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What Causes Cervical Cancer?

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In recent years, there has been a lot of progress in understanding what happens in cervical cells when cancer develops. In addition, several risk factors have been identified that increase the odds that a woman might develop cervical cancer (see Risk Factors for Cervical Cancer).

The development of normal human cells mostly depends on the information contained in the cells’ DNA. DNA is the substance in our cells that makes up our genes, which control how our cells work. We look like our parents because they are the source of our DNA. However, DNA affects more than just how we look.

Some genes control when cells grow, divide, and die:

  • Genes that help cells grow, divide, and stay alive are called oncogenes.
  • Genes that help keep cell growth under control or make cells die at the right time are called tumor suppressor genes.

Cancers can be caused by DNA mutations (gene defects) that turn on oncogenes or turn off tumor suppressor genes.

Human papillomaviruses (HPV) have two proteins, E6 and E7, which turn off some tumor suppressor genes, such as p53 and Rb. This may allow the cells lining the cervix to grow too much and to develop changes in additional genes, which in some cases can lead to cancer.

HPV is not the only cause of cervical cancer. Most women with HPV don’t get cervical cancer, and other risk factors, like smoking and HIV infection, influence which women exposed to HPV are more likely to develop cervical cancer.

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Developed by the American Cancer Society medical and editorial content team with medical review and contribution by the American Society of Clinical Oncology (ASCO).

Jhungran A, Russell AH, Seiden MV, Duska LR, Goodman A, Lee S, et al. Chapter 84: Cancers of the Cervix, Vulva, and Vagina. In: Niederhuber JE, Armitage JO, Doroshow JH, Kastan MB, Tepper JE, eds. Abeloff’s Clinical Oncology. 6th ed. Philadelphia, Pa: Elsevier; 2020.

Yim EK, Park JS. The role of HPV E6 and E7 oncoproteins in HPV-associated cervical carcinogenesis. Cancer Res Treat. 2005;37(6):319–324. doi:10.4143/crt.2005.37.6.319.

Last Revised: July 1, 2025

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