Detection of HPV DNA in Esophageal Lesions: a Cross-Sectional Study

Dinç, Bedia; Altay-Kocak, Aylin; Aydog, Gulden; Kuran, Sedef; Akoğlu, Musa; Özkan, Seçil; Bozdayı, Gülendam

doi:10.7754/clin.lab.2019.190506

Cited by 5 publications

(6 citation statements)

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“…Some of the HPV types detected in our analysis coincide with that reported in our previous study, also using the Luminex technique [35]. These types identified with low frequency are little studied in the literature whose average is 52.4% [53,54].…”

Section: Discussionsupporting

confidence: 88%

Frequency of Human Papillomavirus Detection in Chagasic Megaesophagus Associated or Not with Esophageal Squamous Cell Carcinoma

et al. 2021

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Background: Chagasic megaesophagus (CM) as well as the presence of human papillomavirus (HPV) has been reported as etiological factors for esophageal squamous cell carcinoma (ESCC). Objective: We assessed the prevalence of HPV DNA in a series of ESCCs associated or not with CM. Data obtained were further correlated to the pathological and clinical data of affected individuals. Methods: A retrospective study was performed on 92 formalin-fixed and paraffin-embedded tissues collected from patients referred to 3 different hospitals in São Paulo, Brazil: Barretos Cancer Hospital, Barretos, São Paulo; Federal University of Triângulo Mineiro, Uberaba, Minas Gerais; and São Paulo State University, Botucatu, São Paulo. Cases were divided into 3 groups: (i) 24 patients with CM associated with ESCC (CM/ESCC); (ii) 37 patients with ESCC without CM (ESCC); and (iii) 31 patients with CM without ESCC (CM). Detection of HPV DNA was assessed in all samples by a genotyping assay combining multiplex polymerase chain reaction and bead-based Luminex technology. Results: We identified a high prevalence of high-risk HPV in patients in the CM group (12/31, 38.8%) and CM/ESCC (8/24, 33.3%), compared to individuals in the ESCC group (6/37, 16.3%). The individuals in the groups with cancer (ESCC and CM/ESCC) had a higher frequency of HPV-16 (4/9, 44.5% and 2/8, 25.0%). The other types of high-risk HPVs detected were HPV-31, 45, 51, 53, 56, 66, and 73. We also observed in some samples HPV coinfection by more than one viral type. Despite the high incidence of HPV, it did not show any association with the patient’s clinical-pathological and molecular (TP53 mutation status) characteristics. Conclusion: This is the first report of the presence of HPV DNA in CM associated with ESCC. HPV infection was more presence in megaesophagus lesions. Further studies are needed to confirm and better understand the role of persistent HPV infection in patients with CM.

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Section: Discussionsupporting

confidence: 88%

Frequency of Human Papillomavirus Detection in Chagasic Megaesophagus Associated or Not with Esophageal Squamous Cell Carcinoma

et al. 2021

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“…While our exploration of the SEER-based ESCC incidence data [ 20 ] reveal the known strong disparities of ESCC rates between Blacks and Whites [ 35 ], our results also suggest that there is a significantly higher risk for developing field-defects during childhood for Blacks than for Whites, especially among the earlier birth cohorts when nutritional or other disparities may have been more prevalent among Blacks. Other predisposing factors for ESCC include the possible impact of pathogens such as Human Papilloma Virus (HPV) [ 36 ] and interactions of the microbiome with evolving dietary patterns.…”

Section: Discussionmentioning

confidence: 99%

Modeling historic incidence trends implies early field cancerization in esophageal squamous cell carcinoma

