Version May 2024
INTRODUCTION — Anal cancer is uncommon, with less than 1000 new cases diagnosed annually in the United States [1]. Data on worldwide incidence are available from the GLOBOCAN database.
The incidence of anal cancer in the general population has increased over several decades, both in the United States and elsewhere. An increased incidence has been associated with female sex, infection with human papillomavirus (HPV), lifetime number of sexual partners, genital warts, cigarette smoking, receptive anal intercourse, and infection with HIV [2]. Thus, from an etiologic standpoint, anal cancer is more similar to genital malignancies than it is to gastrointestinal tract cancers.
The pathology and epidemiology of anal cancer will be reviewed here. The clinical features, diagnosis, and treatment are discussed separately. (See "Clinical features and staging of anal cancer".)
ANATOMY AND TYPES OF TUMORS — The anal canal is 2.5 to 3.5 cm long. It begins where the rectum enters the puborectalis sling at the apex of the anal sphincter complex (palpable as the anorectal ring on digital rectal examination and approximately 1 to 2 cm proximal to the dentate line) and ends where the squamous mucosa blends with the perianal skin, which roughly coincides with the palpable intersphincteric groove or the outermost boundary of the internal sphincter muscle (figure 1). Externally, the anal canal is surrounded by the internal and external anal sphincter muscles (figure 1) [3]. The anal canal is divided by the dentate (pectinate) line, a macroscopically visible landmark that overlies the transition from glandular to squamous mucosa; immediately proximal to the dentate line, a narrow zone of transitional mucosa that is similar to urothelium is variably present.
The proximal region of the anus encompasses mucosa of three different histologic types: glandular, transitional, and nonkeratinizing squamous (proximal to distal, respectively). Distally, the squamous mucosa (which is devoid of epidermal appendages, such as hair follicles, apocrine glands, and sweat glands) merges with the perianal skin (true epidermis). This mucocutaneous junction has been referred to as the anal "verge" or margin. This boundary is indistinct on macroscopic examination, and anatomically, its location may vary with the patient's body habitus.
As a result, four distinct categories of tumors arise in the anal region:
●Tumors that develop from any of the three types of mucosa, which cannot be visualized in their entirety while gentle traction is placed on the buttocks, are termed anal cancers [3]:
•Tumors arising in the transitional or squamous mucosa are squamous cell cancers (SCCs) and appear to behave similarly, despite their sometimes variable morphologic appearance. By convention, most series that report outcomes of "anal cancer" refer exclusively to these tumors. The term "anal cancer," by common definition, refers to SCCs arising within the mucosa of the anus, and the two terms will be used interchangeably throughout this review.
•Basaloid (also termed junctional or cloacogenic) carcinoma is a variant of SCC that arises from the epithelial transitional zone. However, these terms have largely been abandoned because these tumors are now recognized as nonkeratinizing types of SCC. Tumors arising within the anal canal above the dentate line are often nonkeratinizing SCCs, while those arising within the anal canal distal to the pectinate (dentate) line are often keratinizing.
•Adenocarcinomas arising from glandular elements within the anal canal are rare, but they appear to share a similar natural history to rectal adenocarcinomas and are treated similarly, with resection plus either preoperative or postoperative chemoradiotherapy. (See "Treatment of anal cancer", section on 'Anal adenocarcinoma'.)
●Tumors arising within the hair-bearing skin at or distal to the squamous mucocutaneous junction have been referred to as anal margin cancers. However, the most recent (eighth) edition of the American Joint Committee on Cancer (AJCC) cancer staging manual and the fifth edition of the World Health Organization (WHO) classification of tumors of the digestive system define tumors that arise within the skin at or distal to the squamous mucocutaneous junction that can be seen in their entirety with gentle traction placed on the buttocks and are within 5 cm of the anus as perianal skin cancers [3,4]. In practice, perianal skin cancers are rare. Most are treated similarly to anal canal cancers, with radiation therapy (RT) and concurrent chemotherapy. However, local treatment (surgery or local RT [electrons]) is used only when the lesion is very separate from the anal verge and is a discrete skin lesion. (See "Treatment of anal cancer", section on 'True perianal skin cancers'.)
