Neuron-specific enolase (gamma enolase, gamma-gamma dimer) expression in Hodgkin's disease and large cell lymphomas

Background. The presence of gamma-enolase, gamma gamma dimer, or neuron-specific enolase (NSE) has been demonstrated in miscellaneous tumors, including malignant lymphomas. Up to now thee results have been interpreted as non-specific, although NSE can be expressed by normal B and T lymphoid cells at a particular stage of differentiation. The aim of the present study was to investigate the expression of NSE in a large series of malignant lymphomas, including Hodgkin's disease, in relation to morphology and immunophenotype. Materials and Methods. Frozen and paraffin embedded sections from 16 cases of Hodgkin's disease (4 lymphocyte predominance, nodular; 4 mixed cellularity; 6 nodular sclerosis; 2 lymphocyte depletion) and 35 cases of non-Hodgkin's lymphomas were investigated in order to evaluate the expression of NSE, its specificity and correlation to immunophenotype or other immunological cell markers. Among the non-Hodgkin's lymphomas, there were 9 Anaplastic Large Cell (CD30+) Lymphomas; 2 Peripheral Large T-Cell Lymphomas; 22 Diffuse Large B-Cell Lymphomas and 2 Primary Mediastinal Large B-Cell Lymphomas. Results. In Hodgkin's disease, NSE showed a diffuse cytoplasmic reaction in Cd30+ Reed-Sternberg cells, whereas the "popcorn" (L&H) cells of lymphocyte predominance, nodular variant cases, were always negative. Among the non-Hodgkin's lymphomas, NSE positivity was found only in lymphomas expressing CD30. All the other cases were negative. No relationship was found between NSE and B- or T-immunophenotype Conclusions. Our results suggest that a link between NSE and CD30 expression exists in malignant lymphomas. However, at the moment this has not been sufficiently investigated and is subject to speculation.

BACKGROUND: The presence of gamma-enolase, gamma gamma dimer, or neuron-specific enolase (NSE) has been demonstrated in miscellaneous tumors, including malignant lymphomas. Up to now these results have been interpreted as non-specific, although NSE can be expressed by normal B and T lymphoid cells at a particular stage of differentiation. The aim of the present study was to investigate the expression of NSE in a large series of malignant lymphomas, including Hodgkin's disease, in relation to morphology and immunophenotype. MATERIALS AND METHODS: Frozen and paraffin embedded sections from 16 cases of Hodgkin's disease (4 lymphocyte predominance, nodular; 4 mixed cellularity; 6 nodular sclerosis; 2 lymphocyte depletion) and 35 cases of non-Hodgkin's lymphomas were investigated in order to evaluate the expression of NSE, its specificity and correlation to immunophenotype or other immunological cell markers. Among the non-Hodgkin's lymphomas, there were 9 Anaplastic Large Cell (CD30+) Lymphomas; 2 Peripheral Large T-Cell Lymphomas; 22 Diffuse Large B-Cell Lymphomas and 2 Primary Mediastinal Large B-Cell Lymphomas. RESULTS: In Hodgkin's disease, NSE showed a diffuse cytoplasmic reaction in CD30+ Reed-Sternberg cells, whereas the "popcorn" (L&H) cells of lymphocyte predominance, nodular variant cases, were always negative. Among the non-Hodgkin's lymphomas, NSE positivity was found only in lymphomas expressing CD30. All the other cases were negative. No relationship was found between NSE and B- or T-immunophenotype. CONCLUSIONS: Our results suggest that a link between NSE and CD30 expression exists in malignant lymphomas. However, at the moment this has not been sufficiently investigated and is subject to speculation.