Baseline human papillomavirus infection, high vaginal parity, and their interaction on cervical cancer risks after a follow-up of more than 10 years

Liao, Shu-Fen; Lee, Wen‐Chung; Chen, Hui‐Chi; Chuang, Li-Chung; Pan, Mei‐Hung; Chen, Chien-Jen

doi:10.1007/s10552-012-9939-4

Cited by 17 publications

(21 citation statements)

References 22 publications

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“…Results from a previous study has shown associations between HPV infection with high parity in developing cervical cancer. 11 Multiparity may increase the risk for maintaining transformation zone in the ectocervical region of the cervix. There was also evidence on the increased number of squamous metaplasia during pregnancy.…”

Section: Discussionmentioning

confidence: 99%

Exploring TLR2 Gene Polymorphisms in Cervical Cancer Development

Panigoro¹,

Susanto²,

Arrazeen³

et al. 2013

mkb

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Human papillomavirus is a pathogen that directly infects cervical keratinocytes and may cause persistent infection that leads to cervical cancer. Toll like receptors (TLRs) play an essential role in initiating antiviral immune responses. Therefore, polymorphisms in TLR gene may contribute to cancer susceptibility. This study aimed to explore the TLR2 gene distribution and susceptibility to cervical cancer. In this case-control study, cervical cancer patients and their controls were recruited from the Department of Obstetrics and Gynecology, Dr. Hasan Sadikin General Hospital. Genomic DNA was extracted from blood of patients with histopathologically confirmed cervical cancer (n=100) and from unrelated, healthy female controls (n=100) during 2011. Three single nucleotide polymorphisms (SNPs) of the TLR2 gene were genotyped on the BeadXpress Reader system (Illumina)®. Chi square test was used to calculate the role of TLR2 and susceptibility to cervical cancer. Only subjects with complete clinical and genetic data were analyzed. Analysis of TLR2 rs3804099, rs4696480 and rs5743708 of cervical cancer patients and controls showed no significant association with the cervical cancer risk (p 0. Polimorfisme Gen TLR2 dan Perkembangan Kanker Serviks AbstrakKanker serviks disebabkan oleh human papillomavirus (HPV), patogen yang dapat langsung menginfeksi keratinosit serviks secara persisten dan dapat berkembang menjadi kanker. Toll like receptors (TLR) berperan dalam merangsang respons imun, sehingga polimorfisme gen TLR dapat berkontribusi dalam kerentanan terhadap kanker. Tujuan penelitian ini adalah untuk mengetahui distribusi gen TLR2 dan peranannya terhadap kerentanan kanker serviks. Pada studi kasus kontrol, DNA genomik diekstraksi dari darah penderita kanker serviks yang terdiagnosis secara histopatologi (n=100) dan kontrol dengan Pap smear normal (n=100) tahun 2011 di Departemen Obstetri dan Ginekologi RSUP Dr. Hasan Sadikin Bandung. Pemeriksaan tiga single nucleotide polymorphisms (SNP) gen TLR2 dilakukan menggunakan BeadXpress Reader system (Illumina). Hanya subyek dengan data klinik dan genetik lengkap yang dianalisis dengan menggunakan uji chi square. Analisis dari TLR2 rs3804099, rs4696480 dan rs5743708 antara pasien dan kontrol tidak menunjukkan perbedaan yang bermakna (p 0.424, p 0.275 dan p 0.209). Di antara pasien dengan klasifikasi FIGO (Fédération Internationale de Gynécologie et d'Obstétrique) tingkat rendah (FIGO I/II) dan tingkat tinggi (FIGO III/IV) juga tidak tampak perbedaan yang bermakna. Dari penelitian ini terbukti polimorfisme TLR2 tidak berperan dalam proses kerentanan maupun perkembangan terjadinya kanker serviks. Kemungkinan TLR yang lain seperti TLR 1, 3, 9 lebih berperan dalam perkembangan terjadinya kanker serviks. [MKB. 2013;45(4):257-62]

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Section: Discussionmentioning

confidence: 99%

Exploring TLR2 Gene Polymorphisms in Cervical Cancer Development

Panigoro¹,

Susanto²,

Arrazeen³

et al. 2013

mkb

View full text Add to dashboard Cite

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“…HPV particles are non-enveloped and assume an icosahedral structure, with a diameter of 55 nm and enclose an 8 kb long double-stranded DNA (Chung et al 2010, Doorbar et al 2015. Clinical, molecular and epidemiological investigations have demonstrated that CC is caused by persistent infection with high-risk HPV, where part of the viral DNA sequence becomes integrated into the host genome (Brake & Lambert 2005, Chung et al 2008, Marks et al 2011, Liao et al 2012. The peak time for a woman to acquire an HPV infection is during the sexually active phase of life (http://www.…”

