Cervical Cancer Prevention Week 19-25 January 2014.
Did you know that it is preventable? Yet 20% of women in the UK decline the invite to be tested. Furthermore, only half of all girls are offered the HPV vaccine.
The cervix (or neck of the uterus) is the lower, narrow part of the uterus which joins to the top end of the vagina. The opening of the cervix is called the os. The cervical os allows menstrual blood to flow out from the vagina during menstruation. During pregnancy, the cervical os closes to help keep the foetus in the uterus until birth. During labour, the cervix dilates, or widens, to allow the passage of the baby from the uterus to the vagina. Approximately half the cervix length is visible with appropriate medical equipment; the remainder lies above the vagina beyond view.
The cervix is covered with a layer of skin-like cells on its outer surface, called the 'ectocervix'. There are also glandular cells lining the inside of the cervix called the endocervix. These cells produce mucus. The skin-like cells of the ectocervix can become cancerous, leading to a squamous cell cervical cancer. Or the glandular cells of the endocervix can become cancerous, leading to an adenocarcinoma of the cervix.
The ectocervix and endocervix have a three main skin layers or zones: * The basal layer--cells are produced here. Older cells are pushed up towards the surface. If you contract HPV, the virus will attack the basal layer cells.
* Midzone--the middle layer of cells. As cells move up from the basal layer they lose their capacity to divide making them fully mature cells.
* Superficial zone--The uppermost surface of the cervix where mature cells eventually die and shed in the normal process of skin shedding (1). Cervical screening takes cells from this area.
The area where cervical cells are most likely to become cancerous is called the transformation zone. This is the area just around the opening of the cervix that leads on to the endocervical canal (the narrow passageway that runs up from the cervix into the womb). The transformation zone is the area that your doctor or nurse will concentrate on during cervical screening.
The vagina is the tube from the outside of the body to the entrance to the womb. The skin-like cells that cover the cervix join with the skin covering the inside of the vagina, so even if you have had your womb and cervix removed, you can still have screening samples taken from the top of the vagina.
Cervical cancer forms in tissues of the cervix (the organ connecting the uterus and vagina). It is usually a slow-growing cancer that may or may not have symptoms but can be prevented through regular screening (a procedure in which cells are taken from the cervix and looked at under a microscope). Cervical cancer is not thought to be hereditary. (2,3,4)
99.7% of cervical cancers are caused by persistent human papillomavirus (HPV) infection which causes changes to the cervical cells. HPV is an extremely common virus; around four out of five people will be exposed to the virus. Anyone who is sexually active can be infected with HPV at some time and the body's immune system will usually clear it up. Generally, most people don't even know they have contracted the virus at all.
Cervical abnormalities are caused by persistant HPV infection. These abnormal cells found through cervical screening are not cancerous but given time (often years) they may go on to develop into cancer. However, often the cells return to normal by themselves. Information from the NHS National Screening Programmes 2010-11 showed that 7-9% of women will have abnormal cells of which only a small percentage will go on to have cancer.
The most effective method of preventing cervical cancer is through regular cervical screening which allows detection of any early changes of the cervix and for younger women the HPV vaccination can help prevent 70% of cervical cancers. Cervical cancer is largely preventable and, if caught early, survival rates are high.
Human papillomavirus (HPV)
Human papillomavirus (HPV) is an extremely common virus. At some point in our life most of us will catch the virus. The world over, HPV is the most widespread sexually transmitted virus; 80% (four out of five) of the world's population will contract some type of the virus once (5). If you catch HPV, in the majority of cases the body's immune system will clear or get rid of the virus without the need for further treatment. In fact you may not even know that you had contracted the virus.
There are over 100 identified types of HPV; each different type has been assigned a number. HPV infects the skin and mucosa (any moist membranes such as the lining of the mouth and throat, the cervix and the anus). Different types affect different parts of the body causing lesions. The majority of HPV types infect the skin on external areas of the body including the hands and feet. For example, HPV types 1 and 2 cause verrucas on the feet (6).
Around 40 of the HPV types affect the genital areas of men and women, including the skin of the penis, vulva (area outside the vagina), anus, and the linings of the vagina, cervix, and rectum (7). Around 20 of these types are thought to be associated with the development of cancer. The WHO International Association for Research on Cancer (IARC) identifies 13 of these types as oncogenic (cancer causing). This means there is direct evidence that they are associated with the development of cervical cancer and are considered high-risk (8). These high risk types of HPV are: 16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, and 68 (9). A person infected with high-risk genital HPV will show no symptoms so they may never even know they have it.