●Primary rectal SCCs, which are very rare, can be difficult to distinguish from anal cancers. They are generally treated according to the same approach as anal cancer. (See "Treatment of anal cancer", section on 'Rectal squamous cell cancers'.)
Histology — Several histologic types of epithelial malignancy arise within the anus, including SCCs (which are the most common), adenocarcinomas, and neuroendocrine tumors (table 1). Due to the variation in anatomy (particularly the transition zone), the anal canal can be quite short in length in some individuals, and the anatomical location as determined by a surgeon or endoscopist should not determine the classification of a tumor. Rather, the histology and location of tumors in the anal region guide the appropriate diagnosis and treatment.
Anal canal tumors — There is no easily identifiable landmark between the rectum and the anus; in addition, the transition zone has a widely variable histologic appearance. As a result, the pathologic classification of tumors arising in this area may be difficult.
●Squamous cell cancer – Tumors arising in the transitional or squamous mucosa are SCCs and appear to behave similarly, despite their sometimes variable morphologic appearance [5,6]. By convention, most series that report outcomes of "anal cancer" refer exclusively to these tumors. The term "anal cancer," by common definition, refers to SCCs arising within the mucosa of the anus, and the two terms will be used interchangeably throughout this review.
Basaloid features are identified in approximately 25 percent of SCCs of the anal canal and must be distinguished from basal cell carcinomas of the perianal skin, which as noted below, are classified as skin cancers. Basaloid (also termed junctional or cloacogenic) carcinoma is a variant of SCC that arises from epithelial transitional zone. However, these terms have largely been abandoned because these tumors are now recognized as nonkeratinizing types of SCC. Tumors arising within the anal canal above the dentate line are termed nonkeratinizing SCCs, while those arising within the anal canal distal to the dentate line are termed keratinizing SCCs.
●Adenocarcinomas – Adenocarcinomas arising from glandular elements within the anal canal are rare, but they appear to share a similar natural history to rectal adenocarcinomas and are treated similarly. (See "Treatment of anal cancer", section on 'Anal adenocarcinoma'.)
Determination of the anatomic site of origin of carcinomas that overlap the anorectal junction can be problematic, particularly since the rectal mucosa may extend to within 1 to 2 cm of the anal verge.
Perianal skin cancers — The clinical distinction between tumors of the anal canal and those that involve the anal "margin" or perianal skin can also be difficult. As noted above, SCCs that arise on any mucosal surface of the anus are treated as anal canal cancers, even if they are located distally at the perianal margin. In contrast, tumors arising within the hair-bearing skin at or distal to the squamous mucocutaneous junction have been termed anal margin cancers. However, the preferred term is perianal skin cancer, since with the exception of melanomas, tumors arising within the perianal skin behave biologically like skin cancers. Although there are essentially no prospective data validating this practice, these tumors had been classified and staged as skin cancers, rather than anal canal cancers, until more recently [7]. The most recent (eighth) edition of the AJCC cancer staging manual and the most recent (fifth) edition of the WHO classification of tumors depart from this practice and stage perianal skin cancers the same as anal cancers (table 2) [3].
Most clinicians treat SCC lesions of the perianal skin similarly to anal canal cancers, using RT and concurrent chemotherapy. Local treatment (surgery, or local RT [electrons]) is appropriate when the lesion is very separate from the anal verge and is a discrete skin lesion. However, it can be very difficult to distinguish between tumors arising on the hair-bearing skin or within the anus/anal cancer. In practice, the distinction between perianal skin cancers and anal canal/margin cancers can be difficult, and the default management by most clinicians is to assume that these are anal margin/canal cancers if there is any doubt, and to treat with initial chemoradiotherapy rather than local therapy alone. (See "Treatment of anal cancer", section on 'True perianal skin cancers'.)
