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Screening for endometrial cancer

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Summary Of Evidence
Significance
Evidence Of Benefit

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Information from PDQ -- for Health Professionals

SUMMARY OF EVIDENCE

Note: Separate PDQ summaries on Prevention of Endometrial Cancer; Endometrial Cancer Treatment; and Uterine Sarcoma Treatment are also available.

Screening by Endometrial Sampling or Transvaginal Ultrasound

There is insufficient evidence to establish whether a decrease in mortality from endometrial cancer occurs with screening by endometrial sampling or transvaginal ultrasound (Levels of Evidence: 3,4,5). The risks associated with endometrial biopsy (sampling) are not systematically reported, but include discomfort, bleeding, infection and rarely uterine perforation. Risks associated with false positive test results include anxiety and additional diagnostic testing and surgery. Endometrial cancers may be missed on endometrial sampling and ultrasound.

Levels of Evidence:

3: Evidence obtained from well designed and conducted cohort or case-control studies

4: Evidence obtained from multiple-time series with or without intervention

5: Opinions of respected authorities based on clinical experience, descriptive studies, or reports of expert committees

Pap Smear and Endometrial Screening

Although the diagnosis of endometrial cancer occasionally originates with an abnormal Pap test of cytological material from the uterine cervix, this method has been evaluated and found to be insensitive for endometrial screening.

Level of Evidence:

5: Opinions of respected authorities based on clinical experience, descriptive studies, or reports of expert committees

SIGNIFICANCE

Status and Trends in Endometrial Cancer Incidence and Mortality

Endometrial cancer is the most common invasive gynecologic cancer in U.S. women, with approximately 39,300 new cases projected to occur in 2002.[1] Age-adjusted endometrial cancer incidence in the United States declined steadily between 1978 and 1988, and has remained fairly constant since 1988. Several factors affect the interpretation of statistics for noncervical endometrial cancer from 1978 onward. From the SEER registries, uterine tumors are classified as cervical, corpus, and NOS (not otherwise specified). Corpus and NOS categories are usually combined to reflect noncervical carcinoma of the uterus. In the mid 1980s, a pathology review of cases in the NOS category found that 11% came from the uterine cervix.[2] The practice of combining corpus with NOS cases, some of which are of cervical origin, overestimates the total amount of noncervical carcinomas of the uterus. Since the 1970s, the percentage of cases in the NOS category has declined to a current level of about 2% or less of the total cases, reducing the opportunity for an overestimate. In addition, rates of endometrial cancer are not adjusted for the substantial, but variable, portion of the female population that has undergone hysterectomy. One study estimated that adjustment for age-specific hysterectomy yielded an endometrial cancer incidence rate that was approximately 20% higher.[3] These examples illustrate how observed trends in the reported incidence of and mortality from endometrial cancer have been affected by temporal factors.

In the United States, it is estimated that approximately 6,600 women will die of endometrial cancer in 2002. The endometrial cancer mortality rate has declined steadily from 1974 to the present, for a decrease amounting to 26%. A transient increase in incidence occurring from 1973 to 1978 was associated with estrogen replacement therapy, but there was no associated increase in mortality.

In the mid 1970s, a noticeable rise and subsequent fall in the U.S. incidence of endometrial cancer occurred in postmenopausal women. The diagnosis of approximately 15,000 cases of endometrial cancers in excess of those expected on the basis of the underlying secular trend, has been related to the use of exogenous estrogen therapy.[4] In addition to the increased risk of developing endometrial cancer that is observed in women who use estrogen replacement therapy unaccompanied by progesterone (which appears to abrogate the risk of cancer), a number of additional risk factors have been identified, and most appear to be related to estrogenic effects. Among these factors are obesity, high fat diet, reproductive factors such as nulliparity, early menarche and late menopause, and tamoxifen use. Hereditary Nonpolyposis Colorectal Cancer (HNPCC) Syndrome is associated with a markedly increased risk of endometrial cancer compared to women in the general population. Among women who are HNPCC carriers, the estimated cumulative incidence of endometrial cancer ranges from 20-60% by the age of 70 (See the genetics summary for health professionals).[5-7] As information about endometrial cancer etiology accumulates, it may be possible to identify screening and prevention interventions that are beneficial to categories of patients with specific risk profiles. The molecular basis for extracolonic tumors in the setting of HNPCC remains undefined.[8]

