Int J Colorect Dis (1990) 5:219 222
Col6ree/al Disease 9 Springer-Verlag 1990
Clinical and pathological correlates of HPV type 16 DNA in anal cancer J.H. Scholefield t, j.G. Palmer 2, N . A . Shepherd 3, S. Love 4, K.J. Miller 1 and J . M . A . Northover 1 1 2 3 4
1CRF Cotorectal Unit, St. Mark's Hospital, London Cumberland Infirmary, Carlisle Gloucestershire Royal Hospital, Gloucester Department of Research Statistics, Imperial Cancer Research Fund, Lincoln's Inn Fields, London, UK
Accepted: 23 August 1990
Abstract. The aetiology o f anal s q u a m o u s cell c a r c i n o m a (SCC) has recently been associated with a sexually transmissible agent - h u m a n papillomavirus (HPV) type 16. In this study clinical and pathological data f r o m a prospective series o f 67 anal SCC collected over a three year period were c o m p a r e d with the H P V type 16 D N A content o f these t u m o u r s to determine whether any o f the clinical o r histological parameters m i g h t predict H P V D N A content in a t u m o u r specimen. O f twelve clinicopathological variables examined n o n e was significantly correlated with H P V D N A c o n t e n t at the p = 0.01 level.
Introduction Evidence o f an association between certain types o f hum a n papillomavirus (HPV) and s q u a m o u s cell c a r c i n o m a o f the uterine cervix is b e c o m i n g increasingly compelling [1]. A t least nine types o f H P V have been identified in association with genital neoplasia, o f which only four are c o m m o n l y encountered in the U n i t e d K i n g d o m . H P V types 6 and 11 are associated with genital warts and some intra-epithelial neoplastic lesions o f the cervix and vulva [2]. H P V types 16 and 18, on the other hand, are f o u n d in association with intra-epithelial neoplasia and invasive cervical, vulval and penile carcinomas [3, 4]. Epidemiological evidence has suggested that anal cancer m a y be associated with a sexually transmissible agent [5, 6]. In the m o s t detailed o f these studies [7] a history o f receptive anal intercourse in males was f o u n d to be associated with anal cancer, c o m p a r e d to controls with colon cancer. This study also showed that cases o f anal cancer o f either sex h a d an increased relative risk o f being smokers and o f a previous history o f genital warts. E m b r y o l o g i c a l parallels between the epithelium o f the cervix and anal canal and the association between papillomaviruses and cervical carcinoma, suggest that H P V type 16 D N A might be involved in the aetiology o f anal s q u a m o u s cell c a r c i n o m a (SCC). This thesis has been tested by examining a series o f anal s q u a m o u s cell car-
cinomas, low rectal carcinomas and n o r m a l anal epithelium using Southern blot analysis and in situ hybridisation [8]. A highly statistically significant association between the presence o f H P V type 16 D N A and anal s q u a m o u s cell c a r c i n o m a was d e m o n s t r a t e d and a n u m ber o f parallels with H P V - a s s o c i a t e d cervical c a r c i n o m a were shown. Several other authors have reported a similar finding in small n u m b e r s o f cases [9-12]. The present study reports a univariate and multivariate analysis o f clinical and histological parameters which might predict the presence o f H P V D N A in these tum o u r s in a prospective series o f 67 perianal SCCs.
Materials and methods Patients were recruited to this study from our own clinical practice and from other surgeons around the UK who knew of our interest in anal cancer. More recently a number of cases have been referred from the UKCCCR Anal Cancer Trial. Clinical details of each patient were collected retrospectively from the medical staff involved in the care of each patient. In addition to basic demographic data including marital status, the following details were collected for each case: presenting complaint, smoking, sexual orientation, previous history of sexually transmissible diseases including genital condylomata, parity, size and site of tumour, systemic spread and operative procedure. Since so many variables were being correlated the level of statistical significance was taken as p =
Col6ree/al Disease 9 Springer-Verlag 1990
Clinical and pathological correlates of HPV type 16 DNA in anal cancer J.H. Scholefield t, j.G. Palmer 2, N . A . Shepherd 3, S. Love 4, K.J. Miller 1 and J . M . A . Northover 1 1 2 3 4
1CRF Cotorectal Unit, St. Mark's Hospital, London Cumberland Infirmary, Carlisle Gloucestershire Royal Hospital, Gloucester Department of Research Statistics, Imperial Cancer Research Fund, Lincoln's Inn Fields, London, UK
Accepted: 23 August 1990
Abstract. The aetiology o f anal s q u a m o u s cell c a r c i n o m a (SCC) has recently been associated with a sexually transmissible agent - h u m a n papillomavirus (HPV) type 16. In this study clinical and pathological data f r o m a prospective series o f 67 anal SCC collected over a three year period were c o m p a r e d with the H P V type 16 D N A content o f these t u m o u r s to determine whether any o f the clinical o r histological parameters m i g h t predict H P V D N A content in a t u m o u r specimen. O f twelve clinicopathological variables examined n o n e was significantly correlated with H P V D N A c o n t e n t at the p = 0.01 level.
Introduction Evidence o f an association between certain types o f hum a n papillomavirus (HPV) and s q u a m o u s cell c a r c i n o m a o f the uterine cervix is b e c o m i n g increasingly compelling [1]. A t least nine types o f H P V have been identified in association with genital neoplasia, o f which only four are c o m m o n l y encountered in the U n i t e d K i n g d o m . H P V types 6 and 11 are associated with genital warts and some intra-epithelial neoplastic lesions o f the cervix and vulva [2]. H P V types 16 and 18, on the other hand, are f o u n d in association with intra-epithelial neoplasia and invasive cervical, vulval and penile carcinomas [3, 4]. Epidemiological evidence has suggested that anal cancer m a y be associated with a sexually transmissible agent [5, 6]. In the m o s t detailed o f these studies [7] a history o f receptive anal intercourse in males was f o u n d to be associated with anal cancer, c o m p a r e d to controls with colon cancer. This study also showed that cases o f anal cancer o f either sex h a d an increased relative risk o f being smokers and o f a previous history o f genital warts. E m b r y o l o g i c a l parallels between the epithelium o f the cervix and anal canal and the association between papillomaviruses and cervical carcinoma, suggest that H P V type 16 D N A might be involved in the aetiology o f anal s q u a m o u s cell c a r c i n o m a (SCC). This thesis has been tested by examining a series o f anal s q u a m o u s cell car-
cinomas, low rectal carcinomas and n o r m a l anal epithelium using Southern blot analysis and in situ hybridisation [8]. A highly statistically significant association between the presence o f H P V type 16 D N A and anal s q u a m o u s cell c a r c i n o m a was d e m o n s t r a t e d and a n u m ber o f parallels with H P V - a s s o c i a t e d cervical c a r c i n o m a were shown. Several other authors have reported a similar finding in small n u m b e r s o f cases [9-12]. The present study reports a univariate and multivariate analysis o f clinical and histological parameters which might predict the presence o f H P V D N A in these tum o u r s in a prospective series o f 67 perianal SCCs.
Materials and methods Patients were recruited to this study from our own clinical practice and from other surgeons around the UK who knew of our interest in anal cancer. More recently a number of cases have been referred from the UKCCCR Anal Cancer Trial. Clinical details of each patient were collected retrospectively from the medical staff involved in the care of each patient. In addition to basic demographic data including marital status, the following details were collected for each case: presenting complaint, smoking, sexual orientation, previous history of sexually transmissible diseases including genital condylomata, parity, size and site of tumour, systemic spread and operative procedure. Since so many variables were being correlated the level of statistical significance was taken as p =
