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Expression of heat shock proteins in classical Hodgkin lymphoma: correlation with apoptotic pathways and prognostic significance
Author(s) -
Santón Almudena,
GarcíaCosío Mónica,
Cristóbal Eva,
Pascual Alejandro,
Muriel Alfonso,
GarcíaLaraña José
Publication year - 2011
Publication title -
histopathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.626
H-Index - 124
eISSN - 1365-2559
pISSN - 0309-0167
DOI - 10.1111/j.1365-2559.2011.03803.x
Subject(s) - apoptosis , heat shock protein , hsp70 , lymphoma , cancer research , biology , heat shock , caspase , tissue microarray , poly adp ribose polymerase , hsp27 , caspase 3 , immunohistochemistry , microbiology and biotechnology , programmed cell death , immunology , polymerase , enzyme , biochemistry , gene
Santón A, García‐Cosío M, Cristóbal E, Pascual A, Muriel A & García‐Laraña J (2011) Histopathology 58, 1072–1080 Expression of heat shock proteins in classical Hodgkin lymphoma: correlation with apoptotic pathways and prognostic significanceAims: Heat shock proteins (HSPs), known to inhibit apoptosis and promote cellular survival, are overexpressed in many tumours. We analysed the expression of relevant HSPs and heat shock factor 1 (HSF1) in classical Hodgkin lymphoma (cHL) and their relationship with caspase signalling pathways and patient outcome. Methods and results: Using tissue microarrays (TMAs), most cases showed strong immunohistochemical expression of HSPs [10, 27, 40, 60, 70, 90, 110, HO1, cell division cycle 37 homolog (CDC37) and HSF1, which points to cHL as a potential candidate to stress‐response inhibitors. Active caspases 3, 8 and 9 were detected in 55.1%, 55.4% and 96.2% of cases although cleaved poly (ADP‐ribose) polymerase (PARP) was observed in only 16.1%, suggesting an improper functioning of apoptosis. Statistical analysis showed associations of HSP70 with active caspase 3 ( P = 0.000); HSP40 with active caspase 9 ( P = 0.031) and p53 ( P = 0.003); HO1 with p53 ( P = 0.006) and p21 ( P = 0.005); and p53 with p21 ( P = 0.015). Conclusions: Correlations between the expression of apoptotic markers and HSPs may suggest a role for the latter in modulating apoptosis in cHL, mainly through the HSP70‐HSP40 system, and in the stabilization of p53. Survival analyses showed that absence of active caspase 8 and HO1 had a negative impact in patient outcome.