Spleen endothelial cells from patients with myelofibrosis harbor the JAK2V617F mutation

Vittorio Rosti, Laura Villani, Roberta Riboni, Valentina Poletto, Elisa Bonetti, Lorenzo Tozzi, Gaetano Bergamaschi, Paolo Catarsi, Elena Dallera, Francesca Novara, Margherita Massa, Rita Campanelli, Gabriela Fois, Benedetta Peruzzi, Marco Lucioni, Paola Guglielmelli, Alessandro Pancrazzi, Giacomo Fiandrino, Orsetta Zuffardi, Umberto MagriniMarco Paulli, Alessandro M. Vannucchi, Giovanni Barosi

Research output: Contribution to journalArticlepeer-review


Increased microvessel density contributes to abnormal BM and spleen microenvironment in myelofibrosis (MF). Taking advantage of the JAK2V617F mutation as a marker of malignancy, in the present study, we investigated whether splenic endothelial cells (ECs) obtained from capillaries by laser microdissection or from fresh spleen tissue by cell culture or cell sorting harbored such mutation in patients bearing the mutation in their granulocytes and undergoing splenectomy for therapeutical reasons. To extend the analysis to the ECs of large vessels, endothelial tissue from the splenic vein was also studied.We found JAK2V617F+ ECs in 12 of 18 patients also bearing the mutation in their granulocytes. In 3 patients, the mutation was found in at least 2 different EC samples obtained by laser microdissection, cell culture, or cell sorting. The mutation was detected in the splenic vein ECs of 1 of 6 patients investigated. In conclusion, we provide evidence that some ECs from the spleen and splenic veins of patients with MF bear the JAK2V617F mutation. We suggest that splenic ECs are involved in the process of malignant transformation in MF.

Original languageEnglish
Pages (from-to)360-368
Number of pages9
Issue number2
Publication statusPublished - Jan 10 2013

ASJC Scopus subject areas

  • Hematology
  • Biochemistry
  • Cell Biology
  • Immunology


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