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Cancer is a group of several hundred diseases in which abnormal cells are not destroyed naturally by the body but instead multiply and spread out of control. Cancers are distinguished from each other by the specific type of cell involved and the place in the body in which the disease began.
Cervical cancer affects the cells of the uterine cervix, which is the lower part (or 'neck') of the uterus where it joins the inner end of the vagina. Cervical cancer develops when abnormal cells in the lining of the cervix begin to multiply out of control and form precancerous lesions. If undetected, these lesions can develop into tumours and spread into the surrounding tissue.
Worldwide, cervical cancer is the fourth most common cancer affecting women and the seventh most common cancer overall; however, the burden of cervical cancer is not equal globally-around 85% of the global burden occurs in the less developed regions, where cervical cancer accounts for almost 12% of all female cancers (IARC 2014). In contrast, in Australia cervical cancer accounts for less than 2% of all female cancers, with a relatively low incidence of 7 new cases per 100,000 women (AIHW 2014).
women (57%) aged 20–69 had a Pap test in the last 2 years.
It has been recognised for some time that cervical cancer is a rare outcome of persistent infection with one or more oncogenic (cancer-causing) types of human papillomavirus (HPV) (Bosch et al. 2002; Walboomers et al. 1999). These oncogenic types of HPV are known as 'high-risk' HPV, and infection with one or more of these is the underlying cause of almost all cases of cervical cancer. Currently 15 high-risk types of HPV are recognised. HPV types 16, 18, and 45 are most predominantly associated with cervical cancer, with HPV types 16 and 18 detected in 70-80% of cases of cervical cancer in Australia (Brotherton 2008).
However, infection with one or more of the 40 genital HPV types is extremely common, with infection rates of this sexually transmitted infection peaking in women in young adulthood (the period following sexual debut). Most HPV infection is asymptomatic and cleared by the immune system within a year; however, in up to 10% of women the infection can persist, and in a very small number of women, persistent infection with high-risk HPV may eventually lead to cervical cancer.
The 4 major steps in cervical cancer development are infection with HPV (from sexual activity), viral persistence (most HPV infections clear with no treatment), progression to precancerous abnormalities (many of which will also regress with no treatment) and invasive cervical cancer (Schiffman et al. 2007). Note that this is not unidirectional, and that most HPV-infected cells return to normal and a large proportion of precancerous abnormalities do not progress to cervical cancer, even in the absence of treatment.
Infection of cervical cells with high-risk HPV interferes with the normal functioning of these cells, leading to abnormalities in the cells that we recognise as precancerous changes.
However, while the cell changes caused by persistent infection with HPV are necessary for the development of precancerous changes to the cervix, there are a range of other factors that will influence whether precancerous changes will progress to cervical cancer, including smoking; multiparity (specifically more than 5 full-term pregnancies); a young age at first full-term pregnancy; oral contraceptive use; and immunosuppression (Cancer Council Australia 2014).
The role HPV plays in the development of cervical cancer allows for the implementation of both primary and secondary strategies for the prevention of cervical cancer, in those countries that have available resources to make cervical cancer prevention a priority.
In Australia, primary prevention of cervical cancer is through vaccination against HPV through the National HPV Vaccination Program to prevent women being infected with high-risk HPV types 16 and 18. Secondary prevention of cervical cancer is through cervical screening through the National Cervical Screening Program to detect and treat abnormalities while they are in the precancerous stage, before any possible progression to cervical cancer. This is possible because cervical cancer is one of the few cancers that has a precancerous stage that lasts for many years prior to the development of invasive disease, which provides an opportunity for detection and treatment (WHO 2014).
Detection of precancerous abnormalities through cervical screening uses cytology from the Papanicolaou smear, or 'Pap test', as the screening tool. During a Pap test, cells are collected from the transformation zone of the cervix-the area of the cervix where the squamous cells from the outer opening of the cervix and glandular cells from the endocervical canal meet. This is the site where most cervical abnormalities and cancers are detected.
Detecting precancerous changes to cells allows for intervention before cervical cancer develops, so high participation in cervical screening reduces both an individual's risk and the incidence and burden of cervical cancer in Australia overall.
It is also important to recognise that some cervical cancers do not have a precancerous stage, and therefore are simply unable to be detected by cervical screening. These tend to be rare but aggressive cancers such as neuroendocrine cancer of the cervix, the two most aggressive types being small cell neuroendocrine carcinoma and large cell neuroendocrine carcinoma, neither of which appear to possess a preinvasive stage (Necervix.com 2014)
The National Cervical Screening Program aims to reduce cervical cancer cases as well as illness and death resulting from cervical cancer through an organised approach to cervical screening aimed at detecting and treating high-grade abnormalities before possible progression to cervical cancer. More women having regular Pap tests means that more of the serious diseases that can lead to cervical cancer can be found and treated. This leads to fewer cases of cervical cancer, and fewer women dying from this disease.
The National Cervical Screening Program recommends Pap tests every two years for women aged 18–20 or over who have ever been sexually active-including women who have been vaccinated against HPV.
For more information on the National Cervical Screening Program, and for the latest cervical screening data, see the latest Cervical screening in Australia report.
For more information on the National Cervical Cancer Screening Program visit www.cancerscreening.gov.au.
AIHW 2014. Cancer in Australia: an overview 2014. Cancer series no. 90. Cat. no. CAN 88. Canberra: AIHW.
Bosch FX, Lorincz A, Muñoz N, Meijer CJ & Shah KV 2002. The causal relation between human papillomavirus and cervical cancer. Journal of Clinical Pathology 55(4):244–65.
Brotherton JM 2008. How much cervical cancer in Australia is vaccine preventable? A meta-analysis. Vaccine 26(2):250–56.
IARC (International Agency for Research on Cancer) 2014. GLOBOCAN 2012: Estimated Cancer Incidence, Mortality and Prevalence Worldwide in 2012. France. Viewed 14 April 2015.
Necervix.com 2014. Neuroendocrine cancer of the uterine cervix: fact sheet PDF. Viewed 9 February 2015.
Schiffman M, Castle PE, Jeronimo J, Rodriguez AC & Wacholder S 2007. Human papillomavirus and cervical cancer. Lancet 370(9590):890–907.
Walboomers JM, Jacobs MV, Manos MM, Bosch FX, Kummer JA, Shah KV et al. 1999. Human papillomavirus is a necessary cause of invasive cervical cancer worldwide. Journal of Pathology 189(1):12–19.
WHO (World Health Organization) 2014. Comprehensive cervical cancer control: a guide to essential best practice. 2nd edn. Geneva: WHO.