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.
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.