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Endometrial cancer


Table of Contents

GENERAL INFORMATION
CELLULAR CLASSIFICATION
STAGE INFORMATION
TREATMENT OPTION OVERVIEW
STAGE I ENDOMETRIAL CANCER
STAGE II ENDOMETRIAL CANCER
Stage IIA
Stage IIB
STAGE III ENDOMETRIAL CANCER
STAGE IV ENDOMETRIAL CANCER
RECURRENT ENDOMETRIAL CANCER

GENERAL INFORMATION

(Separate summaries containing information on screening for endometrial cancer and prevention of endometrial cancer are also available in PDQ.)

Cancer of the endometrium is the most common pelvic gynecologic malignancy and accounts for 13% of all cancers in women. It is a highly curable tumor. To detect endometrial cancer, a technique that directly samples the endometrial tissue is mandatory. The Pap smear is not reliable as a screening procedure in endometrial cancer, although a retrospective study found a strong correlation between positive cervical cytology and high-risk disease (i.e., high-grade tumor and deep myometrial invasion) [1] as well as an increased risk of nodal disease.[2] Degree of tumor differentiation has an important impact on the natural history of this disease and on treatment selection. An increased incidence of endometrial cancer has been found in association with prolonged, unopposed estrogen exposure.[3,4] In contrast, combined estrogen and progesterone therapy prevents the increase in risk of endometrial cancer associated with unopposed estrogen use.[5,6] In some patients, an antecedent history of complex hyperplasia with atypia can be demonstrated. An increased incidence of endometrial cancer has also been found in association with tamoxifen treatment of breast cancer, perhaps related to the estrogenic effect of tamoxifen on the endometrium.[7,8] Because of this increase, patients on tamoxifen should have follow-up pelvic examinations and should be examined if there is any abnormal uterine bleeding.

The pattern of spread is partially dependent on the degree of cellular differentiation. Well-differentiated tumors tend to limit their spread to the surface of the endometrium; myometrial extension is less common. In patients with poorly differentiated tumors, myometrial invasion occurs much more frequently. Myometrial invasion is frequently a harbinger of lymph node involvement and distant metastases and is often independent of the degree of differentiation.[9,10] Metastatic spread occurs in a characteristic pattern. Spread to the pelvic and para-aortic nodes is common. Distant metastases can occur and most commonly involve the lungs, inguinal and supraclavicular nodes, liver, bones, brain, and vagina.

Another factor found to correlate with extrauterine and nodal spread of tumor is involvement of the capillary-lymphatic space on histopathologic examination.[11] Three prognostic groupings of clinical stage I disease become possible by careful operative staging. Patients with grade 1 tumors involving only endometrium and no evidence of intraperitoneal disease (i.e., adnexal spread or positive washings) have a low risk (< 5%) of nodal involvement.[12] Patients with grade 2 or 3 tumors and inner one third superficial myometrial invasion with no intraperitoneal disease have a 5% to 9% incidence of pelvic nodes and a 4% incidence of para-aortic nodes. Patients with deep muscle invasion and high-grade tumors and/or intraperitoneal disease have a significant risk of nodal spread, 20% to 60% to pelvic nodes and 10% to 30% to para-aortic nodes. One study was directed specifically at stage I, grade 1 carcinomas of favorable histologic type. The authors identified 4 statistically significant adverse prognostic factors: myometrial invasion, vascular invasion, 8 or more mitoses per ten high-power fields, and an absence of progesterone receptors.[13]

Another group identified aneuploidy and a high S-phase fraction as predictive of poor prognosis.[14] A Gynecologic Oncology Group (GOG) study related surgical-pathologic parameters and postoperative treatment to recurrence-free interval and recurrence site. For patients without extrauterine spread, the greatest determinants of recurrence were grade 3 histology and deep myometrial invasion. In this study, the frequency of recurrence was greatly increased with positive pelvic nodes, adnexal metastasis, positive peritoneal cytology, capillary space involvement, involvement of the isthmus or cervix, and, particularly, positive para-aortic nodes (includes all grades and depth of invasion). Ninety-eight percent of the cases with aortic node metastases were in patients with positive pelvic nodes, intra-abdominal metastases, or tumor invasion of the outer one third of the myometrium.[15,16]

When the only evidence of extrauterine spread is positive peritoneal cytology, the influence on outcome is unclear. The value of therapy directed at this cytologic finding is not well founded.[17-22] The preponderance of evidence, however, would suggest that other extrauterine disease must be present before additional postoperative therapy is considered.

