Contributions in the domain of cancer research: Review¶Human papillomaviruses and their role in cervical cancer

Abstract

Human papillomaviruses (HPVs) have been linked to a variety of human diseases, most notably cancer of the cervix, a disease responsible for at least 200,000 deaths per year worldwide. Over 100 different types of HPV have been identified and these can be divided into two groups. Low-risk HPV types are the causative agent of benign warts. High-risk HPV types are associated with cancer. This review focuses on the role of high-risk HPV types in cervical tumorigenesis. Recent work has uncovered new cellular partners for many of the HPV early proteins and thrown light on many of the pathways and processes in which these viral proteins intervene. At the same time, structural and biochemical studies are revealing the molecular details of viral protein function. Several of these new avenues of research have the potential to lead to new approaches to the treatment and prevention of cervical cancer.

Evaluation of Human Papillomavirus Infections in Prostatic Disease: a Cross-Sectional Study in Iran

“…Several histopathologic results confirmed that inflammation is much more common in the transition zone and peripheral zone of the prostate gland, which is a prediction for BPH and PCa (Hamid et al, 2011). A relationship between HPV infection and prostate carcinoma has been suggested and some studies demonstrated and confirmed that HPV infection play a main role in the progression and tumorigenesis (Dell and Gaston, 2001;Maghrabi et al, 2007).…”

A DNA recombination-based approach to eliminate papillomavirus infection

“…[1][2][3][4] During productive infection, the virus gains access to the basal epithelium where the viral DNA replicates to a low level of approximately 50 copies per infected cell. [1][2][3][4] Virion production requires terminal differentiation of the host cell during which the virus replicates to high levels, produces the capsid proteins L1 and L2, and mature virions are formed. [1][2][3][4] The shed virions then reinfect the basal epithelium or they can infect new hosts.…”

“…[1][2][3][4] Virion production requires terminal differentiation of the host cell during which the virus replicates to high levels, produces the capsid proteins L1 and L2, and mature virions are formed. [1][2][3][4] The shed virions then reinfect the basal epithelium or they can infect new hosts. PVs infect many different species of animals in nature, and to date more than 100 types of human papillomaviruses (HPVs) have been identified.…”

“…PVs infect many different species of animals in nature, and to date more than 100 types of human papillomaviruses (HPVs) have been identified. [1][2][3][4] Certain mucosatropic HPVs such as types 6 and 11 cause low-grade cervical lesions, while others such as HPV-16, HPV-18, HPV-31, and HPV-45 are strongly associated with cervical cancer and to a lesser degree with other anogenital cancers. [1][2][3][4] The HPV genome often integrates into the host chromosome at the viral E2 locus in these malignancies, and the resulting cells do not express the viral regulatory protein E2.…”

“…[1][2][3][4] Certain mucosatropic HPVs such as types 6 and 11 cause low-grade cervical lesions, while others such as HPV-16, HPV-18, HPV-31, and HPV-45 are strongly associated with cervical cancer and to a lesser degree with other anogenital cancers. [1][2][3][4] The HPV genome often integrates into the host chromosome at the viral E2 locus in these malignancies, and the resulting cells do not express the viral regulatory protein E2. [1][2][3][4] The loss of E2 activity results in the overexpression of the viral E6 and E7 oncoproteins, which inactivate the functions of the cellular tumor suppressor proteins p53 and RB, respectively.…”