The cervix is the opening to the uterus, located at the top of the vagina. Cervical cancer exists when cells of the cervix grow abnormally for a long period of time and then spread to other parts of the body through the blood and lymphatic system.

Cervical cancer is preceded by precancerous changes in cervical cells that can be detected by a simple test called a Pap smear. When these milder degrees of cell abnormalities are present, the condition is called cervical dysplasia.

Since the Pap smear has become a routine part of a woman’s  gynecological checkup, cervical cancer is largely a preventable disease and deaths from cervical cancer in the U.S. have declined by 70 percent. Cervical cancer still occurs in about 15,000 American women a year and kills about 5,000. It is most common among women in their late 30s to their early 60s.

Causes and Risk Factors
The most common cause of cervical cancer is the human papillomavirus or HPV. HPV is found in about 10% of all women and as many as 20% of female college students. Also called genital wart virus or condyloma virus, HPV is spread through sexual contact. Thus, the more sexual partners you have had and/or the more sexual partners they have had, the higher your risk for cervical cancer. Another known risk factor for cervical cancer is smoking, possibly because it weakens the immune system’s ability to destroy abnormal cells.

HPV is actually a group of about 70 viruses, of which some cause cancers and some do not. Sophisticated laboratory tests today can identify the presence of specific types most likely to be aggressive in causing cervical dysplasia or cancer.  Most women who are initially infected with the virus clear it without any treatment and are not at risk for cervical cancer, but in a small percentage the virus persists leading to eventual cancer years later.

There are no symptoms of cervical dysplasia or cervical cancer, except in cases of very advanced cervical cancer that causes bleeding or discharge.

Diagnosis and Treatment Options
The Pap smear detects abnormalities in cervical cells and classifies them as low-grade (mildly abnormal, probably due to infection), high-grade (dysplastic cells are present, further testing needed), or cancer. The Pap smear can also detect certain other kinds of atypical cells that may require further testing.

When further testing is indicated, your doctor may recommend a colposcopy, a test in which the cervix itself may be examined visually under magnification. If it appears that more cells are needed for analysis by a pathologist, your doctor may remove a tiny pinch of the cervix skin in a cervical biopsy.

Cervical dysplasia may be treated with cryotherapy,LEEP (loop electrosurgical excision procedure),laser therapy or cone biopsy. The cure rate for cervical dysplasia is 95%.

Cervical cancer is generally treated with a radical hysterectomy to ensure that the cancer has not spread. The cure rate for cervical cancer is 85%. (parker p 273)

When cancer occurs in the uterus, it usually occurs in the innermost layer — the endometrium — and therefore the terms uterine cancer and endometrial cancer are used interchangeably. As with all cancers, uterine cancer is characterized by changes in the cells that cause them to start growing uncontrollably, although why this happens is not yet fully understood.

When cells start growing abnormally in the uterine lining, they first go through a pre-cancer stage called atypical endometrial hyperplasia. This differs from simple hyperplasia of the uterine lining, a benign condition.

Endometrial cancer is rare, affecting 2 out of every 1,000 postmenopausal women who are not on hormone therapy. It is rarely seen in women under age 40 and is most common among women in their sixties. Taking hormone therapy that includes progesterone, the female hormone responsible for maturing the endometrial lining, reduces the risk to 1 women in 1,000. However, taking only estrogen after menopause increases the risk to 10 women in 1,000. This is why “unopposed estrogen” is no longer recommended for menopausal women.

Causes and Risk Factors
There is no single known cause of endometrial cancer. However, much is known about the factors that appear to increase a woman’s risk of developing it. In general, endometrial cancer is related to imbalances between the two primary female hormones, estrogen and progesterone. Because estrogen promotes growth of endometrial cells and progesterone stops that growth, factors that tip the balance in favor of estrogen may lead to overgrowth of the endometrium. These include being overweight (fat cells convert other hormones into estrogen), missing periods due to a failure to ovulate (and therefore, failing to produce progesterone); and taking unopposed estrogen. There is also a slightly increased risk of uterine cancer in women taking tamoxifen, a drug prescribed for those who have had breast cancer to help prevent recurrence.

Conversely, women who have had multiple full-term pregnancies and women who have taken birth control pills for five years or longer have a lower risk of developing endometrial cancer at any age.

Endometrial cancer causes abnormal uterine bleeding. The precancerous condition also causes abnormal bleeding, and thus, uterine cancer is most often caught in its earliest stages and can usually be cured. This is why it is important for postmenopausal women to report any spotting or unusual bleeding to their gynecologist.