Tumors of the perianal skin are most often SCCs, but other types of cutaneous malignancies (eg, basal cell carcinoma, melanoma, Bowen disease, extramammary Paget disease) can arise within this region.
●Bowen disease (SCC in situ) can occur within the perianal skin as it can in other areas of non-sun-exposed skin. (See "Cutaneous squamous cell carcinoma (cSCC): Clinical features and diagnosis".)
●Melanomas that arise in either the anal canal or perianal skin should be treated according to the same principles commonly applied to this tumor at other sites. (See "Surgical management of primary cutaneous melanoma or melanoma at other unusual sites".)
●Paget disease of the anus, an intraepithelial adenocarcinoma, can be one of two types: a primary cutaneous malignancy in which the tumor cells show sweat gland differentiation, and a lesion in which there is involvement of adjacent squamous epithelium by lateral intramucosal/intraepithelial spread from an underlying adenocarcinoma of the rectum or perianal glands.
Lymphatic drainage — Lymphatic drainage of anal canal and perianal skin cancers is dependent upon the anatomic site of origin (figure 1) [8-10]. Tumors originating above the dentate line, similar to rectal cancers, drain to the mesorectal and internal iliac nodes. In contrast, tumors arising below the dentate line may also spread to the superficial inguinal and external iliac (deep inguinal) nodes. In contrast to earlier editions, in the eighth edition of the AJCC/Union for International Cancer Control (UICC) staging system, metastases in the inguinal, mesorectal, internal, or external iliac are all considered N1 nodes (table 2).
EPIDEMIOLOGY AND RISK FACTORS — Although it remains an uncommon cancer, the incidence of anal cancer is increasing in the United States and other countries [11-16]. In data derived from the United States Cancer Statistics dataset, between 2001 and 2015, incidence rates (IR) for anal squamous cell cancer (SCC) increased 2.7 percent per year, and the most pronounced increases were in young Black males and older females between the ages of 60 and 69 [16]. Stage distribution also changed over this time frame, with a tripling in the incidence of distant-stage disease (annual percentage change in males 8.6 percent and in females 7.5 percent) and a doubling of regional (nodal)-stage disease. The analysis also revealed a concomitant increase in mortality over this same time period (3.1 percent increase per year), with significant increases in groups age 50 and older. The reasons underlying the increased incidence and mortality remain unclear, but anal cancer is one of the fastest accelerating causes of cancer incidence and mortality in the United States, and it may surpass cervical cancer to become the leading human papillomavirus (HPV)-linked cancer in older adult females.
In certain populations, such as males who have sex with other males (MSM) and HIV-infected patients, there is an especially high incidence of anal cancer. The rate of anal cancer was estimated to be as high as 37 per 100,000 among MSM prior to the HIV epidemic [17], rendering its incidence in this population similar to that of cervical cancer in females prior to the introduction of cervical Papanicolaou (Pap) smear screening [6]. The incidence of anal cancer among HIV positive MSM has been estimated to be approximately twice that of HIV negative MSM [18,19].
In contrast to other common malignancies affecting HIV positive individuals (eg, Kaposi sarcoma and non-Hodgkin lymphoma), the incidence of anal cancer has not declined in the era of potent antiretroviral therapy (formerly referred to as highly active antiretroviral therapy [HAART]) [20,21]. This was demonstrated in a study in San Francisco County, in which the age-adjusted incidence of anal cancer in males 40 to 64 years of age (regardless of sexual orientation) more than quadrupled from the pre-HIV period (1973 to 1978) to the present era (1996 to 1999) following the widespread availability of potent antiretroviral therapy [22]. (See "HIV infection and malignancy: Management considerations".)
Risk factors — Certain population groups are known to have a higher than average anal cancer risk, namely persons living with HIV (PLWH), MSM, females diagnosed with human papillomavirus (HPV)-related gynecologic precursor lesions or cancer, solid organ transplant recipients, and individuals with certain autoimmune disorders.