Major differences exist between black and white women in stages of endometrial cancer at detection and subsequent survival. From 1986 to 1993, the stages of disease at detection were more advanced for black women; for example, only 51% of endometrial cancer cases were localized in black women compared with 75% of cases in white women. Even though the incidence of endometrial cancer is lower among black women, mortality is higher. In 1985, the National Cancer Institute initiated a Black/White Cancer Survival Study designed to identify factors that might contribute to observed racial differences in mortality for breast, uterine corpus, colon, and bladder cancer. When the data for endometrial cancer patients were examined, several factors were identified that appeared to be related to excess risk of advanced stage disease for black women. Among these factors was a statistically significant occurrence of higher-grade and more aggressive histologies in black patients with endometrial cancer.[9] Another study has investigated the interval from patient-reported symptom recognition to initial medical consultation and concluded that for patients with cancer of the uterine corpus, there is essentially no black/white difference in this interval, making it unlikely that patient delay after onset of symptoms could explain much of the excess of advanced stage disease found in black women.[10]

References:

  1. American Cancer Society: Cancer Facts and Figures-2002. Atlanta, Ga: American Cancer Society, 2002.
  2. Percy CL, Miller BA, Gloeckler Ries LA: Effect of changes in cancer classification and the accuracy of cancer death certificates on trends in cancer mortality. Annals of the New York Academy of Sciences 609: 87-97, 1990.
  3. Howe HL: Age-specific hysterectomy and oophorectomy prevalence rates and the risks for cancer of the reproductive system. American Journal of Public Health 74(6): 560-563, 1984.
  4. Jick H, Walker AM, Rothman KJ: The epidemic of endometrial cancer: a commentary. American Journal of Public Health 70(3): 264-267, 1980.
  5. Watson P, Vasen HF, Mecklin JP, et al.: The risk of endometrial cancer in hereditary nonpolyposis colorectal cancer. American Journal of Medicine 96(6): 516-520, 1994.
  6. Aarnio M, Mecklin JP, Aaltonen LA, et al.: Life-time risk of different cancers in hereditary non-polyposis colorectal cancer (HNPCC) syndrome. International Journal of Cancer 64(6): 430-433, 1995.
  7. Aarnio M, Sankila R, Pukkala E, et al.: Cancer risk in mutation carriers of DNA-mismatch-repair genes. International Journal of Cancer 81(2): 214-218, 1999.
  8. Cass I, Baldwin RL, Karlan BY: Molecular advances in gynecologic oncology. Current Opinion in Oncology 11(5): 394-400, 1999.
  9. Barrett RJ, Harlan LC, Wesley MN, et al.: Endometrial cancer: stage at diagnosis and associated factors in black and white patients. American Journal of Obstetrics and Gynecology 173(2): 414-423, 1995.
  10. Coates RJ, Click LA, Harlan LC, et al.: Differences between black and white patients with cancer of the uterine corpus in interval from symptom recognition to initial medical consultation (United States). Cancer Causes and Control 7(3): 328-336, 1996.

EVIDENCE OF BENEFIT

Routine screening of women for endometrial cancer is not of any proven benefit. No screening test has been evaluated for its impact on endometrial cancer mortality.[1,2] Published recommendations for screening certain groups of women at high risk for endometrial carcinoma are based on opinion regarding presumptive benefit.[3] Although risk factors include estrogen replacement therapy unopposed by progestins, tamoxifen therapy, and genetic mutations associated with hereditary nonpolyposis colon cancer, no controlled trials have been done to evaluate the effectiveness of screening for endometrial cancer in reducing mortality in these subpopulations.

Pap Test

The Pap test, used successfully for screening for cervical cancer, is too insensitive for detection of endometrial cancer to be used as a screening technique.[4] Occasionally, however, the Pap test may fortuitously identify endometrial abnormalities. Sampling the fluid which collects in the posterior vaginal fornix, as part of the Pap test, in peri- and postmenopausal women may occasionally lead to the detection of endometrial lesions. The presence of endometrial cells in a Pap test from a postmenopausal woman, not taking exogenous hormones, is abnormal and requires further evaluation.[5,6]

Endometrial Aspiration

Endometrial aspiration has been proposed as a potential screening technique. One study evaluating cytologic endometrial screening in asymptomatic patients suggested that the sensitivity of endometrial cytology may approach 80%; however, the study was compromised by the absence of a "gold standard" to fully evaluate the false negative rate of the technique.[7]

Endometrial Sampling

In the setting of abnormal uterine bleeding, endometrial sampling has gained favor largely as an alternative to more invasive procedures such as fractional dilation and curettage; however, issues of access to the endometrial cavity and sampling error limit the clinical significance of a negative result. The limitations of endometrial sampling in the diagnostic setting are even more problematic in adapting its use for screening.

