Pathogenesis of Cervical Cancer
CELL BIOLOGY ESSAY -- PATHOGENESIS OF CERVICAL CANCER
Introduction
According to the Centre for Health Protection of the Department of Health (2011), cervical cancer becomes the tenth commonest cancer in Hong Kong in 2008. Cervical cancer usually arises from sexual activity and human papillomavirus (HPV) (Bellentir, 2002). In this essay, Human papillomavirus would be further discussed. For example, the signal transport pathway of HPV 16 and HPV 18, which many scientists believe that they are closely related of causing cervical cancer, as well as the HPV vaccine and chemotherapy of cervical cancer, would be discussed.
HPV as the Main Cause of Cervical Cancer
Cervical cancer usually starts from the invasion of HPV to the epidermal stratified squamous epithelium of cervix surface (N.D., 2011). HPV embeds with L1 protein. When virus enters the cell, the L1 protein layer degrades and releases the viral DNA in the nucleus of the host cell. And then the viral DNA transcribes to form mRNA, and attaches on the cellular DNA. Thus, the cellular DNA integrates. Finally it continues the translation process and produces E6 and E7 protein. HPV consists of 8 genes, oncogene E6 and E7 genes are closely related to the control of transcription process at human as well as the cell cycle. Once HPV enters the cervix cell, it triggers the HPV to have the transcription for production of viral E6 and E7 mRNA and the translation for production of E6 and E7 protein from double strand of the viral DNA. (Lin & Wu, 1990)
How E7 Protein Affects the Cell Cycle
In the normal cell cycle, after forming the G1Cdk-cyclin complex and inputting of ATP, Rb protein converts from active form to inactive one by phosphorylation (adding of phosphate group). After that, E2F transcription factor releases and triggers the gene transcription, and then mRNA translates for preparing essential materials like enzymes and protein for DNA synthesis phase (S phase). But when E7 enters the cell, it will bind
Introduction
According to the Centre for Health Protection of the Department of Health (2011), cervical cancer becomes the tenth commonest cancer in Hong Kong in 2008. Cervical cancer usually arises from sexual activity and human papillomavirus (HPV) (Bellentir, 2002). In this essay, Human papillomavirus would be further discussed. For example, the signal transport pathway of HPV 16 and HPV 18, which many scientists believe that they are closely related of causing cervical cancer, as well as the HPV vaccine and chemotherapy of cervical cancer, would be discussed.
HPV as the Main Cause of Cervical Cancer
Cervical cancer usually starts from the invasion of HPV to the epidermal stratified squamous epithelium of cervix surface (N.D., 2011). HPV embeds with L1 protein. When virus enters the cell, the L1 protein layer degrades and releases the viral DNA in the nucleus of the host cell. And then the viral DNA transcribes to form mRNA, and attaches on the cellular DNA. Thus, the cellular DNA integrates. Finally it continues the translation process and produces E6 and E7 protein. HPV consists of 8 genes, oncogene E6 and E7 genes are closely related to the control of transcription process at human as well as the cell cycle. Once HPV enters the cervix cell, it triggers the HPV to have the transcription for production of viral E6 and E7 mRNA and the translation for production of E6 and E7 protein from double strand of the viral DNA. (Lin & Wu, 1990)
How E7 Protein Affects the Cell Cycle
In the normal cell cycle, after forming the G1Cdk-cyclin complex and inputting of ATP, Rb protein converts from active form to inactive one by phosphorylation (adding of phosphate group). After that, E2F transcription factor releases and triggers the gene transcription, and then mRNA translates for preparing essential materials like enzymes and protein for DNA synthesis phase (S phase). But when E7 enters the cell, it will bind
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