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2 results on '"Gaisa M"'

1. Risk of Invasive Anal Cancer in HIV-Infected Patients With High-Grade Anal Dysplasia: A Population-Based Cohort Study.

Author

Arens Y, Gaisa M, Goldstone SE, Liu Y, Wisnivesky J, Sigel CS, Swartz TH, and Sigel K

Subjects
Adult, Anus Neoplasms diagnosis, Anus Neoplasms epidemiology, Disease Progression, Female, Follow-Up Studies, Humans, Incidence, Male, Middle Aged, Retrospective Studies, Risk Factors, United States epidemiology, Anal Canal pathology, Anus Neoplasms etiology, HIV, HIV Infections complications, Population Surveillance methods, Precancerous Conditions pathology, SEER Program
Abstract

Background: The progression rate and predictors of anal dysplastic lesions to squamous cell carcinoma of the anus remain unclear. Characterizing these parameters may help refine anal cancer screening guidelines., Objective: This study aimed to determine the rate of progression of high-grade anal dysplasia to invasive carcinoma in HIV-infected persons., Design: Using the Surveillance, Epidemiology, and End Results database linked to Medicare claims from 2000 to 2011, we identified HIV-infected subjects with incident anal intraepithelial neoplasia III. To estimate the rate of progression of anal intraepithelial neoplasia III to invasive cancer, we calculated the cumulative incidence of anal cancer in this cohort. We then fitted Poisson models to evaluate the potential risk factors for incident anal cancer., Settings: This is a population-based study., Patients: Included were 592 HIV-infected subjects with incident anal intraepithelial neoplasia III., Main Outcome Measures: The primary outcome measured was incident squamous cell carcinoma of the anus., Results: Study subjects were largely male (95%) with a median age of 45.7 years. Within the median follow-up period of 69 months, 33 subjects progressed to anal cancer. The incidence of anal cancer was 1.2% (95% CI, 0.7%-2.5%) and 5.7% (95% CI, 4.0%-8.1%) at 1 and 5 years, following a diagnosis of anal intraepithelial neoplasia III. Risk of progression did not differ by anal intraepithelial neoplasia III treatment status. On unadjusted analysis, black race (p = 0.02) and a history of anogenital condylomata (p = 0.03) were associated with an increased risk of anal cancer incidence, whereas prior anal cytology screening was associated with a decreased risk (p = 0.04)., Limitations: The identification of some incident cancer episodes used surrogate measures., Conclusions: In our population-based cohort of HIV-infected subjects with long-term follow-up, the risk of progression from anal intraepithelial neoplasia III to anal squamous cell carcinoma was higher than reported in other studies and was not associated with the receipt of anal intraepithelial neoplasia III treatment. See Video Abstract at http://links.lww.com/DCR/A933.

Published
2019
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2. Chromosomal copy number alterations in anal precancers from people with HIV

Author

Mutetwa, Tinaye, Karlić, Rosa, Houldsworth, Jane, Bowcock M., Anne, Gaisa M., Michael, Liu, Yuxin, Polak, Paz, and Sigel, Kieth

Subjects
Anal cancer, Copy number alteration, FISH, HPV, HIV
Abstract

Background: People living with HIV (PWH) are susceptible to high-risk human papillomavirus (HPV) infection of the anal canal owing to their immunocompromised status. The virus can transform anal squamous epithelia to low-grade squamous intraepithelial lesions (LSILs) and further to high-grade squamous intraepithelial lesions (HSILs). HSILs are well-defined cancer precursors that can progress to invasive cancer if left untreated. HPV-associated cancers commonly carry genomic abnormalities, specifically, a gain of chromosome 3q26 (PIK3CA), 20q13, 5p15 (TERT) and 7 centromere (cen7). We aimed to determine whether HPV-associated anal precancers carry similar genomic abnormalities and if so, to analyze their associations with histological severity and specific HPV types. Methods: Anal lesions from 63 unique patients (36 HSIL, 27 LSIL) were obtained via high-resolution anoscopy (HRA)-directed biopsy. Anal swabs were performed at the time of HRA to collect samples for cytological diagnosis and HPV DNA testing of HPV16, 18, and other (12) high-risk types. FISH-based HPV-associated Cancer Test (FHACT) was performed on the biopsy samples using four-color probes to detect any gain of chromosome 3q, 20q, 5p, and 7. The associations between genomic alterations, histological severity and HPV types were analyzed. Results: Our cohort had a median age of 50, was predominantly (70%) of Black and Hispanic race/ethnicity and 95% had suppressed HIV viral loads. Genomic abnormalities were detected in 47% of anal HSILs and 7% of LSILs (p=0.002). A gain of 3q, 20q, 5p, and cen7 was detected in 42%, 31%, 31%, and 19% of HSILs and 7%, 4%, 0%, and 0% of LSILs, respectively. Genomic abnormalities were more frequent in lesions associated with HPV16/18 infection, compared with those associated with non-16/18 types and negative HPV (42% vs. 24% vs. 9% ; p=0.06). 91% of lesions with 5p gain had gain in 20q. Cen7 gains were only detected in lesions with a gain of 20q13, suggesting a possible sequential order in development of chromosomal gains: 3q26 first, followed by 20q13 or 5p15, and then cen7. Conclusion: Anal precancers frequently demonstrate genomic abnormalities found in other HPV-associated cancers. The most common abnormality was the amplification of chromosome 3q, the location of PIK3CA gene. Our results suggest that PI3- kinase/AKT signaling pathway may play an important role in anal cancer development in PWH.

Published
2021

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