) list essential and desirable diagnostic criteria, which hopefully in the future will help to unify the attempts when approaching this rare pediatric malignancy. Full article
(This article belongs to the Special Issue Chronic Myeloid Leukemia)
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11 pages, 1034 KiB  
Review
Standardization of BCR-ABL1 p210 Monitoring: From Nested to Digital PCR
by Aleksandar Jovanovski, Jessica Petiti, Emilia Giugliano, Enrico Marco Gottardi, Giuseppe Saglio, Daniela Cilloni and Carmen Fava
Cancers 2020, 12(11), 3287; https://doi.org/10.3390/cancers12113287 - 6 Nov 2020
Cited by 7 | Viewed by 4661
Abstract
The introduction of tyrosine kinase inhibitors in 2001 as a targeted anticancer therapy has significantly improved the quality of life and survival of patients with chronic myeloid leukemia. At the same time, with the introduction of tyrosine kinase inhibitors, the need for precise [...] Read more.
The introduction of tyrosine kinase inhibitors in 2001 as a targeted anticancer therapy has significantly improved the quality of life and survival of patients with chronic myeloid leukemia. At the same time, with the introduction of tyrosine kinase inhibitors, the need for precise monitoring of the molecular response to therapy has emerged. Starting with a qualitative polymerase chain reaction, followed by the introduction of a quantitative polymerase chain reaction to determine the exact quantity of the transcript of interest-p210 BCR-ABL1, molecular monitoring in patients with chronic myeloid leukemia was internationally standardized. This enabled precise monitoring of the therapeutic response, unification of therapeutic protocols, and comparison of results between different laboratories. This review aims to summarize the steps in the diagnosis and molecular monitoring of p210 BCR-ABL1, as well as to consider the possible future application of a more sophisticated method such as digital polymerase chain reaction. Full article
(This article belongs to the Special Issue Chronic Myeloid Leukemia)
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