Section: Hpv Involvementmentioning

confidence: 99%

“…Currently, with the epidemiological evidence linking multi-parity and oral contraceptive usage to an increase in CC risk, oestrogens have been speculated to be involved in the development of cervical carcinogenesis (Moreno et al 2002, Muñoz et al 2002, Roura et al 2016. Nevertheless, such carcinogenic transformations due to oestrogens are not physiological and involve a synergistic combination with infection of high-risk human papilloma virus (HPV) as the strongest factor (Brake & Lambert 2005, Chung et al 2008, Marks et al 2011, Liao et al 2012. The successful initiation of HPV-dependent carcinogenesis begins with the infection of HPV in episomal form, initiating the transcription of viral gene products, followed by subsequent genomic integration of HPV oncogenes into the host genome (Senapati et al 2016).…”

Section: Introductionmentioning

confidence: 99%

Functional association of oestrogen receptors with HPV infection in cervical carcinogenesis

Ramachandran¹

2017

Endocrine-Related Cancer

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Repeated parity and usage of oral contraceptives have demonstrated an increased risk of cervical cancer (CC) in HPV-infected women. These lifestyle observations raise the likelihood that oestrogens and HPV infection might act synergistically to affect cancers of the cervix. In vivo studies have indicated the requirement of oestrogens and ERα in the development of atypical squamous metaplasia followed by cervical intraepithelial neoplasia (CIN) I, II and III. CIN II and III are precancerous cervical lesions that can progress over time to CC as an invasive carcinoma. Recently, there has been evidence suggesting that ERα signalling in the tumour epithelium is a preliminary requisite during cancer initiation that is subsequently lost during tumorigenic progression. Conversely, continued expression of stromal ERα gains control over tumour maintenance. This review summarises the current information on the association between oestrogens and HPV infection in contributing to CC and the possibility of SERMs as a therapeutic option.

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“…Hence, it is postulated that both HPV and estradiol enhance the effects of each other, either directly through functional EREs (Estrogen responsive elements) in the viral genome or indirectly encourage uncontrolled cellular proliferation and enhancing malignant proliferation [53]. This synergistic combination between estrogen and HPV is considered as the strongest factor in such carcinogenic transformations [50,[54][55][56][57].…”

Section: How the Hormonal Changes During Pregnancy Favor Cervical Carmentioning

confidence: 99%

Untitled

2017

IPCB

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Statistical reports have shown that breast and cervical malignancies are the most frequent cancers found in the general female population. As more women choose to delay childbearing, the frequency of associated breast cancer is increasing and it is now the most common pregnancy associated carcinoma. The influence of pregnancy on the risk of breast cancer is dependent on several maternal features related to reproductive, genetic and hormonal factors. The effects of pregnancy on the course of breast cancer and its prognosis are complex. It is known that breast cancer is more aggressive in younger women, but whether it is more aggressive during pregnancy in these same women is debatable. One of the reasons for which overall prognosis is diminished in pregnant women is because breast cancer is usually diagnosed at more advanced stage during pregnancy. Ranked second as the most common malignancy in the female population, after breast carcinoma, cancer of the cervix, where HPV (Human papillomavirus) infection is a necessary cause, has a high incidence of 8.9% in all races and a death rate of 2.8%. It is the second cause of cancer death in females aged between 20 and 39 years and it is now known that pregnancy can play an important role in cervical carcinogenesis as well. The aim of this review is to see how the hormonal changes occurring during pregnancy increases the risk of both breast and cervical cancers.

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Baseline human papillomavirus infection, high vaginal parity, and their interaction on cervical cancer risks after a follow-up of more than 10 years

Abstract: A causal-pie modeling based on a women cohort in Taiwan successfully disentangles the roles of virus factors and reproductive factors at study entry, independently or interactively, on subsequent cervical cancer risk.

Cited by 17 publications

References 22 publications

Exploring TLR2 Gene Polymorphisms in Cervical Cancer Development

Exploring TLR2 Gene Polymorphisms in Cervical Cancer Development

Functional association of oestrogen receptors with HPV infection in cervical carcinogenesis

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