Oncogenic potential of Human Papillomavirus (HPV) and its relation with cervical cancer

Faridi, Rabia; Zahra, Amreen; Khan, Khalida; Idrees, Muhammad

doi:10.1186/1743-422x-8-269

Cited by 143 publications

(120 citation statements)

References 70 publications

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“…The product of E5 could downregulate the histocompatibility leucocyte antigen (HLA) expression of the infected cells, facilitating virus immune escape (13,14). E6 and E7 are considered as tumorigenic genes; their products could bind to tumor suppressor protein p53 and arrest cell cycle, impairing the infected cells apoptosis and enhancing their transformation (15). The L1 and L2 proteins are responsible for forming the structural components of the viral capsid.…”

Section: Effect Of Human Papillomavirus Infection On the Immune Systementioning

confidence: 99%

Effect of human papillomavirus infection on the immune system and its role in the course of cervical cancer

et al. 2015

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Abstract. Human papillomavirus (HPV) is widely known as a cause of cervical intraepithelial neoplasia (CIN) and cervical cancer. The mechanisms involved have been studied by numerous studies. The integration of the virus genome into the host cells results in the abnormal regulation of cell cycle control. HPV can also induce immune evasion of the infected cells, which enable the virus to be undetectable for long periods of time. The induction of immunotolerance of the host's immune system by the persistent infection of HPV is one of the most important mechanisms for cervical lesions. The present review elaborates on the roles of several types of immune cells, such as macrophages and natural killer cells, which are classified as innate immune cells, and dendritic cells (DCs), cluster of differentiation (CD)4 + /CD8 + T cells and regulatory T cells, which are classified as adaptive immune cells. HPV infection could effect the differentiation of these immune cells in a unique way, resulting in the host's immune tolerance to the infection. The immune system modifications induced by HPV infection include tumor-associated macrophage differentiation, a compromised cellular immune response, an abnormal imbalance between type 1 T-helper cells (Th1) and Th2 cells, regulatory T cell infiltration, and downregulated DC activation and maturation. To date, numerous types of preventative vaccines have been created to slow down carcinogenesis. Immune response activation-based therapeutic vaccine is becoming more and more attractive for the treatment of HPV-associated diseases.

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Section: Effect Of Human Papillomavirus Infection On the Immune Systementioning

confidence: 99%

Effect of human papillomavirus infection on the immune system and its role in the course of cervical cancer

et al. 2015

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“…Since it is very difficult to realize a longitudinal study that might include patients without any cytological anomalies for decades in order to see the relationship between GST M1 and T1 genetic polymorphisms and HPV HR infections, the present study has included HPV-HR positive patients with LSIL, HSIL or in situ carcinoma, which, accordingly to the known HPV natural history (1,2,4,5,22,23), are due to persistent HPV-HR that cause significant squamous cell modifications.…”

Section: Discussionmentioning

confidence: 99%

“…Cervical neoplasia is the second most prevalent cancer in women after lung cancer, representing one of the major morbidity causes, especially in young women (1,2). Scientific medical research over the past two decades has brought conclusive and unquestionable evidence that cervical neoplasia results from persistent chronic infections with oncogenic types of the human papilloma virus (HPV) known as high-risk HPV (hrHPV).…”

Section: Genetic Polymorphisms Of Glutathione S Transferase and Cervimentioning

confidence: 99%

Genetic polymorphisms of glutathione S transferase and cervical intraepithelial neoplasia

Muresan

Cătană

Popp

et al. 2016

Revista Romana De Medicina De Laborator

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“…In addition to HPV infection, other factors affect the development of CC, including immunological disorders and genetic malfunctions such as point mutations, deletions, amplifications and rearrangements of DNA (6). Previous studies have suggested that epigenetic changes may significantly impact cervical carcinogenesis (6)(7)(8)(9).…”

Section: Introductionmentioning

confidence: 99%

“…CC is a gynecological malignancy associated with oncogenic human papillomavirus (HPV) infection (6,7). In addition to HPV infection, other factors affect the development of CC, including immunological disorders and genetic malfunctions such as point mutations, deletions, amplifications and rearrangements of DNA (6).…”

Section: Introductionmentioning

confidence: 99%

Transcript levels of ten-eleven translocation type 1–3 in cervical cancer and non-cancerous cervical tissues

et al. 2017

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Abstract. Decreased expression of ten-eleven translocation (TET1, TET2 and TET3) proteins has been reported in various types of cancer. However, the expression levels of TET proteins in cervical cancer (CC) remain to be elucidated. The present study determined the levels of TET1, TET2 and TET3 transcripts in cancerous (n=80) and non-cancerous cervical tissues (n=41). The results revealed a significant reduction in TET1 transcripts (P=0.0000001) in cervical tissue samples from patients with primary CC compared with samples from control patients. Significantly decreased TET1 transcript levels, as compared to non-cancerous cervical tissues, were also observed in tissue samples with the following characteristics: Stage I (P=0.016), II (P<0.0001), III (P=0.00007) and grade of differentiation G1 (P=0.026), G2 (P=0.00006), G3 (P=0.0007) and Gx (P=0.0004) and squamous histological type (P<0.00001). TET1 transcript levels were significantly lower in patients aged 45-60 years (P=0.0002) and patients age >60 years (P=0.003), as compared with non-cancerous cervical tissues. TET2 transcript levels were lower in cervical cancer tissues classified as stage II (P=0.043) and TET3 transcript levels were lower in stage III samples (P=0.010), tissue samples with a grade of differentiation of G3 (P=0.025) and tissue with squamous type histology (P=0.047), all compared with non-cancerous cervical tissues. The present study demonstrated a significantly reduced level of TET1 transcripts in cancerous cervical tissues, as compared with non-cancerous tissues. Furthermore, decreased TET1-3 transcript levels were identified when patients with CC were stratified by clinicopathological variables, as compared with non-cancerous cervical tissues.

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Oncogenic potential of Human Papillomavirus (HPV) and its relation with cervical cancer

Cited by 143 publications

References 70 publications

Effect of human papillomavirus infection on the immune system and its role in the course of cervical cancer

Effect of human papillomavirus infection on the immune system and its role in the course of cervical cancer

Genetic polymorphisms of glutathione S transferase and cervical intraepithelial neoplasia

Transcript levels of ten-eleven translocation type 1–3 in cervical cancer and non-cancerous cervical tissues

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