Transvaginal Ultrasound

Transvaginal ultrasound is used to evaluate women with vaginal bleeding but its efficacy in screening for uterine abnormalities among asymptomatic women is unknown. A comparison of transvaginal ultrasound and endometrial aspiration was conducted among asymptomatic women potentially eligible for an osteoporosis prevention trial [8] as part of determination of eligibility for randomization. Transvaginal ultrasound was performed on 1926 women, of these, 93 had endometrial thickness >6 mm. Among the 93 with abnormal endometrial thickness, 42 had endometrial aspiration with one finding of abnormal pathology (defined as adenocarcinoma or atypical hyperplasia). Of the 1833 women with endometrial thickness less than or equal to 6 mm, 1750 women had endometrial aspiration and 5 of these had an abnormal pathologic biopsy. Among this population of asymptomatic postmenopausal women, the estimated sensitivity for transvaginal ultrasound with a threshold value of 6 mm was 17%; 33% for a threshold value of 5 mm.

One study attempted to determine the usefulness of transvaginal ultrasonography as a less-invasive screening method than biopsy, among a cohort of postmenopausal, asymptomatic women receiving hormone replacement therapy. Utilizing the Postmenopausal Estrogen and Progestin Interventions (PEPI) Trial participants who had undergone both transvaginal ultrasonography and endometrial biopsy, sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV) were determined for women who received placebo, estrogen alone, and estrogen-progestin therapy. At a threshold value of 5 mm for endometrial thickness, transvaginal ultrasonography had 90% sensitivity and 48% specificity. Using this threshold, more than half the women would receive a biopsy while only 4% of them had serious disease.[9]

The majority of the evidence for estimating the sensitivity of transvaginal ultrasound comes from studies using ultrasound to evaluate women with abnormal bleeding. A combined analysis of prospective studies of endovaginal ultrasound to evaluate postmenopausal bleeding demonstrated a high sensitivity for detecting endometrial cancer and endometrial disease. Using a 5 mm threshold to define abnormal endometrial thickening, 96% (95% confidence interval (CI) 94%-98%) of women with cancer had an abnormal endovaginal ultrasound, whereas 92% (95% CI 90%-93%) of women with endometrial disease had an abnormal result.[10] Estimated specificity associated with a 5 mm threshold was 81% for endometrial disease and 61% for cancer. Specificity for detection of endometrial disease was 77% among women using hormone replacement therapy (HRT) and 92% among women who did not use HRT. A negative test (<5 mm threshold thickness) reduced the likelihood of cancer by 90%. For example, postmenopausal women with vaginal bleeding not taking HRT have a 10% risk of having cancer, but a negative endovaginal ultrasound reduced the likelihood that cancer is present to 1%; a positive test increased the likelihood of cancer being present to 57%. A comparison of sonography, hydrosonography (sonohysterography), and office hysteroscopy for the evaluation of abnormal uterine bleeding found that sensitivity (95%, 90%, and 78% respectively) and specificity (65%, 83%, and 54% respectively) suggested that the sonographic techniques were preferable to hysteroscopy as well as less costly.[11] Abnormal results from endovaginal ultrasound require additional evaluation. Although transvaginal sonography can be used to evaluate asymptomatic and occult endometrial pathology, the technique has not been evaluated as a screening method for reducing mortality in asymptomatic women.

