Cervical cancer

Cervical cancer forms in tissues of the cervix. The cervix is an organ that connects 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. [1] [2] [3]
 
99.7% of cervical cancers are caused by persistent high risk human papillomavirus (HPV) infection which causes changes to the cervical cells. HPV is an extremely common virus; around four out of five people 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.
 
Cervical abnormalities are caused by persistent high risk 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 2012-13 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 seven out of ten cervical cancers (70%). Cervical cancer is largely preventable and, if caught early, survival rates are high.
 

References

  1. Magnusson P et al., 1999. Genetic link to cervical tumours. Nature 400, 29-30.
  2. Walboomers JMM, et al., 1999. Human papillomavirus is a necessary cause of invasive cancer worldwide. Journal of Pathology, 189 (1), 12–19.
  3. Bosch FX et al. 2002., The causal relation between human papillomavirus and cervical cancer. Journal of Clinical Pathology 55, 244-265.
     
Date last updated: 
11 Feb 2014
Date due for review: 
09 Feb 2016