Additionally there are nine HPV types that may also be associated with the development of cervical cancer these are types: 26, 53, 64, 65, 66, 67, 69, 70, 73, 82. However, currently there is not enough evidence to indicate that these types are high risk for cervical cancer (10).
The remaining genital HPV types have been designated low-risk as they do not cause cervical cancer but they can cause other problems such as genital warts.
HPV and cervical cancer
HPV infection causes changes to the cells of the cervix creating abnormalities, it affects the DNA in the cells meaning new cells will be abnormal. HPV attacks the basal cells of the cervix (these are specific cells found in skin that reproduce new skin cells) (11). These abnormalities can result in the production of damaged and disorganised cervical cells that cannot function correctly. Once these abnormalities become severe they can develop into cancer which is why cervical screening and HPV vaccination are important in helping to prevent cancer.
99.7% of cervical cancers are caused by HPV (12). Around 13 high-risk types of HPV are responsible for causing cervical cancers (13). Within the high-risk group types 16 and 18 are the most prevalent, causing over 70% of cervical cancers (14).
80% of women are infected with genital HPV at some point in their lives, but never know they have been infected because HPV is usually cleared (without treatment) by the body's immune system. However, a small percentage of women do not clear the infection and it can remain 'dormant' (inactive) or persistent in their bodies, sometimes for many years (15,16). We still do not understand why some women are able to clear the infection while in others the virus may lead to the development of abnormal cells and possibly cervical cancer.
The HPV vaccines and preventing cervical cancer.
Each year in the UK, over 3000 women are diagnosed with cervical cancer and around 300,000 women are told they may have some form of cervical abnormality. Cervical cancer is caused by a very common virus called human papillomavirus (HPV). Anyone who is sexually active can contract HPV through contact with someone who already has the virus. Most people are infected with HPV at some point in their lives but may never know they have been infected. Like other viral infections such as a cold, HPV is usually cleared by the body's immune system without the need for other treatment. We do not know why a small percentage of people do not clear the infection, which can remain 'dormant' (inactive) in their bodies sometimes for many years (17,18).
There are around 13 high-risk types of HPV that are responsible for almost all cervical cancers (19). Within the high-risk group, types 16 and 18 are the most prevalent and responsible for 70% of cervical cancers (20). HPV infection can cause changes to the cells of the cervix creating abnormalities. Once these abnormalities become severe they can develop into cancer which is why cervical screening and HPV vaccination are important in helping to prevent cervical cancer.
There are two HPV vaccines which provide protection against the two high risk types of HPV (types 16 and 18) that cause 70% of all cervical cancers. One of the vaccines is also designed to provide protection against genital warts which are caused by low risk types of HPV. Low risk types of HPV do not cause cervical cancer.
Research indicates that the HPV vaccine could prevent two thirds of cervical cancers in women under the age of 30 by 2025 but only if uptake of the HPV vaccination is at 80% (21). To date, the UK has achieved this level each year in the national HPV immunisation programme.
Cervical Screening (smear test)
Each year around five million women in the UK are invited for cervical screening (smear test). Cervical screening is NOT a test to find cancer. It is a screening test to detect abnormalities (pre-cancer) at an early stage in the cells in the cervix.
Please take up your invitation to attend your cervical screening test, it saves lives.
Cervical screening is the process of taking a sample of cells from your cervix which are then examined to detect abnormalities that might develop into cancer in the future. The sample of cells is placed in liquid so that it can be analysed in the laboratory. This process is called liquid based cytology (LBC). Screening can detect precancerous/ abnormal cells and the detection and successful treatment of these cells usually prevents the occurrence of cancer. Changes in these cells are generally caused by certain types of human papillomavirus (HPV). Testing for the HPV virus itself can also be done on the same LBC sample that is examined under the microscope, although at the moment this is not done routinely on all samples in the UK.
Around 3,000 women are diagnosed with cervical cancer in UK each year 22. Regular cervical screening provides a high degree of protection against developing cervical cancer and is offered free on the NHS. It is estimated that early detection and treatment through cervical screening can prevents up to 75% of cervical cancers from developing in the UK (23). Not going for cervical screening is one of the biggest risk factors for developing cervical cancer.
Abnormal cervical cells and treatment
The cervix is covered with a layer of skin-like cells on its outer surface, called the ectocervix. The results of your cervical screening are based on the analysis of the cells from the surface of the ectocervix.
The screening can only detect whether there are abnormal cells present. Depending on the results of your screening, you may be referred to a specialist clinic in the hospital (colposcopy) in order to get a more accurate diagnosis and have treatment if needed. You will need to have a small sample taken from your cervix to analyse the cells from the layer beneath the surface, this is called a biopsy. Usually biopsies are only a few millimetres in size.
