A recurrent pattern of chromosomal aberrations and immunophenotypic appearance defines anal squamous cell carcinomas

Heselmeyer, Kerstin; Manoir, Stanislas du; Blegen, Harald; Friberg, Bertil; Svensson, Christina; Schröck, Evelin; Veldman, Timothy; Shah, Keerti V.; Auer, Gert; Ried, Thomas

doi:10.1038/bjc.1997.547

Cited by 42 publications

(18 citation statements)

References 17 publications

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“…These data support gain of 3q as an important event in the oncogenesis of HPV-related SCCs since, in a previous study, we have shown that a similar proportion of stage 1b HPV-positive cervical SCCs harbour 3q gain (Allen et al, 2000). Gain of 3q has also been detected by others in cervical SCCs (Heselmeyer et al, 1996(Heselmeyer et al, , 1997bDellas et al, 1999;Kirchoff et al, 1999) and in HPV-positive SCC of the anus and its precursor lesions (Heselmeyer et al, 1997a;Haga et al, 2001). Further, we were able to map the smallest region of gain in vulvar SCCs to 3q22 -25, whilst our previous series of cervical cancers showed the smallest area of gain to be 3q24 -26 (Allen et al, 2000).…”

Section: Discussionsupporting

confidence: 87%

Genetic aberrations detected by comparative genomic hybridisation in vulvar cancers

Hammet

et al. 2002

Br J Cancer

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Squamous cell carcinoma of the vulva is a disease of significant clinical importance, which arises in the presence or absence of human papillomavirus. We used comparative genomic hybridisation to document non-random chromosomal gains and losses within human papillomavirus positive and negative vulvar cancers. Gain of 3q was significantly more common in human papillomavirus-positive cancers compared to human papillomavirus-negative cancers. The smallest area of gain was 3q22 -25, a chromosome region which is frequently gained in other human papillomavirus-related cancers. Chromosome 8q was more commonly gained in human papillomavirus-negative compared to human papillomavirus-positive cancers. 8q21 was the smallest region of gain, which has been identified in other, non-human papillomavirus-related cancers. Chromosome arms 3p and 11q were lost in both categories of vulvar cancer. This study has demonstrated chromosome locations important in the development of vulvar squamous cell carcinoma. Additionally, taken together with previous studies of human papillomaviruspositive cancers of other anogenital sites, the data indicate that one or more oncogenes important in the development and progression of human papillomavirus-induced carcinomas are located on 3q. The different genetic changes seen in human papillomavirus-positive and negative vulvar squamous cell carcinomas support the clinicopathological data indicating that these are different cancer types.

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Section: Discussionsupporting

confidence: 87%

Genetic aberrations detected by comparative genomic hybridisation in vulvar cancers

Hammet

et al. 2002

Br J Cancer

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“…In addition, a more recent study un-ambiguously established the central role of 3q for progression from low-grade dysplastic lesions to higher grades and to invasive carcinomas and showed that the gain of 3q can occur in morphologically normal Pap smears of women who developed cervical carcinomas after only a short latency . Gain of chromosomal region 3q is also recurrently observed in other types of cancer, including tonsillar cancer and carcinomas of the anogenital region that are both associated with HPV DNA (Heselmeyer et al, 1997b;Dahlgren et al, 2003;Stoltzfus et al, 2005).…”

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confidence: 99%

Frequent gain of the human telomerase gene TERC at 3q26 in cervical adenocarcinomas

Andersson

Hellström

et al. 2006

Br J Cancer

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The level of genomic amplification of the human telomerase gene TERC, which maps to chromosome band 3q26, was determined in primary cervical adenocarcinomas. Interphase nuclei prepared from archival material of 12 primary cervical adenocarcinomas, eight of which were human papillomavirus positive, were hybridised with a triple colour probe set specific for centromeres of chromosomes 3 and 7 and the TERC gene. We observed high proportions of nuclei with increased absolute copy numbers for TERC in all tumours (mean 3.3; range 2.3 -5.2). Amplification of the human telomerase gene TERC is a consistent aberration in cervical adenocarcinomas. Therefore, application of our probe set may provide an objective genetic test for the assessment of glandular cells in Pap smears and hence for the diagnosis of cervical adenocarcinomas.

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“…In sporadic colorectal cancer, MSI is seen in approximately 15% of cases. The prevalence of MSI in sporadic anal carcinoma is less clear with most studies describing loss of heterozygosity (LOH) at chromosomes 5p, 11q and 18q in relation to integration of HPV DNA and subsequent expression of E6 and E7 genes [27,28]. To our knowledge, there are no reports describing the prevalence of MSI in anal cancer.…”

Section: Introductionmentioning

confidence: 99%

John Cunningham virus T‐antigen expression in anal carcinoma

Ramamoorthy

Devaraj

Miyai

et al. 2010

Cancer

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BACKGROUND: Anal carcinoma is thought to be driven by human papillomavirus (HPV) infection through interrupting function of cell regulatory proteins such as p53 and pRb. John Cunningham virus (JCV) expresses a T‐antigen that causes malignant transformation through development of aneuploidy and interaction with some of the same regulatory proteins as HPV. JCV T‐antigen is present in brain, gastric, and colon malignancies, but has not been evaluated in anal cancers. The authors examined a cohort of anal cancers for JCV T‐antigen and correlated this with clinicopathologic data. METHODS: Archived anal carcinomas were analyzed for JCV T‐antigen expression. DNA from tumor and normal tissue was sequenced for JCV with viral copies determined by quantitative polymerase chain reaction and Southern blotting. HPV and microsatellite instability (MSI) status was correlated with JCV T‐antigen expression. RESULTS: Of 21 cases of anal cancer (mean age 49 years, 38% female), 12 (57%) were in human immunodeficiency virus (HIV)‐positive individuals. All 21 cancers expressed JCV T‐antigen, including 9 HPV‐negative specimens. More JCV copies were present in cancer versus surrounding normal tissue (mean 32.54 copies/μg DNA vs 2.98 copies/μg DNA, P = .0267). There was no correlation between disease stage and viral copies, nor between viral copies and HIV‐positive or ‐negative status (28.7 vs 36.34 copies/μg DNA, respectively, P = .7804). In subset analysis, no association was found between JCV T‐antigen expression and HPV or MSI status. CONCLUSIONS: Anal carcinomas uniformly express JCV T‐antigen and contain more viral copies compared with surrounding normal tissue. JCV and its T‐antigen oncogenic protein, presumably through interruption of cell regulatory proteins, may play a role in anal cancer pathogenesis. Cancer 2011. © 2010 American Cancer Society.

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A recurrent pattern of chromosomal aberrations and immunophenotypic appearance defines anal squamous cell carcinomas

Cited by 42 publications

References 17 publications

Genetic aberrations detected by comparative genomic hybridisation in vulvar cancers

Genetic aberrations detected by comparative genomic hybridisation in vulvar cancers

Frequent gain of the human telomerase gene TERC at 3q26 in cervical adenocarcinomas

John Cunningham virus T‐antigen expression in anal carcinoma

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