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Racial Disparity in Endometrial Cancer

The safety and scientific validity of this study is the responsibility of the study sponsor and investigators. Listing a study does not mean it has been evaluated by the U.S. Federal Government. Read our disclaimer for details. Identifier: NCT00375804
Recruitment Status : Terminated (Funding and logistical difficuties resulted in the withdrawl of the study.)
First Posted : September 13, 2006
Last Update Posted : January 9, 2018
James Graham Brown Cancer Center
Information provided by (Responsible Party):
University of Louisville

Brief Summary:

The objectives for this study:

  1. Investigate some of the causes for the racial disparity of endometrial cancer survival rates among black and white women
  2. Examine the biologic correlates of aggressive behavior such as estrogen receptor status, p53 and HER-2/neu overexpression, and aromatase activity

Condition or disease
Endometrial Cancer

Detailed Description:

Endometrial cancer is the fourth most common cancer among women and the most common gynecologic cancer. Although the incidence of well-differentiated early stage endometrial cancer is higher among white women, there appears to be an increased incidence of aggressive variants with increased mortality rate among blacks.

Reported 5-year survival rate for white women with endometrial cancer is 90% while black women have only 60% survival. (1,2) Black women tend to have more aggressive cancers and more adverse symptoms such as non-endometrioid histology, grade 3 differentiation, and more stage III and IV cancers. (3,7) Many studies have identified and established risk factors and beneficial behaviors for endometrial cancer, most of which are modifiable. Some of the major risks include obesity, hypertension, high fat diet, diabetes, smoking, increased age, hormone replacement therapy, and tamoxifen use. Behaviors associated with decreased risks are use of oral contraceptives, breast feeding, and physical activity. (4)

There is also evidence that biologic factors may contribute to development of malignant endometrial neoplasms. Both mutation and over expression of the p53 tumor suppressor gene is seen in patients with endometrial cancer, especially those in the advanced stages.

Normally, increased levels of p53 are present in cells with damaged DNA. p53 triggers cells to produce more p21, a molecule that binds to cyclin-dependent kinase 2 (Cdk2). In the unbound state, Cdk2 allows cells to progress to the synthesis stage of the cell cycle; therefore, it remains arrested the Gı phase when it is coupled to p21 in an effort to prevent proliferation of abnormal cells. In addition to this mechanism, p53 is thought to be involved in induction of apoptosis. There are indications that black women may exhibit increased incidence of p53 over expression when compared to white women. (5,6,8)

Another biologic factor involved in endometrial cancer is the estrogen receptor. In contrast to p53, presence of estrogen receptors are a positive prognostic factor because they provide a potential avenue for treating endometrial carcinomas. However, the receptors must be functional in order to be advantageous. Some tumors contain mutated estrogen receptors, which cause changes in the metabolic pathway. Individuals with mutated receptors have varying susceptibilities to developing endometrial cancer. (9)

Aromatase is an enzyme involved in converting androgens to estrogens. Both estrogen and aromatase excess has been identified in endometrial cancer, while no aromatase activity has been indicated in the normal endometrium. Most of the aromatase activity appears to be confined to the stromal cells and is correlated with stromal invasion. It may be possible to inhibit aromatase in an effort to decrease estrogen levels and potentially halt cancer growth. (10,11)

Uterine papillary serous carcinoma (UPSC) is an aggressive variant of endometrial cancer characterized by early metastasis, resistance to therapy, and a high mortality rate. Smaller studies suggest that HER-2/neu may be involved in the tumorigenesis of this disease.(13) Overexpression of the HER2/neu receptor in UPSC is an independent variable that is associated with a poorer overall survival, a worse overall prognosis, occurs more frequently in black women, and may contribute to racial disparity in survival. (12,13)

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Study Type : Observational
Actual Enrollment : 43 participants
Observational Model: Cohort
Time Perspective: Other
Official Title: Racial Disparity in Prevalence and Survival Rates in Endometrial Cancer
Study Start Date : June 2003
Actual Primary Completion Date : June 2010
Actual Study Completion Date : June 2010

Information from the National Library of Medicine

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Ages Eligible for Study:   Child, Adult, Older Adult
Sexes Eligible for Study:   Female
Accepts Healthy Volunteers:   No
Sampling Method:   Probability Sample
Study Population
Chart review of subjects diagnosed with endometrial cancer

Inclusion Criteria:

  • Patients diagnosed with a new case of endometrial carcinoma at the University of Louisville Hospital or in the Norton Healthcare system from 1995-2000

Exclusion Criteria:

  • Patients who do not meet the inclusion criteria

Information from the National Library of Medicine

To learn more about this study, you or your doctor may contact the study research staff using the contact information provided by the sponsor.

Please refer to this study by its identifier (NCT number): NCT00375804

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United States, Kentucky
James Graham Brown Cancer Center
Louisville, Kentucky, United States, 40202
Sponsors and Collaborators
University of Louisville
James Graham Brown Cancer Center
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Principal Investigator: Lynn P. Parker, MD University of Louisville, James Graham Brown Cancer Center
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Responsible Party: University of Louisville Identifier: NCT00375804    
Other Study ID Numbers: 357.03
First Posted: September 13, 2006    Key Record Dates
Last Update Posted: January 9, 2018
Last Verified: January 2018
Keywords provided by University of Louisville:
Endometrial Cancer
Additional relevant MeSH terms:
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Endometrial Neoplasms
Uterine Neoplasms
Genital Neoplasms, Female
Urogenital Neoplasms
Neoplasms by Site
Uterine Diseases