Sexual activity and sexually transmitted infections — Initial reports suggesting an increased incidence of the disease in MSM provided a link between sexual activity and the development of anal cancer [17,23]. This relationship has been confirmed in subsequent reports, and linked, in many cases, with sexually transmitted infection, as illustrated by the following observations:
●In a population-based case-control study, females with anal cancer were more likely than controls to have a history of genital warts (relative risk [RR] 32.5), herpes simplex 2 (RR 4.1), or chlamydia trachomatis (RR 2.3), while males with anal cancer were more likely than controls to have never been married (RR 8.6), to have a sexual encounter with another male (ever) (RR 50), to have ever practiced receptive anal intercourse (RR 33), and to have a history of genital warts (RR 27) or gonorrhea (RR 17) [24]. Subsequent studies confirmed the relationship between anal cancer and receptive anal intercourse in males [25-29].
●A second case-control study in heterosexual individuals compared 417 patients with anal cancer, 534 patients with rectal cancer, and 554 normal controls [30]. In multivariate analysis, the strongest risk factors for anal cancer in females were 10 or more lifetime sexual partners (RR 4.5) and a history of anal warts (RR 11.7), genital warts (RR 4.6), gonorrhea (RR 3.3), cervical dysplasia (RR 2.3), or sexual partners with a history of a sexually transmitted disease (RR 2.4). A history of engaging in receptive anal intercourse before the age of 30 and at least two anal intercourse partners were also significant risk factors in females. Among heterosexual males, multivariate analysis revealed significantly elevated risks of anal cancer with 10 or more lifetime sexual partners (RR 2.5), a history of anal warts (RR 4.9), or a history of syphilis or hepatitis (RR 4.0).
HPV and HIV infection are likely responsible for much of this association. However, at least in MSM, there is an elevated risk of anal cancer even amongst those without HIV infection. In a meta-analysis of anal cancer incidence by risk group, the summary IR (cases per 100,000 person-years) for anal cancer were significantly higher for HIV-positive MSM (n = 7 studies, 2,229,234 person-years, IR 85, 95% CI 82-89) but still elevated for HIV-negative MSM (n = 2 studies, 48,135 person-years, IR 19, 95% CI 10-36) [31].
Human papillomavirus infection — HPV infection is the most commonly diagnosed sexually transmitted disease in the United States and provides as least part of the link between sexual activity and anal cancer. A close association exists between infection by oncogenic HPV strains and many premalignant and malignant lesions of the genital tract, anus, and rectum [30,32]. Furthermore, HPV infection is the common link that explains the association between index and second primary anogenital cancers and oral cavity/pharyngeal cancers. (See "Virology of human papillomavirus infections and the link to cancer" and "Epidemiology, staging, and clinical presentation of human papillomavirus associated head and neck cancer", section on 'Epidemiology' and "Second primary malignancies in patients with head and neck cancers", section on 'Incidence'.)
HPV DNA has been isolated from 46 to 100 percent of in situ and invasive SCCs of the anus [30,33-35], and epidemiologic studies have shown that up to 93 percent of anal SCCs are associated with HPV infection. Females are more likely to have HPV associated anal cancer than are males [36]. HPV 16 presence is also associated with a better prognosis [37].
While a number of HPV types can be found in the anogenital tract, only a few have been associated with cancer. The spectrum of HPV types in the anal canal is similar to that described in the cervix and is associated with the same "risk" phenotypes. As in cervical cancer, HPV 16 is the most frequently isolated type in anal malignancies [30,35,38,39], and its presence predicts for preinvasive as well as invasive cancer. HPV 16 associated anal SCC can be identified histologically by immunohistochemical expression of p16 [37]. In contrast, low-grade in situ lesions frequently are associated with other HPV subtypes [29,39,40].
