Notice: Users may be experiencing issues with displaying some pages on stanfordhealthcare.org. We are working closely with our technical teams to resolve the issue as quickly as possible. Thank you for your patience.
 

Learn about the flu shot, COVID-19 vaccine, and our masking policy »

Stanford Health Care

Absence of FTL3 mutations in patients with JAK2(V617F) mutation negative essential thrombocythemia AMERICAN JOURNAL OF HEMATOLOGY Medeiros, B. C., Zhang, T., Lipton, J. H., Kamel-Reid, S. 2007; 82 (4): 293-294

Abstract

A common point mutation in the JAK2 tyrosine kinase leads to constitutive hematopoietic growth factor receptor signaling and was recently described in many patients with myeloproliferative disorders (MPDs). However, this JAK2 mutation is present in only a subset (35-50%) of patients with essential thrombocythemia (ET). Thus, the proliferative signals responsible for MPDs in the absence of JAK2 mutations remain largely unknown. Despite intriguing pre-clinical data, where transgenic mice overexpressing FLT3-ITD developed a MPD resembling ET, none of the patient samples from ET patients who were JAK2(V617F)-negative demonstrated the presence of activating mutations in the FLT3 receptor.

View details for DOI 10.1002/ajh.20765

View details for Web of Science ID 000245464400008

View details for PubMedID 17013813