One report found progesterone receptor levels to be the single most important prognostic indicator of 3-year survival in clinical stage I and II disease. Patients with progesterone receptor levels greater than 100 had a 3-year disease-free survival of 93% compared with 36% for a level less than 100. Only cervical involvement and peritoneal cytology were significant prognostic variables after adjusting for progesterone receptor levels.[23] Other reports confirm the importance of hormone receptor status as an independent prognostic factor.[24] Additionally, immunohistochemical staining of paraffin-embedded tissue for both estrogen and progesterone receptors has been shown to correlate with International Federation of Gynecology and Obstetrics (FIGO) grade as well as survival.[25-27] On the basis of these data, progesterone and estrogen receptors, assessed either by biochemical or immunohistochemical methods, should be included, when possible, in the evaluation of stage I and II patients. Oncogene expression, DNA ploidy, and the fraction of cells in S-phase have also been found to be prognostic indicators of clinical outcome.[27] For example, overexpression of the HER-2/neu oncogene has been associated with a poor overall prognosis.[28] A general review of prognostic factors has been published.[29]

References:

  1. DuBeshter B, Warshal DP, Angel C, et al.: Endometrial carcinoma: the relevance of cervical cytology. Obstetrics and Gynecology 77(3): 458-462, 1991.

  2. Larson DM, Johnson KK, Reyes CN, et al.: Prognostic significance of malignant cervical cytology in patients with endometrial cancer. Obstetrics and Gynecology 84(3): 399-403, 1994.

  3. Ziel HK, Finkle WD: Increased risk of endometrial carcinoma among users of conjugated estrogen. New England Journal of Medicine 293(23): 1167-1170, 1975.

  4. Jick SS, Walker AM, Jick H: Estrogens, progesterone, and endometrial cancer. Epidemiology 4(1): 20-24, 1993.

  5. Jick SS: Combined estrogen and progesterone use and endometrial cancer. Epidemiology 4(4): 384, 1993.

  6. Bilezikian JP: Major issues regarding estrogen replacement therapy in postmenopausal women. Journal of Women's Health 3(4): 273-282, 1994.

  7. van Leeuwen FE, Benraadt J, Coebergh JW, et al.: Risk of endometrial cancer after tamoxifen treatment of breast cancer. Lancet 343(8895): 448-452, 1994.

  8. 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.

  9. Hendrickson M, Ross J, Eifel P, et al.: Adenocarcinoma of the endometrium: analysis of 256 cases with carcinoma limited to the uterine corpus. Gynecologic Oncology 13(3): 373-392,1982.

  10. Nori D, Hilaris BS, Tome M, et al.: Combined surgery and radiation in endometrial carcinoma: an analysis of prognostic factors. International Journal of Radiation Oncology, Biology, Physics 13(4): 489-497, 1987.

  11. Hanson MB, Van Nagell JR, Powell DE, et al: The prognostic significance of lymph-vascular space invasion in stage I endometrial cancer. Cancer 55(8): 1753-1757, 1985.

  12. Takeshima N, Hirai Y, Tanaka N, et al.: Pelvic lymph node metastasis in endometrial cancer with no myometrial invasion. Obstetrics and Gynecology 88(2): 280-282, 1996.

  13. Tornos C, Silva EG, El-Naggar A, et al.: Aggressive stage I grade 1 endometrial carcinoma. Cancer 70(4): 790-798, 1992.