The premalignant condition of cervical intraepithelial neoplasia (CIN or squamous intraepithelial lesions [SIL]) associated with HPV infection of the cervix also occurs with HPV infections involving the anus (termed anal SIL, previously called anal intraepithelial neoplasia [AIN]). Both cervical SIL and anal SIL can be morphologically low grade or high grade. The sometimes confusing terminology associated with anal squamous dysplasia is discussed in detail elsewhere. (See "Anal squamous intraepithelial lesions: Epidemiology, clinical presentation, diagnosis, screening, prevention, and treatment", section on 'Histopathology and nomenclature'.)
HPV infection in the anal canal and perianal region may be subclinical or clinically apparent as condylomata. SIL, particularly high-grade SIL, is considered to be the precursor of anal cancer. Progression of high-grade SIL to invasive anal SCC is related to many factors, including HIV seropositivity, a lower CD4 count, the type of HPV infection, and higher levels of DNA of high-risk HPV types in the anal canal [41]. (See "Anal squamous intraepithelial lesions: Epidemiology, clinical presentation, diagnosis, screening, prevention, and treatment", section on 'Natural history'.)
The prevalence of HPV infection in MSM, a group at high risk for both high-grade SIL and invasive anal cancer, is higher in the presence of HIV infection [42]. (See 'HIV infection' below.)
A substantial minority of anal cancers are not associated with HPV infection. No difference has been noted between HPV positive and HPV negative tumors in regards to patient age, the presence of adjacent dysplasia, ductal differentiation, or prognosis [43].
Vaccines directed against the HPV types associated with cervical and anal neoplasia in females and anal lesions in males have been developed, and their utility for prevention of anal neoplasia is beginning to be studied. As an example, in a randomized trial involving 4065 males, a quadrivalent HPV vaccine was effective in preventing infection with HPV types 6, 11, 16, and 18 and preventing the development of external genital lesions.
In a planned substudy of that trial evaluating the impact of the quadrivalent vaccine on the development of SIL in 602 MSM, there was a 78 percent decrease in the incidence of SIL associated with HPV types 6, 11, 16, and 18 among males who received all three vaccine doses compared with placebo [44]. The results of this trial and recommendations for the use of HPV vaccines are discussed separately. (See "Anal squamous intraepithelial lesions: Epidemiology, clinical presentation, diagnosis, screening, prevention, and treatment", section on 'Prevention' and "Human papillomavirus vaccination".)
HIV infection — It is unclear whether HIV infection itself has a direct effect on the development of anal cancer or if this is mediated through HPV. The data supporting a relationship between HIV, HPV, and anal cancer include the following observations:
●Epidemiologic data indicate that the increasing anal cancer rates in the United States were strongly influenced by the HIV epidemic in males but were independent of HIV infection in females [13,45]. Data are available from an analysis of the HIV/AIDS Cancer Match (HACM) study, a registry-based cohort study linking 12 population-based HIV and cancer registries; these 12 United States regions represent nearly one-third of the United States population, and 44 percent of people living with HIV (PLWH) reside in these 12 regions [45]. Between 2001 and 2015, there were an estimated 16,110 anal SCC cases in these 12 regions, with an estimated 6277 occurring in males and 9833 occurring in females; 14.5 percent of all cases occurred in PLWH. In 2013 to 2015, 33 percent of anal cancers among males occurred in PLWH, but only 3 percent among females. The percentage of anal SCCs among males with HIV increased from 29.1 to 34.9 percent between 2001 and 2015, while for females with HIV the percentage remained stable (2.6 percent in 2001-2004, compared with 2.3 percent in 2013-2015).
●There is a markedly higher incidence of SIL and anal cancer in males living with HIV (MLWH), particularly MSM who are living with HIV (MSMLWH) [42,46-49].
