Spleen neoangiogenesis in patients with myelofibrosis with myeloid metaplasia

Giovanni Barosi, Rosti Vittorio, Massa Margherita, Viarengo G. Luca, Pecci Alessandro, Necchi Vittorio, Ramaioli Isabella, Campanelli Rita, Marchetti Monia, Bazzan Mario, Magrini Umberto

Research output: Contribution to journalArticle

Abstract

Neoangiogenesis is an integral component of bone marrow myeloproliferation in patients with myelofibrosis with myeloid metaplasia (MMM). As extramedullary haematopoiesis is a constitutive feature of MMM, we studied spleen neoangiogenesis by a computerized image analysis in MMM patients. Compared with five normal subjects, spleen CD34-staining capillary vascular density (CVD) was 2.1-3.03 times higher than the upper range of normal in six of the 15 (40%) MMM patients. CD8-staining sinusoidal vascular density (SVD) was constantly normal or lesser than normal and was inversely correlated with CVD (R = -0.53; P = 0.04). In MMM patients who did not receive cytoreductive or radiation therapy in the month before splenectomy (n = 9), the CVD was a significant determinant of spleen size (R = 0.88; P = 0.04). In MMM patients, the number of spleen CD34 + haematopoietic stem cells was increased from 1.2 to 98 times the upper limit of normal, and predicted the expansion of CVD (R = 0.57; P = 0.03). A population of cells expressing the CD34 +/CD133 +/VEGFR-2 + angiopoietic phenotype was present in the blood and spleen of five of seven patients. These results document that neoangiogenesis is an integral component of spleen re-localization of haematopoietic stem cells and suggest a cellular mechanism for spleen neoangiogenesis.

Original languageEnglish
Pages (from-to)618-625
Number of pages8
JournalBritish Journal of Haematology
Volume124
Issue number5
DOIs
Publication statusPublished - Mar 2004

Keywords

  • Angiogenesis
  • CD34 cells
  • Myelofibrosis
  • Myeloid metaplasia
  • Spleen angiogenesis

ASJC Scopus subject areas

  • Hematology

Fingerprint Dive into the research topics of 'Spleen neoangiogenesis in patients with myelofibrosis with myeloid metaplasia'. Together they form a unique fingerprint.

  • Cite this