  14. Friberg LG, Noren H, Delle U: Prognostic value of DNA ploidy and S-phase fraction in endometrial cancer stage I and II: a prospective 5-year survival study. Gynecologic Oncology 53(1): 64-69, 1994.

  15. Morrow CP, Bundy BN, Kurman RJ, et al.: Relationship between surgical-pathological risk factors and outcome in clinical stage I and II carcinoma of the endometrium: a Gynecologic Oncology Group study. Gynecologic Oncology 40(1): 55-65, 1991.

  16. Lanciano RM, Corn BW, Schultz DJ, et al.: The justification for a surgical staging system in endometrial carcinoma. Radiotherapy and Oncology 28(3): 189-196, 1993.

  17. Ambros RA, Kurman RJ: Combined assessment of vascular and myometrial invasion as a model to predict prognosis in stage I endometrioid adenocarcinoma of the uterine corpus. Cancer 69(6): 1424-1431, 1992.

  18. Turner DA, Gershenson DM, Atkinson N, et al.: The prognostic significance of peritoneal cytology for stage I endometrial cancer. Obstetrics and Gynecology 74(5): 775-780, 1989.

  19. Piver MS, Recio FO, Baker TR, et al.: A prospective trial of progesterone therapy for malignant peritoneal cytology in patients with endometrial carcinoma. Gynecologic Oncology 47(3): 373-376, 1992.

  20. Kadar N, Homesley HD, Malfetano JH: Positive peritoneal cytology is an adverse factor in endometrial carcinoma only if there is other evidence of extrauterine disease. Gynecologic Oncology 46(2): 145-149, 1992.

  21. Lurain JR: The significance of positive peritoneal cytology in endometrial cancer. Gynecologic Oncology 46(2): 143-144, 1992.

  22. Lurain JR, Rice BL, Rademaker AW, et al.: Prognostic factors associated with recurrence in clinical stage I adenocarcinoma of the endometrium. Obstetrics and Gynecology 78(1): 63-69, 1991.

  23. Ingram SS, Rosenman J, Heath R, et al.: The predictive value of progesterone receptor levels in endometrial cancer. International Journal of Radiation Oncology, Biology, Physics 17(1): 21-27, 1989.

  24. Creasman WT: Prognostic significance of hormone receptors in endometrial cancer. Cancer 71(4, Suppl): 1467-1470, 1993.

  25. Carcangiu ML, Chambers JT, Voynick IM, et al.: Immunohistochemical evaluation of estrogen and progesterone receptor content in 183 patients with endometrial carcinoma. Part I: clinical and histologic correlations. American Journal of Clinical Pathology 94(3): 247-254, 1990.

  26. Chambers JT, Carcangiu ML, Voynick IM, et al.: Immunohistochemical evaluation of estrogen and progesterone receptor content in 183 patients with endometrial carcinoma. Part II: correlation between biochemical and immunohistochemical methods and survival. American Journal of Clinical Pathology 94(3): 255-260, 1990.

  27. Gurpide E: Endometrial cancer: biochemical and clinical correlates. Journal of the National Cancer Institute 83(6): 405-416, 1991.

  28. Hetzel DJ, Wilson TO, Keeney GL, et al.: HER-2/neu expression: a major prognostic factor in endometrial cancer. Gynecologic Oncology 47(2): 179-185, 1992.

  29. Homesley HD, Zaino R: Endometrial cancer: prognostic factors. Seminars in Oncology 21(1): 71-78, 1994.


CELLULAR CLASSIFICATION

The most common endometrial cancer cell type is endometrioid adenocarcinoma, which is composed of malignant glandular epithelial elements; an admixture of squamous metaplasia is not uncommon. Adenosquamous tumors contain malignant elements of both glandular and squamous epithelium;[1] clear cell and papillary serous carcinoma of the endometrium are tumors that are histologically similar to those noted in the ovary and the fallopian tube, and the prognosis is worse for these tumors.[2] Mucinous, squamous, and undifferentiated tumors are rarely encountered. Frequency of endometrial cancer cell types is as follows:

I. Endometrioid (75%-80%)
A. Ciliated adenocarcinoma

B. Secretory adenocarcinoma

C. Papillary or villoglandular

D. Adenocarcinoma with squamous differentiation

1. Adenoacanthoma

2. Adenosquamous

II. Uterine papillary serous (<10%)

III. Mucinous (1%)

IV. Clear cell (4%)

V. Squamous cell (< 1%)

VI. Mixed (10%)

VII. Undifferentiated

References:

  1. Zaino RJ, Kurman R, Herbold D, et al.: The significance of squamous differentiation in endometrial carcinoma. Cancer 68(10): 2293-2302, 1991.

  2. Gusberg SB: Virulence factors in endometrial cancer. Cancer 71(4, Suppl): 1464-1466, 1993.


STAGE INFORMATION

A hysterectomy is required to determine the degree of myometrial invasion. The following surgical staging has been adopted by the International Federation of Gynecology and Obstetrics (FIGO) and by the American Joint Committee on Cancer (AJCC):[1-3]


-- Stage I --
Stage I endometrial cancer is carcinoma confined to the corpus uteri.
  stage IA:  tumor limited to endometrium
  stage IB:  invasion to less than one half of the myometrium
  stage IC:  invasion to greater than one half of the myometrium

-- Stage II --
Stage II endometrial cancer involves the corpus and the cervix, but has not
extended outside the uterus.
  stage IIA:  endocervical glandular involvement only
  stage IIB:  cervical stromal invasion

-- Stage III --
Stage III endometrial cancer extends outside of the uterus but is confined to
the true pelvis.
  stage IIIA:  tumor invades serosa and/or adnexa and/or positive peritoneal
               cytology
  stage IIIB:  vaginal metastases
  stage IIIC:  metastases to pelvic and/or para-aortic lymph nodes

-- Stage IV --
Stage IV endometrial cancer involves the bladder or bowel mucosa or has
metastasized to distant sites.
  stage IVA:  tumor invasion of bladder and/or bowel mucosa
  stage IVB:  distant metastases, including intra-abdominal and/or inguinal
              lymph nodes

Endometrial cancer can be grouped with regard to the degree of differentiation
of the adenocarcinoma, as follows:
  G1:  5% or less of a nonsquamous or nonmorular solid growth pattern
  G2:  6% to 50% of a nonsquamous or nonmorular solid growth pattern
  G3:  more than 50% of a nonsquamous or nonmorular solid growth pattern

FIGO staging for endometrial cancer:
  Stage IA G123:  tumor limited to endometrium
  Stage IB G123:  invasion to less than one half the myometrium
  Stage IC G123:  invasion to more than one half the myometrium
  Stage IIA G123: endocervical glandular involvement only
  Stage IIB G123: cervical stromal invasion
  Stage IIIA G123:tumor invades serosa and/or adnexa, and/or positive
                  peritoneal cytology
  Stage IIIB G123:vaginal metastases
  Stage IIIC G123:metastases of pelvic and/or para-aortic lymph nodes
  Stage IVA G123: tumor invasion of bladder and/or bowel mucosa
  Stage IVB:      distant metastases including intra-abdominal and/or inguinal
                  lymph nodes

References:

  1. Shepherd JH: Revised FIGO staging for gynaecological cancer. British Journal of Obstetrics and Gynaecology 96(8): 889-892, 1989.

  2. Erratum: FIGO staging for corpus cancer. British Journal of Obstetrics and Gynaecology 99(5): 440, 1992.

  3. Corpus uteri. In: American Joint Committee on Cancer: AJCC Cancer Staging Manual. Philadelphia, Pa: Lippincott-Raven Publishers, 5th ed., 1997, pp 195-200.


