There is no effective treatment
for the myeloproliferative (bone marrow) form of leukemia.
«Microenvironment of hematopoietic stem cells can be a target
for myeloproliferative disorders.»
Not exact matches
The discovery of a new therapeutic target
for certain kinds of
myeloproliferative disease is, without doubt, good news.
The team has shown that the microenvironment that controls hematopoietic stem cells can be targeted
for the treatment of a set of disorders called
myeloproliferative neoplasias, the most prominent of which are chronic myelomonocytic leukemia (CMML), juvenile myelomonocytic leukemia (JMML), and atypical chronic myelogenous leukemia (CML).
Relevance to practice: Identification of the Val617Phe JAK2 mutation lays the foundation
for new approaches to the diagnosis, classification, and treatment of
myeloproliferative disorders.
4/7/2008 From Bench to Bedside in One Year: Stem Cell Research Leads to Potential New Therapy
for Rare Blood Disorder A unique partnership between industry and academia has led to human clinical trials of a new drug
for a rare class of blood diseases called
myeloproliferative disorders (MPD), which are all driven by the same genetic mutation and can evolve into leuk... More...
If you have been diagnosed with
Myeloproliferative neoplasms (MPNs), you can rest assured that our team of experts will provide the best treatment and outcomes
for you.
The Johns Hopkins Center
for the Chronic
Myeloproliferative Disorders coordinates the care of patients with PV and other related disorders and conducts research in these areas.
In 2005, the identification of an activating mutation in JAK2 (the V617F mutation) as a STAT5 - activating and disease - causing genetic alteration in a significant proportion of patients with
myeloproliferative neoplasms (MPNs) has emphasized the oncogenic role of the JAK tyrosine kinases in hematologic malignancies.2 — 5 JAK2 is a member of the Janus tyrosine kinase family comprising three other mammalian non-receptor tyrosine kinases (JAK1, JAK3 and TYK2) that associate with cytokine receptors lacking intrinsic kinase activity to mediate cytokine - induced signal transduction and activation of STAT transcription factors.6 All JAKs share a similar protein structure and contain a tyrosine kinase domain at the C - terminus flanked by a catalytically inactive pseudokinase domain with kinase - regulatory activity, by an atypical SH2 domain and by a FERM domain that mediates association to the membrane - proximal region of the cytokine receptors.7, 8 Soon after the discovery of JAK2 V617F, we and others described that activating JAK1 mutations are relatively common in adult patients with T - cell acute lymphoblastic leukemia (ALL) and participate in ALL development allowing
for constitutive activation of STAT5.9 — 11 Several STAT5 - activating JAK1 mutations were also reported in AML and breast cancer patients.10
FDA Clears Test to Help Diagnose, Identify Blood Cancer Type: The FDA has approved ClearLLab Reagents (T1, T2, B1, B2, M)
for the detection of hematologic malignancies such as acute and chronic leukemias, myelodysplastic syndromes,
myeloproliferative neoplasms, multiple myeloma, and non-Hodgkin lymphoma.
The more recent identification of mutations in calreticulin brought with it a sense of completeness, with most patients with
myeloproliferative neoplasm now having a biological basis
for their excessive myeloproliferation.