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Background. The Epstein‐Barr virus (EBV) has been linked to several human malignancies, including Hodgkin's disease (HD). In addition, epidemiologic studies have shown differences in HD occurrence in different parts of the world. The authors studied 27 cases of Hodgkin's disease from Mexico to determine the prevalence of EBV in HD in this developing nation. Methods. The Epstein‐Barr virus was investigated using in situ hybridization with the EBER1 probe. Immunohistochemical studies were performed on paraffin sections. Cases from both adult and pediatric age groups were included. Correlations with histologic subtype, clinicopathologic features, and immunophenotype were determined. Results. Epstein‐Barr virus sequences were identified in 18/27 (67%) cases. Positivity correlated with histologic subtype: 0/1 lymphocyte predominant; 6/13 (46%) nodular sclerosis; 7/7 mixed cellularity (MC) (100%); and 5/6 (83%) lymphocyte depleted (LD). The proportion of cases classified as MC and LD (13 of 27) was greater than that found in the United States and other developed countries. The immunophenotypic profile was appropriate for Hodgkin's disease, with all cases of classic Hodgkin's disease positive for CD30 (Ber‐H2) and 18 cases expressing CD15. One case of lymphocyte‐predominant Hodgkin's disease was CD20 (L26)‐positive as were three cases of classic Hodgkin's disease. Patient age ranged from 5 to 65 years, with a median of 29 years. Conclusions. The EBV is associated highly with HD in Mexico, and this prevalence rate is found in all age groups. A strong correlation between EBV expression and histologic subtype was confirmed, with 92% of MC and LD subtypes found to be positive. Cancer 1995;75:1360‐6.

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Anaplastic large cell lymphoma (ALCL) is a subtype of CD30+ large T-cell lymphoma (TCL) that comprises ~2% of all adult non-Hodgkin lymphomas. Based on the presence/absence of the rearrangement and expression of anaplastic lymphoma kinase (ALK), ALCL is divided into ALK+ and ALK-, and both differ clinically and prognostically. This review focuses on the historical points, clinical features, histopathology, differential diagnosis, and relevant cytogenetic and molecular alterations of ALK- ALCL and its subtypes: systemic, primary cutaneous (pc-ALCL), and breast implant-associated (BIA-ALCL). Recent studies have identified recurrent genetic alterations in this TCL. In systemic ALK- ALCL, rearrangements in DUSP22 and TP63 are detected in 30% and 8% of cases, respectively, while the remaining cases are negative for these rearrangements. A similar distribution of these rearrangements is seen in pc-ALCL, whereas none have been detected in BIA-ALCL. Additionally, systemic ALK- ALCL—apart from DUSP22-rearranged cases—harbors JAK1 and/or STAT3 mutations that result in the activation of the JAK/STAT signaling pathway. The JAK1/3 and STAT3 mutations have also been identified in BIA-ALCL but not in pc-ALCL. Although the pathogenesis of these alterations is not fully understood, most of them have prognostic value and open the door to the use of potential targeted therapies for this subtype of TCL.