Myelofibrosis Stem Cell Therapy Development

Myelofibrosis is a myeloproliferative disease caused by the proliferation of collagen in the bone marrow hematopoietic tissue, whose fibrous tissue severely affects hematopoietic function. Currently, allogeneic stem cell transplantation is available for the treatment of this disease. However, further research is needed due to the demanding conditions of transplantation. Therefore, CD BioSciences has launched myelofibrosis stem cell therapy development services.

Overview of Myelofibrosis

A myeloproliferative neoplasm (MPN) known as primary myelofibrosis (PMF) is characterized by clonal myeloproliferation derived from stem cells. Additional symptoms of the disease include cachexia, leukemic progression, extramedullary hematopoiesis (EMH), anemia, hepatosplenomegaly, bone marrow reticulin/collagen fibrosis, aberrant inflammatory cytokine expression, and shortened survival.

Myelofibrosis Molecular Markers

Molecular markers are phenotypic traits that are unique to a given disease, and they can shed light on previously unknown disease-specific mechanisms. One of the most significant genetic discoveries in non-Philadelphia chromosome myeloid malignancies in MF was the JAK2^V617F mutation. Recent studies have found a large number of non-JAK2 clonal markers in MF, including the genes MPL, TET2, ASXL1, IDH1/2, DNMT3A, EZH2, CBL, and SH2B3 (LNK).

• Myelofibrosis Molecular Marker JAK2
  JAK2 is a member of the JAK family of proteins, which also includes JAK1, JAK3, and TYK2. These cytoplasmic non-receptor tyrosine kinases play a significant role in the survival and proliferation of hematopoietic stem cells (HSC). The JAK2^V617F mutation has been linked to some MF phenotypes and is crucial for the self-reprogramming abilities of HSC. Erythropoietin (EPO) binding to a receptor leads to JAK2 receptor dimerization. This dimerization results in the phosphorylation of STAT3 and STAT5, the formation of stable homodimers and heterodimers, and the transcription of genes governing cell survival and proliferation. In the absence of any additional triggers, the JAK2^V617F mutation can result in the repetitive activation of the STAT pathway.

Activated JAK-STAT signaling drives myelofibrosis. (Schieber, M. et al. 2019)

Stem Cell Transplant for the Treatment of Myelofibrosis

Myelofibrosis (MF), a myeloproliferative neoplasm without a Philadelphia chromosome, can develop as a primary or secondary condition to polycythemia vera or essential thrombocythemia. For patients with MF, allogeneic hemopoietic stem cell transplantation (HSCT) continues to be the only effective treatment.

• Hematopoietic Stem Cell Transplantation in the Era of JAK Inhibitors
  According to a number of studies, patients who respond to ruxolitinib therapy have a better chance of surviving after HCT than nonresponders or patients who lose response, indicating that HCT should be started when JAKi is responding the best. It is not clear, though, whether the improved HCT results are directly attributable to JAKi or merely reflect a more benevolent disease biology in these patients. Prospective analysis of the advantages of early versus delayed HCT in the context of JAKi therapy is merited.

Our Services

CD BioSciences offers aplastic anemia stem cell therapy development services. We have sophisticated experimental techniques and perfect experimental conditions. Based on our professional laboratory team, we can contribute to the development of stem cell therapy for myelofibrosis.

As a pioneer in biotechnology, CD BioSciences has grown into one of the largest independent biotechnology companies in the world. CD BioSciences is committed to providing professional and efficient service to our customers around the world. If you are interested in our service, please contact us.

References

1. Mbdf, A. et al. (2021). Application of stem cell therapy in myelofibrosis. Hematology/oncology clinics of North America. 35(2), 391-407.
2. Schieber, M. et al. (2019). Myelofibrosis in 2019: moving beyond JAK2 inhibition. Blood Cancer Journal.