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This section features synopses of pertinent practical publications that appear in Pathology journals in the respective sub-specialties. The summaries are mere guidelines and personal opinions of the two authors. The articles selected are diverse but occasionally reflect the authors' bias and are from the more widely read pathology journals. It is not intended to be an assiduous search of every publication in every Pathology journal, but more of a general indication of some of the monthly highlights through the eyes of the authors.
Hopefully, these snippets will provide the reader with enough to glean some facts and tips, as well as encourage them to read the entire article if necessary.
British Journal of Haematology
Bock O, Muth M, Theophile K, et al. Identification of new target molecules PTK2, TGFBR2 and CD9 overexpressed during advanced bone marrow remodelling in primary myelofibrosis. Br J Haematol 2009;146:510–20.
Primary myelofibrosis is characterised by angiogenesis and fibrosis within the bone marrow and bone remodelling. As the disease progresses, stromal changes preclude bone marrow aspiration and investigation of the underlying molecular mechanisms. In this innovative paper, the authors develop a low-density array to study 45 candidate genes. There was increased expression of 11 of these genes, which were in turn associated with matrix components, collagen processing, matrix synthesis and stroma remodelling. Three genes were of particular interest. The TGFβ type II receptor (TGFBR2) showed increased expression in primary myelofibrosis, in contrast to other myeloproliferative disorders, and may be of diagnostic significance. In concert with protein kinase 2 and CD9, TGFBR2 provides a positive feedback loop to drive angiogenesis and stroma remodelling. The interruption of this loop may be a therapeutic strategy and warrants further investigation.
Nteliopoulos G, Marley SB, Gordon MY. Influence of PI-3K/Akt pathway on Wnt signalling in regulating myeloid progenitor cell proliferation. Evidence …
Provenance and peer review Not commissioned; not externally peer reviewed.
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