Volumen: 17 # Number : 1
Publication Date : Enero - Abril Year: 2013
Authors: Carlos Ponzinibbio
Abstract: More than a century passed since its initial morphological
recognition as an indicator of Hodgkin’s lymphoma until the clarification of the origin of Hodgkin and Reed-Sternberg cell in a B-cell that failed in its genetic recombination
during germinal-central somatic hypermutation. After establishing the cell’s origin entity and clonality, it was still needed to explain the mechanisms by which it escapes apoptosis and stimulates proliferation. The aberrant phenotypic expression of HRS cells and the constitutive
activation of signaling channels, such as NF-kB and JAK- STAT, partly helped explain these mechanisms. The discovery of the Epstein-Barr virus as a pathogenic mechanism in almost half of the cases also helped find an explanation. The remarkable interaction of HRS cells with cellular microenvironment, in which scarce tumor cells have vast potential over the stroma that constitutes most of the tumor mass, is also subject to analysis and the mutual interdependence has been made clear through the production of multiple cyto and chemokines.
Key words: Reed Stenberg cell, Hodgkin´s lymphoma, Apoptosis.
Pages : 46-54
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