et al. 2021

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Patterns of cancer incidence, viewed over extended time periods, reveal important aspects of multistage carcinogenesis. Here we show how a multistage clonal expansion (MSCE) model for cancer can be harnessed to identify biological processes that shape the surprisingly dynamic and disparate incidence patterns of esophageal squamous cell carcinoma (ESCC) in the US population. While the dramatic rise in esophageal adenocarcinoma (EAC) in the US has been largely attributed to reflux related increases in the prevalence of Barrett’s esophagus (BE), the premalignant field in which most EAC are thought to arise, only scant evidence exists for field cancerization contributing to ESCC. Our analyses of incidence patterns suggest that ESCC is associated with a premalignant field that may develop very early in life. Although the risk of ESCC, which is substantially higher in Blacks than Whites, is generally assumed to be associated with late-childhood and adult exposures to carcinogens, such as from tobacco smoking, alcohol consumption and various industrial exposures, the temporal trends we identify for ESCC suggest an onset distribution of field-defects before age 10, most strongly among Blacks. These trends differ significantly in shape and strength from field-defect trends that we estimate for US Whites. Moreover, the rates of ESCC-predisposing field-defects predicted by the model for cohorts of black children are decreasing for more recent birth cohorts (for Blacks born after 1940). These results point to a potential etiologic role of factors acting early in life, perhaps related to nutritional deficiencies, in the development of ESCC and its predisposing field-defect. Such factors may explain some of the striking racial differences seen in ESCC incidence patterns over time in the US.

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“…Globally, 570,000 female and 60,000 male cancer-related cases are attributable to HPV each year, demonstrating an increasing trend ( 7 ). Although the association between HPV and ESCA is generally controversial, studies have found that ESCA samples are accompanied by HPV infection, and HPV infection is a negative prognostic factor for patients with ESCA ( 8 , 9 ). It has been previously demonstrated by the authors' laboratory that HPV18 E6E7 induces the immortalization and malignant transformation of human embryonic esophageal epithelial cells ( 10 , 11 ).…”

Section: Introductionmentioning

confidence: 99%

“…Although there are limited studies available on whether HPV affects pyroptosis, it has also been confirmed that HPV can inhibit the occurrence of pyroptosis ( 18 ). HPV is one of the key carcinogenic factors of ESCA, and the majority ESCA samples are also accompanied by HPV infection ( 8 , 9 ). However, the mechanisms through which HPV is involved in ESCA occurrence and particularly the mechanisms through it affects cell death pathways in ESCA, warrant further investigation.…”

Section: Introductionmentioning

confidence: 99%

Transcriptomic analysis of the effects of the HPV18 E6E7 gene on the cell death mode in esophageal squamous cell carcinoma

et al. 2023

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Human papillomavirus (HPV) infection is one of the main causes of esophageal carcinoma (ESCA), and its carcinogenic mechanisms in ESCA require further investigation. E6 and E7 are HPV oncogenes, and their genomic integration is a crucial reason for the transformation of host cells into cancer cells. In order to reveal the role of oncogenes E6 and E7 in ESCA cells, the RNA-Seq raw data for HPV18-positive and -negative esophageal squamous cell carcinoma (ESCC) samples derived from the NCBI BioProject database were analyzed, and the differentially expressed genes were identified. Moreover, differentially expressed genes were enriched significantly in multiple cell death pathways, including apoptosis (cyclin-dependent kinase inhibitor 2A, plakophilin 1 and desmoglein 3), pyroptosis (gasdermin A, gasdermin C, NLR family pyrin domain containing 3, absent in melanoma 2, NLR family pyrin domain containing 1 and Toll like receptor 1) and autophagy (Unc-51 like autophagy activating kinase 1, adrenoceptor beta 2). Consequently, the effects of cisplatin-induced apoptosis and Hank's balanced salt solution-induced autophagy, and α-ketoglutarate-induced pyroptosis in the ESCC-expressing E6 and E7 cells were verified. Therefore, the expression of E6E7 may culminate in the inhibition of multiple cell death modes, which may also be one of the mechanisms of oncogene-induced carcinogenesis.

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Detection of HPV DNA in Esophageal Lesions: a Cross-Sectional Study

Cited by 5 publications

References 0 publications

Frequency of Human Papillomavirus Detection in Chagasic Megaesophagus Associated or Not with Esophageal Squamous Cell Carcinoma

Frequency of Human Papillomavirus Detection in Chagasic Megaesophagus Associated or Not with Esophageal Squamous Cell Carcinoma

Modeling historic incidence trends implies early field cancerization in esophageal squamous cell carcinoma

Transcriptomic analysis of the effects of the HPV18 E6E7 gene on the cell death mode in esophageal squamous cell carcinoma

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