The Estrogen-Progestin Replacement Therapy Setting

Endometrial sampling is not required prior to or during estrogen-progestin replacement therapy (ERT) unless abnormal bleeding occurs.[12,13]

Tamoxifen

Because the risk of endometrial cancer may be increased for women who are treated with tamoxifen and even more in that subset of women who have a history of prior estrogen replacement therapy,[14] the question has been raised as to whether special surveillance is required.[15] Beyond a routine gynecologic examination eliciting any history of abnormal bleeding, it has been recommended that screening studies and procedures for detecting endometrial pathology in women taking tamoxifen should be left to the discretion of the individual gynecologist.[16] More importantly, any abnormal uterine bleeding should be completely evaluated. The annualized risk of developing endometrial cancer while taking tamoxifen has been estimated to be 2 per 1,000, but special surveillance uncovers other endometrial changes of uncertain clinical significance.[17] For example, in a series of 111 postmenopausal women randomized to either tamoxifen or placebo as part of a breast cancer prevention study, the prevalence of atypical endometrial hyperplasia in the tamoxifen group was 16% compared to none in the placebo group.[18] An ACOG Committee has interpreted results such as these as being suggestive that hyperplastic endometrial lesions developing during tamoxifen treatment may seldom evolve into invasive endometrial cancer. There are no data from well-controlled trials currently available that support the use of routine annual screening for the detection of tamoxifen-associated endometrial cancer.[19,20]

A number of clinical investigators have reported their efforts to use transvaginal ultrasound for the evaluation of the endometrium in postmenopausal tamoxifen-treated breast cancer patients. Repeatedly, it has been observed that 40% or more of postmenopausal women treated with tamoxifen have an endometrial stripe on ultrasound that is thickened beyond 5 mm, the usual threshold for further investigation of women who are not being treated with tamoxifen.[21-26] Although a positive correlation between duration of tamoxifen use and endometrial thickness was observed in 1 of these studies,[21] no correlation could be demonstrated in several others.[22,23] Although increased thickness of the endometrium is associated with tamoxifen treatment, 1 study obtained baseline ultrasound studies that suggested pre-existing thickness was predictive of likelihood to increase or remain abnormal. It was observed that patients with an endometrial stripe less than 4 mm prior to treatment with tamoxifen seldom had an increase in mucosal thickness.[24] At baseline, approximately 35% of breast cancer patients (15 of 42) prior to tamoxifen treatment had an endometrial stripe wider than 5 mm
which was unlikely to decrease with tamoxifen.

Consideration has been given to using an 8 mm threshold of endometrial thickness in triaging tamoxifen-treated patients to further evaluation. One study reported that the positive predictive value of 8 mm of thickness for identifying endometrial pathology was 100%.[18] In spite of the high positive predictive value of the 8 mm cut-off, with either 5 or 8 mm, the negative predictive value is low. Another study identified 134 asymptomatic, tamoxifen-treated breast cancer patients with an endometrial stripe greater than 5 mm, who underwent outpatient hysteroscopy for clinical-pathological correlation. Atrophic endometrium was the histological finding in 46% of these patients.[21] The apparently high false negative rate of endometrial thickness of 5 mm or greater on ultrasound for predicting histological abnormalities of the uterine epithelium on biopsy was observed in other tamoxifen-treated, breast cancer patient cohorts.[25,26]

A study attempted to evaluate the value of transvaginal ultrasound in the endometrial screening of postmenopausal breast cancer patients receiving tamoxifen. The endometrium was prospectively followed by TVS every 6 months for up to 5 years in 247 tamoxifen-treated women and 98 controls. Participants with endometrial thickening >10 mm were scanned every 3 months. After 3 years of tamoxifen treatment, the mean endometrial thickness tripled in cases and was significantly thicker compared to controls. Fifty-two asymptomatic patients with endometrial thickening had hysteroscopy and dilation and curettage (D&C) performed , which resulted in 4 uterine perforations. Endometrial cancer was found in one case. Among 20 women who reported vaginal bleeding, 2 endometrial cancers were found. The authors conclude that TVS has a high false positive rate, even with a cutoff value of 10 mm for endometrial thickness in tamoxifen-treated patients. The false positives result in unnecessary invasive procedures and therefore make TVS a poor screening tool for the tamoxifen-treated population.[27]