TREATMENT OPTION OVERVIEW

Patients with endometrial cancer who have localized disease are usually curable by hysterectomy and bilateral salpingo-oophorectomy. Best results are obtained with either of 2 standard treatments: hysterectomy or hysterectomy and adjuvant radiation therapy (when deep invasion of the myometrial muscle [one half the depth] or grade 3 tumor with myometrial invasion is present). Some patients have regional and distant metastases that, although occasionally responsive to standard hormone therapy, are rarely curable. For these patients, standard therapy is inadequate.

Progestational agents have been evaluated as adjuvant therapy in a randomized clinical trial of stage I disease and have been shown to be of no benefit. These studies, however, were not stratified according to level of progesterone receptor in the primary tumor. No trials of adjuvant progestins in more advanced disease are reported. Determination of progesterone receptors in the primary tumor is encouraged, and entry onto an appropriate adjuvant trial (if receptor levels are high) should be considered. If no trial is available, data from receptors on the primary tumor may help guide therapy for recurrent disease, should it occur.

The designations in PDQ that treatments are "standard" or "under clinical evaluation" are not to be used as a basis for reimbursement determinations.


STAGE I ENDOMETRIAL CANCER

Treatment options:

Standard:

If the tumor is well or moderately differentiated, involves the upper
two thirds of the corpus, has negative peritoneal cytology, is without
vascular space invasion, and has less than 50% myometrial invasion, a total
abdominal hysterectomy and bilateral salpingo-oophorectomy should be done.
Selected pelvic lymph nodes may be removed. If they are negative, no
postoperative treatment is indicated. Postoperative treatment with a
vaginal cylinder is advocated by some.[1]

For all other cases and cell types, a periaortic and selective pelvic node
sampling should be combined with the total abdominal hysterectomy and
bilateral salpingo-oophorectomy if there are no medical or technical
contraindications. One study found that node dissection per se did not
significantly add to the overall morbidity from hysterectomy.[2] If both
periaortic and selective pelvic node sampling are negative, the patient
should receive pelvic irradiation because of the frequency of pelvic and
vaginal cuff recurrence. While the irradiation will reduce the incidence of
local and regional recurrence, improved survival has not been proven.[3-5]

If the pelvic nodes are positive and the periaortic nodes are negative,
total pelvic irradiation, including the common nodes, should be given. This
careful patient selection for postoperative external-beam radiation is
mandated because external radiation can be associated with complications.
The incidence of bowel complications is approximately 4%, and it can be even
higher if the radiation is given after pelvic lymphadenectomy.[6] If the
surgery is done using a retroperitoneal approach, the toxic effects are
lessened. If the periaortic nodes are positive, the patient is a candidate
for clinical trials that could include radiation and/or chemotherapy.
Patients who have medical contraindications to surgery should be treated with
radiation therapy alone, but inferior cure rates below those attained with
surgery may occur.[1,7,8]

References:

  1. Eltabbakh GH, Piver MS, Hempling RE, et al.: Excellent long-term survival and absence of vaginal recurrences in 332 patients with low-risk stage I endometrial adenocarcinoma treated with hysterectomy and vaginal brachytherapy without formal staging lymph node sampling: report of a prospective trial. International Journal of Radiation Oncology, Biology, Physics 38(2): 373-380, 1997.

  2. Homesley HD, Kadar N, Barrett RJ, et al.: Selective pelvic and periaortic lymphadenectomy does not increase morbidity in surgical staging of endometrial carcinoma. American Journal of Obstetrics and Gynecology 167(5): 1225-1230, 1992.

  3. Aalders J, Abeler V, Kolstad P, et al.: Postoperative external irradiation and prognostic parameters in stage I endometrial carcinoma. Clinical and histopathologic study of 540 patients. Obstetrics and Gynecology 56(4): 419-427, 1980.

  4. Morrow CP, Bundy BN, Kurman RJ, et al.: Relationship between surgical-pathological risk factors and outcome in clinical stage I and II carcinoma of the endometrium: a Gynecologic Oncology Group study. Gynecologic Oncology 40(1): 55-65, 1991.

