Presencia del virus de Epstein-Barr en casos colombianos de linfoma de Hodgkin y su relación con la respuesta al tratamiento.

Sandra Quijano, Carlos Saavedra, Susana Fiorentino, Oscar Orozco, María Mercedes Bravo

Producción: Contribución a una revistaArtículorevisión exhaustiva

7 Citas (Scopus)

Resumen

The role of Epstein-Barr virus as etiologic agent in Hodgkin lymphoma (HL) development has been supported by the detection of viral DNA in the Reed-Sternberg cell in a subset of HL, and the high levels of latent membrane protein 1 expression in these tumors. To gain further evidence of this relationship, lymph nodes from 67 patients with HL were analyzed for the presence of Epstein-Barr virus using EBERs in situ hybridization and LMP-1 immunohistochemistry. Virus presence was related to histological subtype, patients' treatment response and tumor infiltrating lymphocytes phenotype. EBERs transcripts were found in 67% of the cases and LMP-1 in the Reed-Sternberg tumor cells at a 56.7% rate. The prevalence, as determined by histological subtype, was 69.81% for nodular sclerosing, 85.71% for mixed cellularity and 40% for lymphocyte-rich. Epstein-Barr virus presence was more frequent in children (84.2%) in comparison with adults (60.4%). Positive patients presented higher failure-free survival rates than Epstein-Barr virus negative patients. CD4 positive infiltrating T cells were present in a higher proportion in relation to CD8 positive T infiltrating cells, the mean percentages for both subsets were higher in Epstein-Barr virus positive cases. A high percentage of Epstein-Barr virus was present in HL with a probable association with treatment response. This suggests an application of Epstein-Barr virus detection to use as a prognosis marker in treatment response for HL cases.

Título traducido de la contribuciónEpstein-Barr virus presence in Colombian Hodgkin lymphoma cases and its relation to treatment response
Idioma originalEspañol
Páginas (desde-hasta)163-173
Número de páginas11
PublicaciónBiomedica
Volumen24
N.º2
DOI
EstadoPublicada - jun. 2004
Publicado de forma externa

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