•In a report of data from 13 cohorts (11 clinic-based, including 34,189 HIV infected and 114,260 HIV uninfected individuals) that were included in the North American AIDS Cohort Collaboration on Research and Design (NA-ACCORD) for the years 1996 to 2007, the unadjusted anal cancer IR per 100,000 person-years were 131 for MSMLWH, 46 for other MLWH, and 2 for MSM without HIV [49].
•In a meta-analysis of anal cancer incidence by risk group, the summary IR (cases per 100,000 person-years) for anal cancer were significantly higher for MSMLWH (n = 7 studies, 2,229,234 person-years, IR 85, 95% CI 82-89) compared with MLWH but not practicing MSM (n = 5 studies, 1,626,448 person-years, IR 32, 95% CI 30-35) [31].
●The incidence of HPV infection and HPV associated preinvasive and invasive malignancy is higher in people living with HIV (PLWH), regardless of sexual practice [29,50-54].
●Among HPV infected individuals, the prevalence of high-grade SIL and anal carcinoma is higher in PLWH compared with those without HIV [55].
●In a meta-analysis of 53 studies, the prevalence of both high-risk anal HPV subtypes (74 versus 34 percent) and anal cancer (45.9 versus 5.1 per 100,000 men) was significantly higher among MSMLWH as compared with MSM without HIV [42].
Despite these observations, the overall impact of HIV infection on IR of anal cancer remains unclear, since population-based studies have produced conflicting results [13,18,19,56-58]. The following observations illustrate the range of findings:
●An increased incidence of anal cancer was noted in some reports during the peak of the AIDS epidemic [57]. In New York City, for example, there was a 10-fold increase in the incidence of anal cancer among males age 20 to 49 from 1979 to 1985, concurrent with the onset of the AIDS epidemic and a marked rise in Kaposi sarcoma and non-Hodgkin lymphoma in this population [57]. In contrast, case-control studies of single males living in San Francisco did not find a significant rise in the incidence of anal cancer from before the appearance of AIDS in about 1980 to the late 1980s, a period in which there was an increased incidence of both Kaposi sarcoma and non-Hodgkin lymphoma [28,59,60]. (See "HIV infection and malignancy: Management considerations" and "HIV infection and malignancy: Epidemiology and pathogenesis".)
●In an American series linking registries reporting both AIDS and cancer, the RR of developing anal cancer in PLWH was much higher than that in the general population (standardized incidence ratio 19.1, 95% CI 18.1-20.0) [61]. The anal cancer incidence was highest among MSM, with increased age, and in those with AIDS.
●PLWH who have a longer duration of HIV infection have a substantially higher rate of anal cancer, but in contrast to other AIDS-associated cancers, the use of potent antiretroviral therapy has not led to a decline in the incidence of anal cancer [62,63].
Without controlling for receptive anal intercourse and prior HPV infection, it is difficult to discern the true effect of HIV on the incidence of anal cancer. It is possible that HIV infection interacts with HPV to predispose to anal cancer. In a cohort of 346 MSMLWH and 262 MSM without HIV, infection with multiple anal HPV types was more common in the MSMLWH (73 versus 23 percent) and was associated with significant immunosuppression (CD4 count below 200/microL) [64]. This finding could reflect increased HPV replication in patients with AIDS, which would allow more HPV types to reach a detectable concentration. Infection with more than one type of HPV is associated with an increased risk of abnormal anal cytology [46,65]. (See "Virology of human papillomavirus infections and the link to cancer".)
Chronic immunosuppression in HIV infection is also associated with a higher risk of anal cancer and of progression from low-grade SIL to high-grade SIL or invasive cancer [29,41,66]. As an example, within a nested case-control study in the Swiss HIV cohort study, low CD4 counts were significantly associated with anal cancer, both at nadir and at the time of cancer diagnosis [66]. The influence of CD4 counts appeared to be strongest six to seven years prior to the diagnosis of anal cancer (odds ratio for <200 versus ≥500 cells/microL 14.0, 95% CI 3.85-50.9).