  5. Marchetti DL, Caglar H, Driscoll DL, et al.: Pelvic radiation in stage I endometrial adenocarcinoma with high-risk attributes. Gynecologic Oncology 37(1): 51-54, 1990.

  6. Greven KM, Lanciano RM, Herbert SH, et al.: Analysis of complications in patients with endometrial carcinoma receiving adjuvant irradiation. International Journal of Radiation Oncology, Biology, Physics 21(4): 919-923, 1991.

  7. Stokes S, Bedwinek J, Kao MS, et al.: Treatment of stage I adenocarcinoma of the endometrium by hysterectomy and adjuvant irradiation: a retrospective analysis of 304 patients. International Journal of Radiation Oncology, Biology, Physics 12(3): 339-344, 1986.

  8. Grigsby PW, Kuske RR, Perez CA, et al.: Medically inoperable stage I adenocarcinoma of the endometrium treated with radiotherapy alone. International Journal of Radiation Oncology, Biology, Physics 13(4): 483-488, 1987.


STAGE II ENDOMETRIAL CANCER

Many combinations of preoperative intracavitary and external-beam radiation therapy with hysterectomy and bilateral salpingo-oophorectomy are used for treatment of stage II endometrial cancer, with careful biopsy of the para-aortic nodes at the time of surgery. When microscopic cervical stromal involvement is found, postoperative irradiation (external-beam and vaginal irradiation) should be used.


Stage IIA

Stage IIA (endocervical glandular involvement only) should be treated the same as stage I disease.


Stage IIB

Treatment options:

Standard:

1. Hysterectomy, bilateral salpingo-oophorectomy, and node sampling followed by postoperative irradiation.

2. Preoperative intracavitary and external-beam radiation therapy followed by hysterectomy and bilateral salpingo-oophorectomy. (A biopsy of the para-aortic nodes should be done at the time of surgery.)

3. Radical hysterectomy and pelvic lymphadenectomy in selected cases.


STAGE III ENDOMETRIAL CANCER

Treatment options:

Standard:

In general, these patients are treated with surgery and radiation therapy.
These patients may be inoperable if the tumor extends to the pelvic wall,
and in this case, they should be treated with radiation therapy. The usual
approach is to use a combination of intracavitary and external-beam
radiation therapy. Patients who are not candidates for either surgery or
irradiation may be treated with progestational agents. Postoperative
radiation therapy is used in patients who were thought to have had more
localized disease (clinical stage I or II) but are found during hysterectomy
to have positive lymph nodes or adnexa. Studies of patterns of failure have
found a high rate of distant metastases in the upper abdominal and extra-
abdominal sites. For this reason, patients with stage III disease may be
candidates for innovative clinical trials.[1]

Under clinical evaluation:
Clinical trials.[2]

References:

  1. Greven KM, Curran WJ, Whittington R, et al.: Analysis of failure patterns in stage III endometrial carcinoma and therapeutic implications. International Journal of Radiation Oncology, Biology, Physics 17(1): 35-39, 1989.

  2. Axelrod JH, Gynecologic Oncology Group: Phase II Study of Whole-Abdominal Radiotherapy in Patients with Papillary Serous Carcinoma and Clear Cell Carcinoma of the Endometrium or with Maximally Debulked Advanced Endometrial Carcinoma (Summary Last Modified 05/91), GOG-94, clinical trial, closed, 02/24/1992.


STAGE IV ENDOMETRIAL CANCER

Treatment options:

Standard:

Treatment of stage IV endometrial cancer is dictated by the site of
metastatic disease and symptoms related to disease sites. For bulky pelvic
disease, radiation therapy consisting of a combination of intracavitary and
external-beam irradiation is used. When distant metastases,
especially pulmonary metastases, are present, hormonal therapy is indicated
and useful.

