FAP patients occasionally have extracolonic mani- festations, which can be life threatening. Our patient has survived without recurrent malignancy. We emphasize that patients with APC mutations should undergo careful follow-up examination of other organ systems, including the alimentary tract, gynaecological organs and biliary system, to ensure relatively long survival, as in the present case. H Hirano A Okimura K Nakasho T Nishigami K Uematsu K Tamura 1 The Second Department of Pathology and 1 Laboratory of Hereditary Tumours, Institute for Advanced Medical Sciences, Hyogo College of the Medicine, Hyogo, Japan 1. Garber JE. Follow-up study of a family group exhibiting dominant inheritance for a syndrome including intestinal polyps, osteomas, fibromas and epidermal cysts. Am. J. Hum. Genet. 1962; 14; 1376– 1390. 2. Gurbuz AK, Giardiello FM, Petersen GM et al. Desmoid tumours in familial adenomatous polyposis. Gut 1994; 35; 377–381. 3. Lees CD, Hermann RE. Familial polyposis coli associated with bile duct cancer. Am. J. Surg. 1981; 141; 378–380. 4. Honore LH, Davey SJ. Endometrial carcinoma in young women. A report of four cases. J. Reprod. Med. 1989; 34; 845–849. 5. Beroud C, Soussi T. APC gene: database of germline and somatic mutations in human tumors and cell lines. Nucleic Acids Res. 1996; 24; 121–124. 6. Knudson AG Jr. Mutation and cancer: statistical study of retino- blastoma. Proc. Natl Acad. Sci. USA 1971; 68; 820–823. Familial pleural mesothelioma with environmental asbestos exposure: losses of DNA sequences by comparative genomic hybridization (CGH) Sir: Familial clustering of malignant mesothelioma (MM) is well-documented. 1 In most families, meso- thelioma develops among related individuals, in asso- ciation with asbestos exposure due to work or the domestic environment. More rarely, tumours have been diagnosed in related patients without evidence of asbestos exposure, indicating that the predisposition to MM might be expressed through different oncogenic pathways. To date, only two familial clusters have been genetically studied; Ascoli et al. 2 detected losses at 1p, 6q, 9p, 13q, and 14q chromosomes, while Musti et al. 3 found only a loss at 9p chromosome. In both families, a previous professional or residential exposure to asbestos was reported. These genetic alterations were similar to those observed in sporadic cases. 4 Here, we report on two cases of pleural MM affecting two young sisters (23 and 32 years old) of a nine- member family, who were environmentally exposed to asbestos. Their familial and clinical histories were previously described by Bisconti et al. 5 and Serio et al. 6 The patients were also affected with Marfan’s syn- drome and they died 39 and 24 months, respectively, after the histological diagnosis. In both cases, the histological features of the tumour were identified as deciduoid subtype, a rare morphological variant of epithelioid malignant mesothelioma (Figure 1a,c). We described it in a previously published paper in Histopathology. 6 We performed comparative genomic hybridization (CGH) on paraffin-embedded samples following a con- ventional technique. 7 CGH analysis showed largely concordant cytogenetic aberrations in both cases. Gains, including amplifica- tions, were more frequent than losses in both cases. In case 1 the amplified DNA sequences were on chromosomes 1p31.3-pter; 2q36-qter; 4p15.3-pter; 5p14-pter, q31.3-qter; 7q33-qter; 8q24.1-qter; 9q33- qter; 10q25.1-qter; 11q12-q13.3, q22.1-qter; 12q24.1- qter; 14q31-qter; 15q13-qter; 16q23-qter; 17 trisomy; 19 trisomy; 20 trisomy; 22q trisomy; in contrast, DNA losses were on chromosomes 6q12-q21 and 13q21.1- q22 (Figure 1b). In case 2 the amplifications were on chromosomes 1p31.3-pter; 4p15.3-pter; 5q33.2-qter; 8q24.1-qter; 10q25.1-qter; 11q12-q13.5, q22.2-qter; 12q24.1-qter; 15q22.2-q25; 16p11.2-p13.1; 17p11.2-p13, 17q tri- somy; 19 trisomy; 20q trisomy; 22q trisomy; while DNA losses were found on chromosomes 2q32.1-q33; 4p13-q21.1; 6q12-q14; 9p22-pter; and 13q21.1-q22 (Figure 1d). At present, the biology of this tumour is poorly understood. Unfortunately, previous cytogenetic studies have demonstrated dissimilar karyotypic abnormalities which could not serve as diagnostic markers in meso- theliomas. Nevertheless, some authors have shown, using different methods, loss or structural rearrange- ment of 1p, 3p, 4, 6q, 9p, 13q, 14q, 15q, 22q, and increases in chromosomes 5, 6p, 7, 8p, 15q, 17q, 19q, or 20q. 1,4 In our study, CGH analysis allowed the identification of critical chromosome regions possibly involved in the pathogenesis of the MM. Similar chromosomal altera- tions were found in both cases with identical amplified Correspondence 643 Ó 2004 Blackwell Publishing Ltd, Histopathology, 45, 642–656.