Special Issue "Myeloproliferative Neoplasms: From Genetic Landscape to Therapeutic Targets"
A special issue of Cells (ISSN 2073-4409).
Deadline for manuscript submissions: closed (15 August 2021).
Interests: hematopoietic stem cell differentiation; erythropoiesis; megakaryocytopoiesis; platelets; myeloproliferative neoplasms; cell signalling; protein kinase C
The biological, molecular and clinical landscape of Philadelphia-negative myeloproliferative neoplasms (MPNs) has dramatically changed in the last decades, leading to a better understanding of the pathophysiology of these disorders and to a significant improvement of the therapeutic armamentarium for MPN patients.
In addition to the so called “phenotypic-driver mutations”, the widespread adoption of next-generation sequencing technology has provided key insights into the molecular mechanisms of MPNs, leading to the identification of mutations in genes involved in epigenetic methylation, RNA splicing, transcriptional regulation and signal transduction, significantly affecting disease course and outcome. Moreover, genome wide association studies revealed that other genetic factors, such as germline predisposition factors, also impact the disease.
Different mouse models recapitulating the main features of these disorders have also been generated, enabling to define the role of each genetic lesion in determining the disease phenotype, the long-term effects of the single mutant gene and the function of MPN-initiating cells. All this information led to the implementation of patient risk stratification systems for tailored treatment options.
We currently know that all three MPNs, but primarily myelofibrosis (MF), are typified by aberrant megakaryocytopoiesis, and that the megakaryocytic clone is the main source of a plethora of cytokines responsible for local (bone marrow) and systemic inflammation. Indeed, MPNs are considered a model of onco-inflammatory disorders and, in this scenario, distinct MPNs could be more appropriately seen as a “biological continuum”, in which polycythemia vera (PV) and essential thrombocythemia (ET) represent early stages followed by an advanced, burnout phase (MF), that in turn may develop into secondary acute myeloid leukemia. The primary focus of this special issue will be to provide the state of the art of the genetic landscape of MPNs and of its inflammatory environment, to cover the recent advances in cell signaling alterations during the aberrant differentiation of the MPN hematopoietc stem cell and to discuss how all this impacts on therapeutic strategies based on new molecular targets.
Dr. Marco Vitale
Dr. Elena Masselli
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 papers will be 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. Cells is an international peer-reviewed open access monthly 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 2000 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.
- Myeloproliferative Neoplasms
- Polycythemia Vera
- Essential Thrombocythemia
- CD34+ cells
- Mouse models
- Somatic mutation
- Prognostic models