Abstract
To investigate the differences in Langerhans cells (LCs) populations between HIV-positive and negative anal squamous cell carcinomas patients. Twenty five patients (14 HIV-positive and 11 HIV-negative) were evaluated. Paraffin-block transversal thin sections from biopsies of anal squamous cell carcinomas (ASCC) were stained using the anti-CD1A antibody that identifies activated LCs. LCs counts were performed using histometry at 20 different sites, at baseline in the ASCC cases. These were then compared with LCs counts in anal canal specimens from HIV-negative and positive patients without ASCC (controls groups). In patients with ASCC, the LC count was greater among HIV-negative individuals than among HIV-positive individuals (p<0.05). The LC count was greater in the control HIV-negative group than in HIV-positive patients with ASCC (p<0.05). There was a lower amount of activated LCs in HIV-positive patients with anal squamous cell carcinomas than in HIV-negative patients, thereby suggesting worsening of the immune response.
Highlights
Anal squamous cell carcinomas (ASCC) are 20 to 30 times less frequent than colorectal carcinomas[1]. They can be divided into anal canal tumors, present in 85% of such patients, and those of the anal verge, which are similar to skin carcinomas[2]
All of these patients were in stage II and IIIB, according to the TNM classification of the American Joint Committee on Cancer (AJCC)[25]
The maximum value for patient distribution in Group B was lower than the median value of the control HIV-negative group, and its median value was close to zero
Summary
Anal squamous cell carcinomas (ASCC) are 20 to 30 times less frequent than colorectal carcinomas[1]. A change in this epidemiological profile has been taken place since the onset of the AIDS epidemics. The incidence of this kind of tumor has increased among HIV-infected men aged 30 to 40 years who practice anal receptive sex[5,6]. In this group of patients, ASCC is 25 to 50 times more frequent than among HIV-negative men of the same age[7], suggesting that immunological suppression and HIV infection are important in carcinogenesis
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