Cervical cancerIntroduction

Cervical cancer starts on the surface of the cervix, which is the lower part of the uterus (womb) that opens at the top of the vagina. The cervix surface has two types of cells: squamous and columnar. The majority of cervical cancers are from squamous cells.

The development of cervical cancer is usually very slow. It starts as a precancerous condition called dysplasia, which can be detected by a Pap smear and is 100% treatable.

Worldwide, cervical cancer is the third most common type of cancer in women. It is much less common in the United States because of the routine use of Pap smears. Most women who are diagnosed with cervical cancer today have not had regular Pap smears, or they have not followed up on abnormal results.

Undetected, precancerous changes can develop into cervical cancer and spread to the bladder, intestines, lungs, and liver. It can take years for precancerous changes to turn into cervical cancer. Patients with cervical cancer do not usually have problems until the cancer is advanced and has spread.

Almost all cervical cancers are caused by HPV (human papilloma virus). HPV is a common virus that is spread through sexual intercourse. There are many different types of HPV, and many do not cause problems. However, only certain strains of HPV actually lead to cervical cancer. (Other strains may cause genital warts.)
https://health.google.com/health/ref/Cervical+cancer

Both smoking and second-hand smoke increase the risk of cervical cancer1. Smoking may reduce the likelihood that the epithelial (surface) cells of the cervix have tight junctions. This same effect has been observed for epithelial cells in the lungs2. Once the epithelial cells lose their tight junctions, it is much easier for HPV to penetrate. 

Page last edited: 22 August 2011

References

  1. Tsai HT, Tsai YM, Yang SF, Wu KY, Chuang HY, Wu TN, Ho CK, Lin CC, Kuo YS, Wu MT. Lifetime cigarette smoke and second-hand smoke and cervical intraepithelial neoplasm–a community-based case-control study. Gynecol Oncol. 2007 Apr; 105 (1): 181-8.
  2. Shaykhiev, R. Otaki, F. Bonsu, P. Dang, D. T. Teater, M. Strulovici-Barel, Y. Salit, J. Harvey, B. G. Crystal, R. G. Cigarette smoking reprograms apical junctional complex molecular architecture in the human airway epithelium in vivo. Cell Mol Life Sci. 2010 Sep 6;