These preliminary findings suggest an association between silicone breast prostheses and ALCL, although the absolute risk is exceedingly low due to the rare occurrence of ALCL of the breast (11 cases in The Netherlands in 17 years). These findings require confirmation in other studies.

We studied the relative importance of class I and class II major histocompatibility complex (MHC) immunoregulation in the control of Tand B-cell lymphomas induced by murine leukemia virus. Previously, we have described a mink cell focus-inducing (MCF) murine leukemia virus, MCF 1233, which induces not only lymphoblastic T-cell lymphomas but also follicle center cell or lymphoblastic B-cell lymphomas. We now report that the outcome of neonatal infection with MCF 1233 in H-2-congenic C57BL/10 and C57BL/6 mice is decisively influenced by the H-2 I-A locus. A total of 64% of H-2 I-Ak, d mice [B1O.BR, B10.D2, B10.A(2R), B10.A(4R), and B10.MBR] developed T-cell lymphomas after MCF 1233 infection (mean latency, 37 weeks). In contrast, H-2 I-Ab [B10, B10.A(5R), B6], H-2 I_Ab/k [(B10.A x B10)F1 and (BlO x B10.A)F1], and H-2 * Corresponding author.

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We present the case of a 63-year-old Caucasian male who complained of persistent rhinitis and sinusitis accompanied by a total left-sided nasal blockage. The diagnosis nasal T/NK cell lymphoma was established by histopathological investigation. This case was diagnosed as stage IE lymphoma as no other sites were involved. The patient was treated with CHOP (cyclophosfamide, doxorubicin, vincristin and prednisone) chemotherapy and involved-field radiotherapy. The nasal T/NK cell lymphoma is a rare malignancy, which is known to have an extremely aggressive and destructive course. The mainstay of treatment is locoregional radiotherapy combined with chemotherapy, depending on disease stage. A high index of clinical suspicion is imperative to ensure early diagnosis and ultimately improve disease outcome.

It is well established that MHC-restricted T cell responses decisively influence the outcome of virus infection (1-3). In the rejection of murine leukemia virus-induced lymphomas, Th and cytotoxic T (Tc) t cells are considered essential effector cells, besides the effects of MuLVspecific antibodies, which can neutralize the virus and inhibit its spread (reviewed in reference 4). Many attempts have been made to characterize the viral antigens that are important in recognition by murine leukemia virus (MuLV)-specific T cells. The presence of viral proteins on the cell surface of MuLV induced tumor cell lines has been documented in a number of serological studies. These cell surface viral proteins, which in processed form are potential target molecules for recognition by Th and Tc cells (5), include the viral env gene-encoded products gPr85env, gp70, and p15(E) and the gag gene-encoded gP95g°g, gP85g°g, p10, pp12, p30, and p15 (reviewed in reference 6). In addition to this, recent data indicate that viral proteins that are not detectable at the surface of cells by serology can also serve as targets for T cells (7). DNA-mediated gene transfer experiments, in which single MuW viral antigens together with particular MHC class I antigens were expressed in heterologous cell lines, and the availability of Tc clones have provided a more subtle analysis of MHC and viral antigen recognition (8, 9). A highly complex picture emerged from these studies, which collectively indicate that both MHC and non-MHC genes determine which viral antigens are recognized in the context of MHC.Recently, substantial progress has been made in the understanding of MHCrestricted recognition ofantigens by T cells. It now appears that T cells usually recognize relatively short antigenic peptides, derived by processing of the native antigen (10, 11). This holds for MHC class II-restricted antigen recognition at the surface of APC by Th cells, but also for MHC class I-restricted antigen recognition by Tc cells, which results in lysis of the antigenic peptide-bearing cells (7,12). The MHCpeptide interaction required for T cell recognition is rather MHC allele specific, which implies that the nature of viral antigens preferentially recognized differs from individual to individual (7,(13)(14)(15)(16)(17) .

We performed a cytogenetic study on 16 murine mature B-cell lymphomas and 10 T-cell lymphomas, using G-banding techniques. All tumors, with the exception of 3 spontaneous B-cell tumors, were induced by various slowly transforming murine leukemia viruses (MuLV). Metaphases were obtained from primary (10 B-cell tumors) and first or second transplant generation lymphomas (6 B-cell and 10 T-cell tumors), all of which were well characterized with respect to phenotypic, histologic and genotypic features. In the T-cell tumors we found relatively simple karyotypic abnormalities, including various numerical aberrations, such as trisomy 15, in line with many earlier reports. However, the majority of B-cell tumors showed a great variety of both structural and numerical chromosomal anomalies. Three B-cell lymphomas had an apparently normal karyotype. No single cytogenetic abnormality occurred commonly in the B-cell lymphomas, but some structural abnormalities were found in more than one stemline, in particular, ins (II) (A1; A2) in 3 tumors, and deletions involving the D-region of chromosome 14 in 3 other lymphomas. These cytogenetic results clearly indicate that the pathogenic mechanisms involved in MuLV-induced (long latency) B-cell lymphomagenesis and (short latency) T-cell lymphomagenesis differ considerably.