No abstract

The use of registered names, trademarks etc. in this publication does not imply, even in the absence of a specific statement, that such names are exempt from the relevant laws and regulations and therefore free for general use.The publisher makes no representation, express or implied, with regard to the accuracy of the information contained in this book and cannot accept any legal responsibility or liability for any errors or omissions that may be made. Typesetting by EXPO Holdings, Malaysia 34/3830-543210 Printed on acid-free paper SPIN 10682008 DEDICATIONS To mum, Mike and especially to Andrew. DJH To Sue, Tim, Emma and mum, but particularly my father Peter, who sadly died during the preparation of this book. MTS

VIN is thought to be the precursor of some VSCCs because it is monoclonal, frequently occurs contiguously with VSCC and shares similar risk factors with a subgroup of VSCC. There has been no conclusive molecular evidence supporting this assumption. We performed X-chromosome inactivation analysis on 9 cases of lone VIN, 10 cases of VSCC and associated contiguous VIN and 11 cases of VSCC and associated noncontiguous VIN. Eight of the 9 cases of lone VIN appeared to be monoclonal. All 7 informative and monoclonal cases of VIN with contiguous VSCC and 6/9 informative cases of VIN with noncontiguous VSCC showed patterns of X-chromosome inactivation consistent with a common monoclonal origin for both VIN and VSCC. Two of the 9 cases of VIN with noncontiguous VSCC showed X-chromosome inactivation patterns consistent with a separate clonal origin. We performed LOH analysis at 6 chromosomal loci on these samples and 7 cases with lymph node metastases. Identical losses occurred 7 times in VIN and contiguous VSCC (random probability 1.2 ؋ 10 -9 ), twice in VIN and noncontiguous VSCC (random probability 1.5 ؋ 10 -3 ) and 3 times in VSCC and associated metastases (random probability 1.8 ؋ 10 -5 ). Some losses occurring in VSCC did not appear in the contiguous VIN or associated metastases and vice versa. These data provide molecular evidence that VIN is the precursor of VIN-associated VSCC, that multifocal disease may arise via either different clones or a single clone and that continued divergent clonal evolution may occur in vulval neoplasia. © 2002 Wiley-Liss, Inc. Key words: vulval intraepithelial neoplasia; vulval cancer; loss of heterozygosity; X-chromosome inactivation; vulval squamous cell carcinomaVIN has long been thought to be a premalignant condition that may progress to invasive VSCC. This assumption is based on observations that VIN frequently occurs contiguously with VSCC, 1 that VIN and a subgroup of VSCC are associated with similar risk factors (smoking, 2 immunosuppression 3 and HPV infection 2,4 ) and that VIN and VSCC are monoclonal neoplastic conditions. 5,6 Confirmation of this hypothesis is important for gaining insight into the process of vulval carcinogenesis. Furthermore, identifying molecular markers for risk of progression of VIN to VSCC is possible only if molecular evidence is compatible with a common monoclonal origin of the 2 conditions. We first wanted to confirm that VIN is a monoclonal condition. We then wanted to document the patterns of LOH events and X-chromosome inactivation in VSCC samples and contiguous and noncontiguous VIN, to examine whether VIN and VSCC could have arisen from the same clone. Because we had already studied the frequency of LOH at 6 chromosomal loci in lone VIN and VSCC, 7 it was possible to calculate the odds of identical losses occurring by chance in both VSCC and associated VIN. Finally, as primary cancers and their metastases are thought to have the same clonal origin, we compared the number of identical losses occurring in primaries and their metastases with the...

We describe two patients, who presented with erythematous facial plaques, in keeping with neutrophilic eccrine hidradenitis, during chemotherapy for acute myeloid leukaemia. Both patients were neutropaenic and febrile. Histology showed a dermal neutrophilic infiltrate around the eccrine glands with gland destruction. The importance of recognizing this disorder is to prevent the inappropriate use of antibiotics as it is self limiting.