Incidence and time trends of anal cancer among people living with HIV in Australia

Abstract

Background: Anal cancer incidence increased markedly in people living with HIV (PLWHIV) after the introduction of HAART, but in a few setting settings, recent declines have been reported. We report the incidence and time trends of anal cancer in PLWHIV in Australia. Study design: A data linkage study between the National HIV Registries and the Australian Cancer Database. Methods: Cases of anal squamous cell carcinoma (ASCC) in Australians aged 16 years and above diagnosed with HIV between 1982 and 2012 were identified. Standardized incidence ratios (SIRs) were calculated to compare incidence with that of the general population. Poisson regression models were developed to describe the time trends of ASCC over time and to compare ASCC risk within subgroups of PLWHIV. Results: Among 28 696 individuals, a total of 129 cases of ASCC were identified. The crude incidence was 36.3 per 100 000 person-years and it increased sharply from 14.8 to 62.1 per 100 000 person-years between 1982-1995 and 2009-2012 (P trend <0.001). The SIR was 35.3 (95% confidence interval 29.5-42.0), and there was an inverse association between SIR and increasing age (P trend <0.001). In multivariate analyses, ASCC incidence was significantly higher in recent years (P trend <0.001), in those who acquired HIV through male homosexual contact (P=0.002), and in those who had a history of AIDS (P < 0.001). Conclusion: PLWHIV in Australia are at markedly higher risk of anal cancer. Unlike in some industrialized countries with a mature HIV epidemic, the incidence of anal cancer is still increasing in this population in Australia.

ART is key to clearing oncogenic HPV genotypes (HR-HPV) in anal mucosa of HIV-positive MSM

“…Since the first HIV epidemic, the incidence of this neoplasia has increased in seropositive patients, mainly in elderly MSM with AIDS [34]. Recently published data from the Australian HIV and Cancer National Registry showed that the incidence of ASCC rose from 14.8/100,000 people/yr between 1982 and 1995 to 62.1/100,000 people/yr between 2009 and 2012 (p <0.001) [35], similar to the present findings.…”

“…Both samples were immersed in thinlayer liquid medium and sent to the pathology laboratory of the hospital. Genotypes 16,18,26,31,33,35,39,45,[51][52][53]56,58,59,66,68,73, and 82 were considered to be HR-HPV genotypes. Genotypes 6,11,34,40,[42][43][44]54,55,57,61,[70][71][72]81,83,84, and 89 were considered to be low-risk (LR-HPV) genotypes.…”

“…Genotypes 6,11,34,40,[42][43][44]54,55,57,61,[70][71][72]81,83,84, and 89 were considered to be low-risk (LR-HPV) genotypes. Genotypes 39, 45, 59, and 68 were classified as subtypes of HPV genotype 18; and genotypes 31,33,35,52,58, and 67 as subtypes of HPV 16 [17].…”

Risk factors for ≥high-grade anal intraepithelial lesions in MSM living with HIV and the response to topical and surgical treatments

“…Since the first HIV epidemic, the incidence of ASCC has increased in seropositive patients, mainly in MSM with AIDS [ 17 ]. After the initiation of our screening/treatment program in 2010, the ≥HSIL rate significantly decreased among HIV-infected MSM patients for six years and then subsequently stabilized, with no progression to ASCC in patients with treated HSIL.…”

The Roles of the Virome in Cancer

“…Possible involvement of EBV in gastric cancer and precursor lesions [35]; patients with EBV-positive gastric cancer had a better response to chemotherapy and better survival [36] EBV (HHV4) Hepatic EBV infections detected in HCC tissues [37] EBV (HHV4) Lymphoma (DLBCL) EBV RNA detected in B-cell lymphoma samples [38] EBV (HHV4) Lymphoma (PTCL) EBV expression associated with some subtypes of peripheral T-cell lymphomas [39] EBV (HHV4) Oral Higher proportion of EBV-positive oral squamous cell carcinoma in industrialized countries [40] EBV (HHV4) Skin and mucosal EBV DNA frequently detected in skin and mucosal cancers [26] HHV6 Lymphoma (DLBCL) HHV6 RNA detected in B-cell lymphoma samples [38] HHV6 Malignant melanoma HHV6 DNA frequently detected in malignant melanoma [26] HHV7 Bladder HHV7 DNA frequently detected in bladder cancer [26] HHV7 Lymphoma (CTCL) HHV7 DNA frequently detected in cutaneous T-cell lymphoma (Mycosis fungoides) [26] HHV7 Oral HHV7 DNA frequently detected in oral cavity cancer [26] HSV (HHV1/2) Oral Higher proportion of HSV-positive oral squamous cell carcinoma in industrialized countries [40] KSHV (HHV8) Kaposi sarcoma In HIV-infected individuals, KSHV infection is associated with Kaposi sarcoma [41] Polyomaviridae BKV Bladder Possible association of BKV with bladder cancer [26] BKV Colorectal Possible association of BKV with colorectal cancer [42,43], however, other studies found no association [16,44] JCV Colorectal JCV is associated with colorectal cancer [44,45] and may be involved in carcinogenesis [46], specifically in chromosomal instability [47]; JCV Tantigen is expressed in early stage colorectal cancer [48], however, another study found no association [16] MCV Merkel cell carcinoma MCV is the major causative factor for Merkel cell carcinoma [49,50] Retroviridae HIV Anal HIV-positive people have increased risk for anal cancer [51,52] and worse overall colostomy-free survival rates [53] HIV Cervical Cervical cancer...…”