Diagnosis and Treatment Options
Your doctor may first use a sonogram to see whether your uterine lining appears thickened. If it does, either an endometrial biopsy or a hysteroscopy may be performed to collect cells for examination by a trained pathologist. If either atypical hyperplasia or uterine cancer is found, a hysterectomy is generally recommended and cures the cancer in 95% of women.  A D&C only samples tissue of the lining of the uterus and has no curative value.

Another rare cancer that can form in the uterine muscle wall is leiomyosarcoma, which may appear as a fibroid. Leiomyosarcoma may be suspected in postmenopausal women who have an enlarged uterus and have certain MRI changes. The only way to know for sure whether this growth is cancerous or not is to remove it surgically and have the cells analyzed in the pathology lab. If cancer is found to be present, a hysterectomy is recommended.

Ovarian cancer, like other cancers, is the uncontrolled growth of cells. Most of the time, ovarian cancer forms in the outer covering of the ovary, called the epithelium. These cells first go through precancerous changes, as they do with other cancers. The problem with ovarian cancer is that there is no good way to screen for these changes at an early stage, and thus, by the time ovarian cancer becomes evident, it may be fairly advanced.

Ovarian cancer mostly occurs in postmenopausal women. About 1 in 1,500 women aged 60 will develop ovarian cancer – a rate comparable to that of uterine cancer. The lifetime risk is about 1 in every 100 women, or 1%. However, there is a genetic component that increases risk among some women. Caucasian women have a higher risk than women of African or Asian descent. In particular, Jewish women of Eastern European descent have a higher risk due to the prevalence of an inherited gene mutation in this population.

Causes and Risk Factors
Presence of the inherited BRCA gene increases the risk of developing ovarian cancer to 25-50%. Having a close family relative with the disease increases risk five- to seven-fold. Despite these genetic links, the vast majority of cases (90%) have no family history of ovarian cancer.

Eating a diet high in saturated fat has been associated with increased risk, and conversely, eating a diet high in fiber may be associated with decreased risk.

Other factors that are associated with decreased risk include having children, taking birth control pills (the longer, the better), and having a shorter reproductive lifespan either because of late onset of menstruation (after age 12) or early menopause (before age 45). The reason these factors may be protective is that they all reduce the total number of times a woman ovulates, thereby reducing the number of times the ovary has been open to potential carcinogens.

Unfortunately, early ovarian cancer is characterized only by vague symptoms such as bloating, abdominal discomfort and pelvic cramps, all of which are quite common and usually have other causes. A change in the ovary size or surface that can be felt by your gynecologist during a pelvic exam is a signal that additional tests for ovarian cancer should be conducted.

Diagnosis and Treatment Options
A sonogram can show an ovarian cyst and detect certain cell patterns that are suggestive of cancer, but a sonogram cannot provide a conclusive diagnosis. Another test used in postmenopausal women is the CA-125 blood test, which measures the amount of a substance that may be elevated in women with ovarian cancer. However, this test has only 50% accuracy in postmenopausal women and even less in premenopausal women.

One promising diagnostic tool being investigated is measurement of a certain pattern of proteins in the blood (proteomics), and in preliminary studies this test showed great accuracy in detecting early ovarian cancers.

At present, the only way to know with 100% certainty if there is cancer in an ovary is to biopsy or remove surgically and look at the tissue under a microscope. If cancer is present, an oophorectomy with hysterectomy will be recommended.


  1. American Cancer Society. Learn About Cancer.
  2. American College of Obstetricians and Gynecologists. Gynecological Problems: Cancer of the Ovary. 2007.
  3. American College of Obstetricians and Gynecologists. Gynecological Problems: Cancer of the Uterus. 2006.
  4. American College of Obstetricians and Gynecologists. Gynecological Problems: Cancer of the Cervix. 2004.
  5. National Cancer Institute. http://www.
  6. Ovarian epithelial/patient. 9.16.2007.7. Parker WH. A Gynecologist’s Second Opinion. (c)2003; A Plume Book; Published by the Penguin Group, New York, NY.8. Schiffman et al. Human papillomavirus and cervical cancer. Lancet. 2007;370(9590):890-907.
Copyright 2023 AAGL. By using this site, you agree to our Terms of Service and Privacy Policy
Last updated on Jun 9, 2023