Chronic immunosuppression not due to HIV
Solid organ transplant recipients — Other causes of chronic immunosuppression, such as solid organ transplantation, also may be associated with the development of high-grade SIL and invasive anal carcinoma [31,67-69].
●In a meta-analysis of anal cancer incidence by risk group, the summary IR (cases per 100,000 person-years) for anal cancer among solid organ transplant recipients (n = 5 studies, 1,946,206 person-years, IR 13, 95% CI 12-15) [31]. By ten years post-transplant, this IR reached 24.5 for males and 49.6 for females.
●Among renal transplant recipients, the risk of anogenital cancer may be increased as much as 100-fold; this high risk level has been associated with persistent HPV infection [68,69].
This subject of post-transplantation malignancy is discussed in detail elsewhere. (See "Malignancy after solid organ transplantation".)
Other immunocompromised patients — Autoimmune disease also is a risk factor for subsequent anal cancer, in part related to treatment with chronic glucocorticoid therapy [70,71]. In a meta-analysis of anal cancer incidence by risk group, the summary IR (cases per 100,000 person-years) for anal cancer among individuals with systemic lupus erythematosus was 10 (95% CI 5-19), for ulcerative colitis it was 6 (95% CI 3-11), and for Crohn's disease it was 3 (95% CI 2-4). (See "Major adverse effects of systemic glucocorticoids".)
Cigarette smoking — Several case-control studies have noted a statistically significant risk of anal cancer in smokers, especially current smokers [25,35,66,72-75]. In one series, cigarette smoking was associated with a significantly increased risk of anal cancer (RR 1.9 for 20 pack-years, RR 5.2 for 50 pack-years) [25]. Cigarette smoking is highly associated with cervical neoplasia and is thought to act as a cocarcinogen for anogenital SCC [76]. (See "Cervical cancer screening tests: Techniques for cervical cytology and human papillomavirus testing".)
INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)
●Basics topic (see "Patient education: Anal cancer (The Basics)")
SUMMARY
●Anatomy and tumor types
•Four distinct categories of tumors arise in the anal region (see 'Anatomy and types of tumors' above):
-Tumors that develop from any of the three types of lining mucosa (glandular, transitional, and squamous) that cannot be visualized in their entirety while gentle traction is placed on the buttocks are termed anal canal cancers. The vast majority are squamous cell cancers (SCCs). (See 'Anatomy and types of tumors' above.)
-Perianal skin cancers arise within the hair-bearing skin at or distal to the squamous mucocutaneous junction; by definition, they can be seen in their entirety with gentle traction placed on the buttocks and are within 5 cm of the anus as perianal skin cancers.
-Adenocarcinomas are thought to arise from glandular elements within the anal canal.
-Primary rectal SCCs, which are very rare, can be difficult to distinguish from anal cancers.
•The majority of tumors arising in the transitional or squamous mucosa of the anal canal are SCCs. The term "anal cancer," by common definition, refers to SCCs arising within the mucosa of the anal canal. In contrast, adenocarcinomas arising from glandular elements within the anal canal are rare but appear to share a similar natural history to rectal adenocarcinomas. They are treated in a manner that is similar to rectal carcinoma rather than anal cancer. (See 'Anal canal tumors' above.)
●Epidemiology and risk factors
•Although it remains an uncommon cancer, the incidence of anal cancer is increasing in the United States and other countries. (See 'Epidemiology and risk factors' above.)
•An increased incidence has been associated with sexual activity, including anal receptive intercourse and the lifetime number of sexual partners; infection with human papillomavirus (HPV); infection with HIV; other causes of chronic immunosuppression, including solid organ transplantation, and cigarette smoking. Thus, from an etiologic standpoint, anal cancer is more similar to genital malignancies than it is to gastrointestinal tract cancers. (See 'Risk factors' above.)
ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges David P Ryan, MD, who contributed to earlier versions of this topic review.
آیا می خواهید مدیلیب را به صفحه اصلی خود اضافه کنید؟
