AI Article Synopsis
- Myelofibrosis (MF) is a serious subtype of myeloproliferative neoplasm (MPN) with a typically poor prognosis, highlighting the need for better understanding of its causes.
- Key mutations in three genes (JAK2, CALR, and MPL) frequently appear in MPN and can trigger the disease in animal models, indicating their significance in MF development.
- Research using these animal models has provided insights into MF's progression from earlier stages of MPN, like essential thrombocythemia and polycythemia vera, and has opened doors to potential new therapies.
Article Abstract
Myelofibrosis (MF) is subtype of myeloproliferative neoplasm (MPN) characterized by a relatively poor prognosis in patients. Understanding the factors that drive MF pathogenesis is crucial to identifying novel therapeutic approaches with the potential to improve patient care. Driver mutations in three main genes (janus kinase 2 (), calreticulin (), and myeloproliferative leukemia virus oncogene ()) are recurrently mutated in MPN and are sufficient to engender MPN using animal models. Interestingly, animal studies have shown that the underlying molecular mutation and the acquisition of additional genetic lesions is associated with MF outcome and transition from early stage MPN such as essential thrombocythemia (ET) and polycythemia vera (PV) to secondary MF. In this issue, we review murine models that have contributed to a better characterization of MF pathobiology and identification of new therapeutic opportunities in MPN.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7563264 | PMC |
| http://dx.doi.org/10.3390/cancers12092381 | DOI Listing |
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