The reason that ultrasound evaluation has poor specificity as a screening test for identifying endometrial abnormalities in tamoxifen users may arise from the nature of a tamoxifen-associated uterine change described as tamoxifen-induced subepithelial stromal hypertrophy. With instillation of fluid into the uterine cavity, this lesion is observable on ultrasound as irregular subendothelial sonolucency at the junction between the endothelium and myometrium.[26,28,29] This finding appears to account for the many instances where normal or atrophic endometrium is found on aspiration of biopsy despite the appearance of a thickened endometrium on ultrasound. Given the technical limitations of transvaginal ultrasound and aspiration for endometrial screening, it does not appear that either approach offers an advantage in detecting endometrial cancer over the comprehensive evaluation of abnormal uterine bleeding in either postmenopausal women using tamoxifen or in women who have become amenorrheic while taking tamoxifen. Also to be factored into the risk/benefit assessment of endometrial sampling as a stand-alone screening test or in follow-up to ultrasound is the pain and potential for complications of the procedure. Additionally, the risk of endometrial cancer among tamoxifen-treated women remains low. Endometrial cancers which occur in this population are very similar to those cancers occurring in the general population, with respect to stage, grade, and histology. Prognosis tends to be good and early detection does not appear to improve outcome. The authors estimate that annual screening among the tamoxifen-treated population would only result in a 0.03% decrease in endometrial cancer mortality.[30]

One study prospectively followed 67 women with breast cancer treated with tamoxifen. Every 6 months, participants underwent pelvic examination, cervical cytology, TVS, and endometrial biopsy. Three of the women developed hyperplasia while 1 developed carcinoma; each had symptoms of abnormal uterine bleeding. The 1 participant who developed carcinoma had an endometrial lining which measured 3 mm.[31]

Although sonohysterography (hydrosonography) is able to separate space occupying endometrial lesions from an abnormal endometrial-myometrial junction, evidence is lacking that routine screening sonohysterography will confer clinical benefit.

From 1995 to 1997, women entering the Breast Cancer Prevention Trial comparing tamoxifen with a placebo underwent baseline endometrial sampling followed by annual screening with endometrial sampling or ultrasound.

References:

  1. Pritchard KI: Screening for endometrial cancer: is it effective? Annals of Internal Medicine 110(3): 177-179, 1989.
  2. Eddy D: ACS report on the cancer-related health checkup. CA: A Cancer Journal for Clinicians 30(4): 193-240, 1980.
  3. Burke W, Petersen G, Lynch P, et al.: Recommendations for follow-up care of individuals with an inherited predisposition to cancer, I: hereditary nonpolyposis colon cancer. Cancer Genetics Studies Consortium. JAMA: Journal of the American Medical Association 277(11): 915-919, 1997.
  4. Burk JR, Lehman HF, Wolf FS: Inadequacy of papanicolaou smears in the detection of endometrial cancer. New England Journal of Medicine 291(4): 191-192, 1974.
  5. Ng AB, Reagan JW, Hawliczek S, et al.: Significance of endometrial cells in the detection of endometrial carcinoma and its precursors. Acta Cytologica 18(5): 356-361, 1974.
  6. Yancey M, Magelssen D, Demaurez A, et al.: Classification of endometrial cells on cervical cytology. Obstetrics and Gynecology 76(6): 1000-1005, 1990.
  7. Koss LG, Schreiber K, Oberlander SG, et al.: Detection of endometrial carcinoma and hyperplasia in asymptomatic women. Obstetrics and Gynecology 64(1): 1-11, 1984.
  8. Fleischer AC, Wheeler JE, Lindsay I, et al.: An assessment of the value of ultrasonographic screening for endometrial disease in postmenopausal women without symptoms. American Journal of Obstetrics and Gynecology 184(2): 70-75, 2001.
  9. Langer RD, Pierce JJ, O'Hanlan KA, et al.: Transvaginal ultrasonography compared with endometrial biopsy for the detection of endometrial disease. New England Journal of Medicine 337(25): 1792-1798, 1997.
  10. Smith-Bindman R, Kerlikowske K, Feldstein VA, et al.: Endovaginal ultrasound to exclude endometrial cancer and other endometrial abnormalities. JAMA: Journal of the American Medical Association 280(17): 1510-1517, 1998.
  11. Saidi MH, Sadler RK, Theis VD, et al.: Comparison of sonography, sonohysterography, and hysteroscopy for evaluation of abnormal uterine bleeding. Journal of Ultrasound in Medicine 16(9): 587-591, 1997.
  12. Committee on Gynecologic practice: ACOG committee opinion: routine cancer screening - Number 185, September, 1997. International Journal of Gynecology and Obstetrics 59(2): 157-161, 1997.
  13. Korhonen MO, Symons JP, Hyde BM, et al.: Histologic classification and pathologic findings for endometrial biopsy specimens obtained from 2964 perimenopausal and postmenopausal women undergoing screening for continuous hormones as replacement therapy (CHART 2 Study). American Journal of Obstetrics and Gynecology 176(2): 377-380, 1997.
  14. Bernstein L, Deapen D, Cerhan JR, et al.: Tamoxifen therapy for breast cancer and endometrial cancer risk. Journal of the National Cancer Institute 91(19): 1654-1662, 1999.
  15. Suh-Burgmann EJ, Goodman A: Surveillance for endometrial cancer in women receiving tamoxifen. Annals of Internal Medicine 131(2): 127-135, 1999.
  16. ACOG committee opinion. Tamoxifen and endometrial cancer. Number 169, February 1996. Committee on Gynecologic Practice. American College of Obstetricians and Gynecologists. International Journal of Gynecology and Obstetrics 53(2): 197-199, 1996.
  17. Fisher B, Costantino JP, Redmond CK, et al.: Endometrial cancer in tamoxifen-treated breast cancer patients: findings from the National Surgical Adjuvant Breast and Bowel Project (NSABP) B-14. Journal of the National Cancer Institute 86(7): 527-537, 1994.
  18. Kedar RP, Bourne TH, Powles TJ, et al.: Effects of tamoxifen on uterus and ovaries of postmenopausal women in a randomised breast cancer prevention trial. Lancet 343(8909): 1318-1321, 1994.
  19. Wilking N, Isaksson E, von Schoultz E: Tamoxifen and secondary tumours: an update. Drug Safety 16(2): 104-117, 1997.
  20. Barakat RR: Tamoxifen and endometrial neoplasia. Clinical Obstetrics and Gynecology 39(3): 629-640, 1996.
  21. Love CD, Muir BB, Scrimgeour JB, et al.: Investigation of endometrial abnormalities in asymptomatic women treated with tamoxifen and an evaluation of the role of endometrial screening. Journal of Clinical Oncology 17(7): 2050-2054, 1999.
  22. Nahari C, Tepper R, Beyth Y, et al.: Long-term transvaginal ultrasonographic endometrial follow-up in postmenopausal breast cancer patients with tamoxifen treatment. Gynecologic Oncology 74(2): 222-226, 1999.
  23. Bertelli G, Venturini M, Del Mastro L, et al.: Tamoxifen and the endometrium: findings of pelvic ultrasound examination and endometrial biopsy in asymptomatic breast cancer patients. Breast Cancer Research and Treatment 47(1): 41-46, 1998.
  24. Friedrich M, Villena-Heinsen C, Mink D, et al.: Ultrasonography of the endometrium and endometrial pathology under tamoxifen treatment. European Journal of Gynaecological Oncology 19(6): 536-540, 1998.
  25. Willen R, Lindhal B, Andolf E, et al.: Histopathologic findings in thickened endometria, as measured by ultrasound in asymptomatic, postmenopausal breast cancer patients on various adjuvant treatment including tamoxifen. Anticancer Research 18(1B): 667-676, 1998.
  26. Mourits MJ, Van der Zee AG, Willemse PH, et al.: Discrepancy between ultrasonography and hysteroscopy and histology of endometrium in postmenopausal breast cancer patients using tamoxifen. Gynecologic Oncology 73(1): 21-26, 1999.
  27. Gerber B, Krause A, Muller H, et al.: Effects of adjuvant tamoxifen on the endometrium in postmenopausal women with breast cancer: a prospective long-term study using transvaginal ultrasound. Journal of Clinical Oncology 18(20): 3464-3470, 2000.
  28. Goldstein SR: Unusual ultrasonographic appearance of the uterus in patients receiving tamoxifen. American Journal of Obstetrics and Gynecology 170(2): 447-451, 1994.
  29. Achiron R, Lipitz S, Sivan E, et al.: Sonohysterography for ultrasonographic evaluation of tamoxifen-associated cystic thickened endometrium. Journal of Ultrasound in Medicine 14(9): 685-688, 1995.
  30. Barakat RR, Gilewski TA, Almadrones PE, et al.: Effect of adjuvant tamoxifen on the endometrium in women with breast cancer: a prospective study using office endometrial biopsy. Journal of Clinical Oncology 18(20): 3459-3463, 2000.
  31. Seoud M, Shamseddine A, Khalil A, et al.: Tamoxifen and endometrial pathologies: a prospective study. Gynecologic Oncology 75(1): 15-19, 1999.
Date Last Modified: 08/2002

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