Anal cancer is responsible for approximately 2.1% of digestive system malignancies with 6230 new cases estimated in the United States in 2012 (1). Anal cancer was once believed to be caused by chronic inflammation of the anal canal and treated with abdominoperineal resection (APR). Research has now shown that the development of anal cancer is associated with human papillomavirus (HPV) infection and has a pathophysiology similar to that of cervical cancer. Concurrent chemotherapy and external beam radiation therapy (EBRT) regimens have essentially replaced APR as primary treatment and have allowed for a great majority of patients to be cured with preservation of the anal sphincter.
The anal canal extends from the junction of the puborectalis portion of the levator ani muscle and the external anal sphincter to the anal verge. The length of the canal averages 4 cm. The anal canal is divided by the transitional zone, or dentate line, which represents the transition from squamous mucosa to glandular mucosa. There is no easily identifiable landmark between the rectum and anus, so clinicians should rely on the pathologic classification of tumors in this area rather than surgical or endoscopic classification. Anal cancers are primarily keratinizing or non-keratinizing squamous cell carcinomas. Adenocarcinomas of the anal canal comprise about 20% of anal tumors, and share the natural history of rectal adenocarcinomas and should be treated as such.
There are two sites of lymphatic drainage from the anal canal. Tumors above the dentate line drain to the perirectal and perivertebral nodes, while tumors below the dentate line drain to the inguinal and femoral lymph nodes. For this reason, patients who present with anal masses should undergo examination of the inguinal lymph nodes, and patients who present with squamous cell cancers in the inguinal lymph nodes should be evaluated for primary anal tumors.
The incidence of anal cancer has been rising in the United States. In a review of the SEER database from 1973 to 2000, the incidence of anal cancer in men and women has risen from 1.06 and 1.39 per 100,000 persons to 2.04 and 2.06 per 100,000 persons (2). In 2013, an estimated 7,060 cases were diagnosed in the United States. Although the incidence of anal cancer has risen in both sexes, the rate of rise for men is higher, particularly in patients diagnosed with HIV (3, 4). This increase in incidence may be due to better screening techniques and an increased rate of risk factors for anal cancer within the U.S. population that has occurred over time. Survival for patients with anal cancer is consistently worse for men compared to women and for black patients compared to white patients. Several risk factors have been associated with anal cancer: