tion for EBER did not show any evidence of EBV infection. The bone marrow trephine biopsy, received following chemotherapy, was focally infiltrated by MCL but there was no evidence of HL. The unaffected marrow showed normal haematopoiesis. An attempt was made to demonstrate immunoglob- ulin gene rearrangements. Only fixed, processed tissue was available from this referral case. DNA was extrac- ted using a standard Proteinase K digestion procedure. It was unfortunately not possible to demonstrate gene rearrangements due to poor DNA quality, related to DNA degradation. The study of composite lymphoma cases provides an insight into the complex interrelationship between the different components of the lymphoid system. Studies of composite lymphomas using molecular techniques have shown them to demonstrate true biclonality as well as a common origin from the same clonal progenitor cell, suggesting different biological mecha- nisms in different tumours. 5 The derivation of classical HL from germinal centre or post germinal centre B cells has been established. The evidence that Reed–Sternberg cells are derived from a germinal centre B cell is supported by an investigation of a composite HL and a follicular B-cell NHL, in which most of the somatic mutations in the two types of lymphoma cells were identical 5 and a theoretical relationship between HL and NHL therefore exists. The extreme rarity of composite MCL and HD is perhaps not surprising considering the cells of origin of classical HL and MCL which are not thought to be closely related. Reed–Sternberg cells in classical HL are derived in more than 98% of cases from mature B cells at the germinal centre stage of differentiation. Mantle cell lymphoma is thought to be derived from naive CD5+ B cells (small resting lymphocytes), which circulate in the blood and occupy primary lymphoid follicles and follicle mantle zones. Our case showed an absence of CD5 staining in MCL, which is recognized. 6 It was necessary to confirm our morphological diagnosis by using immunohistochem- ical staining for cyclin D1 and FISH. HRS cells were negative for cyclin D1. This negative result does not help us in establishing the clonal relationship between the components of this composite lesion. If HRS cells had been shown to be positive for cyclin D1, it would have strongly suggested a clonal relationship. Composite lymphomas consisting of NHL and HL often show EBV positivity, 7,8 suggesting an origin from a common EBV-infected progenitor cell. Our case represents a distinct example of composite MCL and CHL showing negativity of all of the HRS cells within the tumour for EBV, as shown by in situ hybridization for EBV EBER. S J Hayes S S Banerjee 1 Y Cook 2 J B Houghton 3 L P Menasce 1 Department of Histopathology, Salford Royal Hospitals, Salford, 1 Department of Histopathology and 2 Department of Cytogenetics, Christie Hospital, Manchester, and 3 Department of Haematology, Salford Royal Hospitals, Salford, UK 1. Caleo A, Sa ´nchez-Aguilera A, Rodriguez S et al. Composite Hodgkin lymphoma and mantle cell lymphoma. Am. J. Surg. Pathol. 2003; 27; 1577–1580. 2. Tinguely M, Rosenquist R, Sundstro ¨m C et al. Analysis of a clonally related mantle cell and Hodgkin lymphoma indicates Epstein–Barr virus infection of a Hodgkin ⁄ Reed–Sternberg cell precursor in a germinal center. Am. J. Surg. Pathol. 2003; 27; 1483–1488. 3. Cachia AR, Diss TC, Isaacson PG. Composite mantle-cell lym- phoma and plasmacytoma. Hum. Pathol. 1997; 28; 1291– 1295. 4. Fend F, Quintanilla-Martinez L, Kumar S et al. Composite low grade B-cell lymphomas with two immunophenopypically distinct cell populations are true biclonal lymphomas. Am. J. Pathol. 1999; 154; 1857–1866. 5. Brauninger A, Hansmann M, Strickler JG et al. Identification of common germinal-center B-cell precursors in two patients with both Hodgkin’s disease and non-Hodgkin’s lymphoma. N. Engl. J. Med. 1999; 340; 1239–1246. 6. Watson P, Wood KM, Lodge A et al. Monoclonal antibodies recognizing CD5, CD10 and CD23 in formalin-fixed, paraffin- embedded tissue: production and assessment of their value in the diagnosis of small B-cell lymphoma. Histopathology 2000; 36; 145–150. 7. Jaffe ES, Zarate-Osorno A, Kingma DW, Raffeld M, Medeiros LJ. The interrelationship between Hodgkin’s disease and non-Hodg- kin’s lymphomas. Ann. Oncol. 1994; 5; S7–S11. 8. Kingma DW, Medeiros LJ, Barletta J et al. Epstein–Barr virus is infrequently identified in non-Hodgkin’s lymphomas associated with Hodgkin’s disease. Am. J. Surg. Pathol. 1994; 18; 48–61. Intracellular spread of Ewing’s sarcoma within skeletal muscle fibres: is there a role for cytotoxic tumour-infiltrating lymphocytes? DOI: 10.1111/j.1365-2559.2005.02297.x Sir: Intramyofibre invasion (IMI) is a particular pheno- menon in which malignant cells exhibit intracellular spread into skeletal muscle cells. According to Sarma, 1 Correspondence 623 Ó 2006 Blackwell Publishing Ltd, Histopathology, 48, 605–626.