Integration of human papillomavirus 16 in esophageal carcinoma samples
Abstract Background Esophageal carcinoma (EC) is one of the major cancers in China. In 1982, Syrjanen first hypothesized the relationship between human papillomavirus (HPV) infection and the development of esophageal cancer. Since then, many reports in the field have supported this viewpoint. This s...
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| Format: | Article |
| Language: | English |
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BMC
2017-10-01
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| Series: | Infectious Agents and Cancer |
| Subjects: | |
| Online Access: | http://link.springer.com/article/10.1186/s13027-017-0164-3 |
| _version_ | 1828408678994149376 |
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| author | Shuying Li Haie Shen Zhanjun Liu Ning Li Suxian Yang Ke Zhang Jintao Li |
| author_facet | Shuying Li Haie Shen Zhanjun Liu Ning Li Suxian Yang Ke Zhang Jintao Li |
| author_sort | Shuying Li |
| collection | DOAJ |
| description | Abstract Background Esophageal carcinoma (EC) is one of the major cancers in China. In 1982, Syrjanen first hypothesized the relationship between human papillomavirus (HPV) infection and the development of esophageal cancer. Since then, many reports in the field have supported this viewpoint. This study investigated the etiological relationship between HPV infection and the occurrence of esophageal carcinoma at Tangshan City of the Hebei province in China. Methods 189 samples of esophageal carcinoma patients were collected. DNA and RNA were isolated from samples, HPV DNA was detected by polymerase chain reaction (PCR) using My09/11 for HPV L1, and HPV16 was determined using type-specific primer sets for HPV16 E6. The HPV16 integration site was verified by amplification of papillomavirus oncogene transcripts, and HPV16 oncogene transcript products were ligated to the pMD-18 T vector and sequenced to confirm the physical location of HPV16 integration. Results 168 HPV-positive samples were detected in 189 samples, and among them 76 specimens were HPV16 positive. Approximately 600 bp of the HPV16 oncogene transcript were detected in nine esophageal cancer samples. Sequence analysis revealed that HPV16 E7 integrated into human chromosome 2 in three samples, into human chromosome 5 in one sample, into human chromosome 6 in one sample, into human chromosome 8 in two samples, and into human chromosome 17 in two samples. The results verified that the integrated HPV16 E7 in five samples harbored one mutation of viral DNA compared with the HPV16 sequence provided in GenBank (K02718). Conclusions The high prevalence of HPV16 suggests that HPV16 may play an etiological role in the development of esophageal cancer. The integration of HPV16 into host cell chromosomes suggests that persistent HPV infection is key for esophageal epithelial cell malignant transformation and carcinogenesis. |
| first_indexed | 2024-12-10T11:43:14Z |
| format | Article |
| id | doaj.art-f186c027e57d498690326631644f624c |
| institution | Directory Open Access Journal |
| issn | 1750-9378 |
| language | English |
| last_indexed | 2024-12-10T11:43:14Z |
| publishDate | 2017-10-01 |
| publisher | BMC |
| record_format | Article |
| series | Infectious Agents and Cancer |
| spelling | doaj.art-f186c027e57d498690326631644f624c2022-12-22T01:50:11ZengBMCInfectious Agents and Cancer1750-93782017-10-011211910.1186/s13027-017-0164-3Integration of human papillomavirus 16 in esophageal carcinoma samplesShuying Li0Haie Shen1Zhanjun Liu2Ning Li3Suxian Yang4Ke Zhang5Jintao Li6North China University of Science and Technology (Hebei Key Laboratory for Chronic Diseases, Tangshan Key Laboratory for Preclinical and Basic Research on Chronic Diseases)North China University of Science and Technology (Hebei Key Laboratory for Chronic Diseases, Tangshan Key Laboratory for Preclinical and Basic Research on Chronic Diseases)North China University of Science and Technology (Hebei Key Laboratory for Chronic Diseases, Tangshan Key Laboratory for Preclinical and Basic Research on Chronic Diseases)North China University of Science and Technology (Hebei Key Laboratory for Chronic Diseases, Tangshan Key Laboratory for Preclinical and Basic Research on Chronic Diseases)North China University of Science and Technology (Hebei Key Laboratory for Chronic Diseases, Tangshan Key Laboratory for Preclinical and Basic Research on Chronic Diseases)North China University of Science and Technology (Hebei Key Laboratory for Chronic Diseases, Tangshan Key Laboratory for Preclinical and Basic Research on Chronic Diseases)College of Life Science and Bio-engineering, Beijing University of TechnologyAbstract Background Esophageal carcinoma (EC) is one of the major cancers in China. In 1982, Syrjanen first hypothesized the relationship between human papillomavirus (HPV) infection and the development of esophageal cancer. Since then, many reports in the field have supported this viewpoint. This study investigated the etiological relationship between HPV infection and the occurrence of esophageal carcinoma at Tangshan City of the Hebei province in China. Methods 189 samples of esophageal carcinoma patients were collected. DNA and RNA were isolated from samples, HPV DNA was detected by polymerase chain reaction (PCR) using My09/11 for HPV L1, and HPV16 was determined using type-specific primer sets for HPV16 E6. The HPV16 integration site was verified by amplification of papillomavirus oncogene transcripts, and HPV16 oncogene transcript products were ligated to the pMD-18 T vector and sequenced to confirm the physical location of HPV16 integration. Results 168 HPV-positive samples were detected in 189 samples, and among them 76 specimens were HPV16 positive. Approximately 600 bp of the HPV16 oncogene transcript were detected in nine esophageal cancer samples. Sequence analysis revealed that HPV16 E7 integrated into human chromosome 2 in three samples, into human chromosome 5 in one sample, into human chromosome 6 in one sample, into human chromosome 8 in two samples, and into human chromosome 17 in two samples. The results verified that the integrated HPV16 E7 in five samples harbored one mutation of viral DNA compared with the HPV16 sequence provided in GenBank (K02718). Conclusions The high prevalence of HPV16 suggests that HPV16 may play an etiological role in the development of esophageal cancer. The integration of HPV16 into host cell chromosomes suggests that persistent HPV infection is key for esophageal epithelial cell malignant transformation and carcinogenesis.http://link.springer.com/article/10.1186/s13027-017-0164-3Esophageal carcinomaHuman papillomavirusInfectionIntegrationEtiology |
| spellingShingle | Shuying Li Haie Shen Zhanjun Liu Ning Li Suxian Yang Ke Zhang Jintao Li Integration of human papillomavirus 16 in esophageal carcinoma samples Infectious Agents and Cancer Esophageal carcinoma Human papillomavirus Infection Integration Etiology |
| title | Integration of human papillomavirus 16 in esophageal carcinoma samples |
| title_full | Integration of human papillomavirus 16 in esophageal carcinoma samples |
| title_fullStr | Integration of human papillomavirus 16 in esophageal carcinoma samples |
| title_full_unstemmed | Integration of human papillomavirus 16 in esophageal carcinoma samples |
| title_short | Integration of human papillomavirus 16 in esophageal carcinoma samples |
| title_sort | integration of human papillomavirus 16 in esophageal carcinoma samples |
| topic | Esophageal carcinoma Human papillomavirus Infection Integration Etiology |
| url | http://link.springer.com/article/10.1186/s13027-017-0164-3 |
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