The most common hormonal treatment has been progestational agents,
which produce good antitumor responses in up to 15% to 30% of patients.
These responses are associated with significant improvement in survival.
Progesterone and estrogen hormone receptors have been identified in
endometrial carcinoma tissues. Responses to hormones are correlated with
the presence and level of hormone receptors and the degree of tumor
differentiation. Standard progestational agents include
hydroxyprogesterone (Delalutin), medroxyprogesterone (Provera), and
megestrol (Megace).[1]

Under clinical evaluation:
There is no standard chemotherapy program for patients with metastatic
uterine cancer, although doxorubicin has activity. Some studies have
demonstrated activity of doxorubicin-containing combinations, although there
has been no prospective comparison of single-agent versus combination
chemotherapy that has demonstrated superiority of the combinations.[2,3]
Paclitaxel has demonstrated antitumor activity and has been evaluated.[4]
All patients with advanced disease should be considered for clinical trials
that evaluate single-agent or combination therapy for this disease.

References:

  1. Lentz SS: Advanced and recurrent endometrial carcinoma: hormonal therapy. Seminars in Oncology 21(1): 100-106, 1994.

  2. Hancock KC, Freedman RS, Edwards CL, et al.: Use of cisplatin, doxorubicin, and cyclophosphamide to treat advanced and recurrent adenocarcinoma of the endometrium. Cancer Treatment Reports 70(6): 789-791, 1986.

  3. Seski JC, Edwards CL, Herson J, et al.: Cisplatin chemotherapy for disseminated endometrial cancer. Obstetrics and Gynecology 59(2): 225-228, 1982.

  4. Ball HG, Blessing JA, Lentz SS, et al.: A phase II trial of paclitaxel in patients with advanced or recurrent adenocarcinoma of the endometrium: a Gynecologic Oncology Group study. Gynecologic Oncology 62(2): 278-281, 1996.


RECURRENT ENDOMETRIAL CANCER

For localized recurrences (pelvis and periaortic lymph nodes) or distant metastases in selected sites, irradiation may be an effective palliative therapy. In rare instances, pelvic irradiation may be curative in pure vaginal recurrence when no prior radiation has been used. Patients positive for estrogen and progesterone receptors respond best to progestin therapy. Among 115 patients with advanced endometrial cancer who were treated with progestins, 75% (42 of 56) of those with detectable progesterone receptors in their tumors before treatment responded, compared to only 7% without detectable progesterone receptors (4 of 59).[1] A receptor-poor status may predict not only poor response to progestins, but also a better response to cytotoxic chemotherapy.[2] There is evidence to suggest that tamoxifen (20 milligrams twice a day) will give a response rate of 20% in those who do not respond to standard progesterone therapy.[3] Clinical trials are appropriate for patients whose disease recurs with distant metastases and who are unresponsive to hormonal therapy.[4] Doxorubicin is the most active anticancer agent employed, with useful but temporary responses obtained in up to one third of patients with metastatic disease. Paclitaxel also has significant activity.[5]

References:

  1. Kauppila A: Oestrogen and progestin receptors as prognostic indicators in endometrial cancer: a review of the literature. Acta Oncologica 28(4): 561-566, 1989.

  2. Kauppila A, Friberg LG: Hormonal and cytotoxic chemotherapy for endometrial carcinoma: steroid receptors in the selection of appropriate therapy. Acta Obstetricia et Gynecologica Scandinavica. Supplement (101): 59-64, 1981.

  3. Quinn MA, Campbell JJ: Tamoxifen therapy in advanced/recurrent endometrial carcinoma. Gynecologic Oncology 32(1): 1-3, 1989.

  4. Cornelison TL, Baker TR, Piver MS, et al.: Cisplatin, adriamycin, etoposide, megestrol acetate versus melphalan, 5-fluorouracil, medroxyprogesterone acetate in the treatment of endometrial carcinoma. Gynecologic Oncology 59(2): 243-248, 1995.

  5. Ball HG, Blessing JA, Lentz SS, et al.: A phase II trial of paclitaxel in patients with advanced or recurrent adenocarcinoma of the endometrium: a Gynecologic Oncology Group study. Gynecologic Oncology 62(2): 278-281, 1996.

Date Last Modified: 05/1999



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