HPV16 viral characteristics in primary, recurrent and metastatic vulvar carcinoma

Lillsunde-Larsson, Gabriella; Kaliff, Malin; Sorbe, Bengt; Helenius, Gisela; Karlsson, Mats G.

doi:10.1016/j.pvr.2018.10.008

Cited by 4 publications

(4 citation statements)

References 52 publications

(80 reference statements)

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“…Although VL somewhat varied between time points, the results in individual patients were relatively constant. The authors concluded that time elapsed and new milieu (lymph node or metastasis) seem to have no influence on VL [21]. The patients enrolled in that study were treated with surgery, and therefore the influence of treatment was negligible.…”

Section: Discussionmentioning

confidence: 95%

“…We found that HPV16 VL was higher in treatment-naive than in recurrent cancer, but the difference was not statistically significant. As we were not able to find any study comparing HPV16 VL between treatment naive and recurrent anal cancer, we referred to a study on primary and recurrent HPV-dependent vulvar cancer [21]. There were no differences in HPV16 VL between primary vulvar squamous cell cancer and matched local recurrences and/or metastases.…”

Section: Discussionmentioning

confidence: 99%

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Significance of HPV16 Viral Load Testing in Anal Cancer

Małusecka

Chmielik

Suwiński

et al. 2020

Pathol. Oncol. Res.

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Human papilloma virus (HPV) is highly frequent among patients with anal squamous cell carcinoma, but the viral load (VL) differs between patients. This study aimed to compare the rate of HPV positivity, HPV16VL, p16 INK4A and p53 expression between treatment naive and recurrent anal cancer patients. HPV was genotyped via AmpliSens® HPV HCR-genotype-titre-FRT kit. HPV16 VL was determined via quantitative polymerase chain reaction-based in-house test. p16 INK4A and p53 expression was tested via immunohistochemistry. The cohort comprised 13 treatment-naive and 17 recurrent anal SCC patients. High-risk HPV was detected in 87% of cases, and HPV16 (73%) was the predominant genotype. The rate of HPV positivity was higher among women and nonsmokers, and majority of HPV-positive cases were also p16 INK4A-positive. All p53-negative tumors were HPV16-positive. The most predominant p53 staining pattern in the HPV-positive group was scattered type, whereas it was diffuse type in the HPV-negative group. The HPV16 VL was higher in the treatment-naive group. Further, in the treatment-naive group, cases with scattered staining pattern of p53 had higher HPV16 VL than cases with diffuse staining pattern. The opposite result was noted in the recurrent cancer group. Moreover, p16-positive cases with scattered p53 staining pattern in the treatment naive group had higher HPV16 VL than their counterparts in the recurrent cancer group. In conclusion, the HPV VL, as is the association between VL and p16 INK4A /p53, is in an inversed trend in treatment naive and recurrent cancer patients, highlighting the importance of HPV VL measurement in anal SCC.

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Section: Discussionmentioning

confidence: 95%

Section: Discussionmentioning

confidence: 99%

Significance of HPV16 Viral Load Testing in Anal Cancer

Małusecka

Chmielik

Suwiński

et al. 2020

Pathol. Oncol. Res.

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“…The prognostic role of HPV in vulvar SCC is still a matter of debate; however, increasing evidence suggests that HPV-associated tumors are less aggressive (14). A large meta-analysis by Faber et al (16) included > 5000 vulvar cancer patients; the prevalence of HPV was 39.7%. Our HPV-tested patients had a higher percentage of positive results.…”

Section: Discussionmentioning

confidence: 99%

Clinicopathologic characteristics of patients with vulvar cancer treated between 1994 and 2017 at the University Medical Centre Maribor

Lovrec

Kozar

Takač

et al. 2021

AMB

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Purpose: Vulvar cancer is one of the rarest forms of cancer. Vulvar cancer represents 3%–7% of all gynecologic cancers. Eighty percent of patients with vulvar cancer are > 60 years of age. The vulvar cancer, analyze the epidemiology, and describe the clinical characteristics, treatment modalities, and factors that influence the development of vulvar cancer. Methods: This retrospective study included patients treated at the University Medical Centre Maribor for vulvar cancer between 1994 and 2017. Patient demographics, disease characteristics, clinical features, histologic findings, and type of therapy were recorded. Associations among various demographic factors, tumor characteristics, treatments, and risk factors of vulvar cancer were evaluated. Results: We collected data from 124 patients between 22 and 92 years of age. The average age of the patients was 71 years. Six different tumor types were identified, of which the most common histologic type of vulvar cancer was squamous cell carcinoma. Forty-five patients were tested for the presence of HPV types, which was confirmed in 71% (32/45) of the tested patients.Conclusion: Squamous cell carcinoma was the most common form of vulvar cancer in patients treated at the University Medical Centre Maribor. Undoubtedly, one of the risk factors for vulvar cancer is HPV infection. HPV 16 was the most frequently diagnosed HPV type in our patients. For more comprehensive and more representative conclusions, data from other medical centers in Slovenia should be included.

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“…Further investigation of CD36 and LAMA3 protein expression in these samples is warranted to understand whether these proteins are disrupted and whether that may have played a role in metastasis. Our assessment of tumor clonality was limited to HPV genotype and HPV integration site, which other groups have also used to demonstrate tumor clonality [ 43 , 44 ], but future work will include mutational profiling of cellular genes to strengthen our ability to assess the clonal nature of these samples. This work was somewhat limited by having access to only FFPE tissue, resulting in a lack of quality RNA for integrated viral transcript analysis.…”

Section: Discussionmentioning

confidence: 99%

Viral Integration Analysis Reveals Likely Common Clonal Origin of Bilateral HPV16-Positive, p16-Positive Tonsil Tumors

Pinatti

Walline

Carey

et al. 2020

Arch Clin Med Case Rep

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Infections with high-risk human papilloma viruses (HPV) are responsible for a significant number of oropharyngeal squamous cell carcinoma (OPSCC), with infection rates currently rising at epidemic rates in the western world. Synchronous bilateral HPV+ tumors of both tonsils are a very rare event whose understanding, however, could provide important insights into virus-driven tumor development and progression and whether such integration events are of clonal origin. In this study we analyzed a single case of a bilateral tonsillar p16+ HPV+OPSCC. The viral integration status of the various tumor samples was determined by integration-specific PCR methods and sequencing, which identified viral insertion sites and affected host genes. Integration events were further confirmed by transcript analysis. Analysis of the tumors revealed common viral integration events involving the CD36 gene, as well as a unique event in the LAMA3 gene which resulted in loss of LAMA3 exon one in both tissues that had lost the complex viral LAMA3 integration event. In addition, there were several integration events into intergenic regions. This suggests a common origin but individual evolution of the tumors, supporting the single-clone hypothesis of bilateral tumor development. This hypothesis is further supported by the fact that the two cellular genes LAMA3 and CD36 as targets of viral integration are involved in cell migration and ECM-receptor interactions, which provides a possible mechanism for clonal migration from one tonsil to another.

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HPV16 viral characteristics in primary, recurrent and metastatic vulvar carcinoma

Cited by 4 publications

References 52 publications

Significance of HPV16 Viral Load Testing in Anal Cancer

Significance of HPV16 Viral Load Testing in Anal Cancer

Clinicopathologic characteristics of patients with vulvar cancer treated between 1994 and 2017 at the University Medical Centre Maribor

Viral Integration Analysis Reveals Likely Common Clonal Origin of Bilateral HPV16-Positive, p16-Positive Tonsil Tumors

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