Human papillomaviruses (HPVs) can lead to cancers in both males and females at multiple anatomic sites including cervical (90%), vulvar (70%), vaginal (70%), anal (90%), oropharyngeal (70%), and penile cancers (more than 60%). High risk HPV E6/E7 expression initiate malignant transformation processes including bypass of cell cycle control, inhibition of apoptosis and transcriptional activation of genes that promote proliferation. HPV in vitro and transgenic mouse models have been generated and characterized. These models provide information regarding the biological properties of HPV genes. However, further investigation into the molecular profiles between HPV-positive and HPV-negative cancers is needed to understand whether specific alterations may accelerate the HPV related tumorigenesis.
This Research Topic will highlight the role of HPV in different cancers, including molecular pathways of HPV associated cancers and experimental models for studying HPV associated cancers. Understanding how HPV associated pathways lead to carcinogenesis will advance our understanding of HPV carcinogenesis and will provide much needed data to aid studies on prevention, early detection, prognosis, and development of therapeutic agents to reduce the morbidity and mortality from HPV associated cancers. We invite Review and Research Articles that include mechanism and role of viral integration in mediating carcinogenesis, in vivo models to study HPV associated cancers, gene alterations in HPV associated cancers, differences in immune microenvironment between HPV+ vs HPV cancers, limitations of current experimental models among other topics associated with the molecular aspects of HPV in cancer.
Please note: manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by validation (independent cohort or biological validation in vitro or in vivo) are out of scope for this section and will not be accepted as part of this Research Topic.
Human papillomaviruses (HPVs) can lead to cancers in both males and females at multiple anatomic sites including cervical (90%), vulvar (70%), vaginal (70%), anal (90%), oropharyngeal (70%), and penile cancers (more than 60%). High risk HPV E6/E7 expression initiate malignant transformation processes including bypass of cell cycle control, inhibition of apoptosis and transcriptional activation of genes that promote proliferation. HPV in vitro and transgenic mouse models have been generated and characterized. These models provide information regarding the biological properties of HPV genes. However, further investigation into the molecular profiles between HPV-positive and HPV-negative cancers is needed to understand whether specific alterations may accelerate the HPV related tumorigenesis.
This Research Topic will highlight the role of HPV in different cancers, including molecular pathways of HPV associated cancers and experimental models for studying HPV associated cancers. Understanding how HPV associated pathways lead to carcinogenesis will advance our understanding of HPV carcinogenesis and will provide much needed data to aid studies on prevention, early detection, prognosis, and development of therapeutic agents to reduce the morbidity and mortality from HPV associated cancers. We invite Review and Research Articles that include mechanism and role of viral integration in mediating carcinogenesis, in vivo models to study HPV associated cancers, gene alterations in HPV associated cancers, differences in immune microenvironment between HPV+ vs HPV cancers, limitations of current experimental models among other topics associated with the molecular aspects of HPV in cancer.
Please note: manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by validation (independent cohort or biological validation in vitro or in vivo) are out of scope for this section and will not be accepted as part of this Research Topic.