Want to know more or want to help? Visit Jo's cervical cancer trust at http:// www.jostrust.org.uk/about-cervicalcancer/
(1.) Dunleavey R (2009) Cervical Cancer: a guide for nurses. Wiley-Blackwell, UK. pp.9
(2.) Magnusson P, Sparen P, and Gyllensten UB (1999) Genetic link to cervical tumours. Nature 400, 29-30.
(3.) Walboomers JMM, Jacobs MV, Manos MM, Bosch FX, Kummer JA, Shah KV, Snijder PJ, Peto J, Meijer CJ and Munoz Nl (1999) Human papillomavirus is a necessary cause of invasive cancer worldwide. Journal of Pathology, 189 (1), 12-19.
(4.) Bosch FX et al. (2002) The causal relation between human papillomavirus and cervical cancer. Journal of Clinical Pathology 55, 244-265
(5.) Koutsky L. 1997. Epidemiology of genital human papillomavirus infection. The American Journal of Medicine, 102 (5A), 3-8.
(6.) Lacey CJ et al., 2006. Chapter 4: Burden and management of non-cancerous HPV-related conditions: HPV-6/11 disease. Vaccine, 24 (3), S3/35-41.
(7.) Giuliano AR et al., 2008. Epidemiology of human papillomavirus infection in men, cancers other than cervical and benign conditions. Vaccine, 26 (10), K17-28.
(8.) Walboomers JMM et al.,1999 Human papillomavirus is a necessary cause of invasive cancer worldwide. Journal of Pathology, 189 (1), 12-19.
(9.) Szarewski A. 2012. Cervarix: a bivalent vaccine against HPV types 16 and 18, with cross-protection against other high-risk HPV types. Expert Review Vaccines 11(6), 645-657.
(10.) Bouvard et al., 2009. A review of human carcinogens--Part B: biological agents. Lancet Oncology 10, 321-322.
(11.) Dunleavey R. 2009. Cervical Cancer: a guide for nurses. Wiley-Blackwell, UK, 9.
(12.) Walboomers JMM et al.,1999. Human papillomavirus is a necessary cause of invasive cancer worldwide. Journal of Pathology, 189 (1), 12-19.
(13.) Li N et al., 2011. Human papillomavirus type distribution in 30,848 invasive cervical cancers worldwide: variation by geographical region, histological type and year of publication. International Journal of Cancer 128, 927-935.
(14.) Bosch FX et al., 2008. Epidemiology and natural history of human papillomavirus infections and type-specific implications in cervical neoplasia. Vaccine 26 (10), K1-16.
(15.) Munoz N et al., 2009. Persistence of HPV infection and risk of high-grade cervical intraepithelial neoplasia in a cohort of Colombian women. British Journal of Cancer 100, 1184-1190.
(16.) Moscicki AB et al., 1998. The natural history of human papillomavirus infection as measured by repeat DNA testing in adolescent and young women. Journal of Pediatr, 132, 277-284.
(17.) Munoz N, et al., 2009. Persistence of HPV infection and risk of high-grade cervical intraepithelial neoplasia in a cohort of Colombian women. British Journal of Cancer 100, 1184-1190.
(18.) Moscicki, AB, et al., 1998. The natural history of human papillomavirus infection as measured by repeat DNA testing in adolescent and young women. Journal of Pediatr 132, 277-284.
(19.) Li N et al., 2011. Human papillomavirus type distribution in 30,848 invasive cervical cancers worldwide: variation by geographical region, histological type and year of publication. International Journal of Cancer 128, 927-935.
(20.) Bosch, F.X., et al., Epidemiology and natural history of human papillomavirus infections and type-specific implications in cervical neoplasia. Vaccine, 2008. 26 (10), K1-16.
(21.) Cuzick J, Castanon A, and Sasieni P. 2010. Predicted impact of vaccination against human papillomavirus 16/18 on cancer incidence and cervical abnormalities in women aged 20-29 in the UK. British Journal of Cancer 102, 933-939.
(22.) Cancer Research UK website: http ://www. cancerresearchuk.org/cancerinfo/cancerstats/types/cervix/mortality/. Accessed 30.05.2013.
(23.) Peto et al., 2004. The cervical cancer epidemic that screening has prevented in the UK. Lancet, 35, 249-56.
Additional thanks to Jo's cervical cancer trust. http://www.jostrust.org.uk/about-cervical cancer/
National Awareness Days http://www.national awareness-days.com
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|Title Annotation:||HEALTH AWARENESS WEEK; European Cervical Cancer Association|
|Date:||Jan 1, 2014|
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