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Ovarian low malignant potential tumor


Table of Contents

DISEASE DESCRIPTION

DISEASE DESCRIPTION

Tumors of low malignant potential (borderline tumors) account for 15% of all epithelial ovarian cancers. Nearly 75% of these are stage I at the time of diagnosis. These tumors must be recognized, since their prognosis and treatment is clearly different from the frankly malignant invasive carcinomas. A review of 22 series (953 patients) with a mean follow-up of 7 years revealed a survival rate of 92% for advanced stage tumors if patients with so-called invasive implants were excluded. The cause of death was determined to be benign complications of disease (e.g., small bowel obstruction), complications of therapy, and only rarely (0.7%), malignant transformation.[1] In one series, the 5-, 10-, 15-, and 20-year survival rates of patients with low malignant potential tumors (all stages), as demonstrated by clinical life table analysis, were 97%, 95%, 92%, and 89%.[2] In this series, mortality was stage dependent: 0.7%, 4.2%, and 26.8% of patients with stages I, II, and III respectively, died of disease.[2] One large study showed early stage, serous histology, and younger age to be associated with a more favorable prognosis.[3] In contrast to the excellent survival rates for early stage disease generally reported, the FIGO Annual Report (#21) included 529 stage I tumors with a 5- year actuarial survival rate of 89.1%. Nonetheless, these survival rates are clearly in contrast with the 30% survival rate for invasive tumors (all stages). The less common endometrioid tumor of low malignant potential should not be regarded as malignant since it seldom, if ever, metastasizes. Malignant transformation can, however, occur and may be associated with a similar tumor outside of the ovary; such tumors are the result of either a second primary or rupture of the primary endometrial tumor.[4]

In early stage disease (stage I/II), no additional treatment is indicated for a completely resected tumor of low malignant potential.[5] When it is desirable to retain childbearing potential, a unilateral salpingo-oophorectomy is adequate therapy.[3,6] In the presence of bilateral ovarian cystic neoplasms, or a single ovary, partial oophorectomy can be employed when fertility is desired by the patient.[7] Some stress the importance of limiting ovarian cystectomy to stage IA patients in whom the margins of the cystectomy specimens are free of tumor.[8] In one large series, the relapse rate was higher with more conservative surgery (cystectomy >unilateral oophorectomy >TAH, BSO); differences, however, were not statistically significant and survival was nearly 100% for all groups.[2,9] When childbearing is not a consideration, a total abdominal hysterectomy and bilateral salpingo-oophorectomy is appropriate therapy. Once a woman has completed her family, most, but not all,[8] physicians favor removal of remaining ovarian tissue as it is at risk of recurrence of a borderline tumor, or even rarely, a carcinoma.[3,10]

The value of complete staging has not been demonstrated for early stage cases, but the opposite ovary should be carefully evaluated for evidence of bilateral disease. Although the impact of surgical staging on therapeutic management is not defined, in one study 7 of 27 patients with presumed localized disease were upstaged following complete surgical staging.[11] In two other studies, 16% and 18% of patients with presumed localized tumors of low malignant potential were upstaged as a result of a staging laparotomy.[10,12] In one of these studies, the yield for serous tumors was 30.8% (4/13) compared to 0% (0/12) for mucinous tumors.[8] In yet another study, patients with localized intraperitoneal disease and negative lymph nodes had a low incidence of recurrence (5%), whereas patients with localized intraperitoneal disease and positive lymph nodes had a statistically significantly higher incidence of recurrence (50%).[2]

Patients with advanced disease should undergo a total hysterectomy, bilateral salpingo-oophorectomy, omentectomy, node sampling, and aggressive cytoreductive surgery. Patients with stage II/III disease with no gross residual tumor have had a 100% survival rate in some series regardless of the follow-up duration.[13,14] The 7-year survival rate of patients with gross residual disease was only 69% in one large series,[2] and appears to be inversely proportional to the length of follow-up.[2]

For patients with more advanced stage disease and microscopic or gross residual disease, chemotherapy and/or radiation therapy may be indicated. There is scant evidence, however, that postoperative chemotherapy or radiation therapy alters the course of this disease in any beneficial way.[2,9,13,15,16] In one study of 364 patients without residual tumor, adjuvant therapy had no effect on disease-free or corrected survival when stratified for disease stage.[3] Patients without residual tumor who received no adjuvant treatment had a survival rate equal to or greater than the treated groups. There have been no controlled studies comparing postoperative treatment with no treatment.

In a review of 150 patients with borderline ovarian tumors, the survival of patients with a residual tumor of less than 2 centimeters was significantly better than those with a residual tumor from 2 to 5 centimeters and greater than 5 centimeters.[17] Whether invasive implants imply a worse prognosis remains an unsettled question. Some investigators have correlated invasive implants with poor prognosis [18] while others have not.[14,19] Some studies have suggested that it may be possible to use DNA ploidy of the tumors to identify those patients who will develop aggressive disease.[20,21] A study could not correlate DNA ploidy of the primary serous tumor with survival but found that aneuploid invasive implants were associated with a poor prognosis.[22] There is no evidence that treatment of patients with aneuploid tumors would have an impact on survival. No significant association was found between p53 and Her-2/neu overexpression and tumor recurrence or survival.[23]

In the face of clinical progression, further tumor reductive surgery followed by chemotherapy is certainly indicated. If the symptom-free interval is long, using chemotherapy after a secondary cytoreductive procedure may not be advisable. If, on the other hand, the disease symptomatically recurs rapidly, chemotherapy may be beneficial. Reports have surgically documented the efficacy of chemotherapy on some patients with microscopic or gross residual disease.[24,25] A GOG study used melphalan chemotherapy for patients with progressive disease, with cisplatin for melphalan failures.[26]

References:

  1. Kurman RJ, Trimble CL: The behavior of serous tumors of low malignant potential: are they ever malignant? International Journal of Gynecological Pathology 12(2): 120-127, 1993.

  2. Leake JF, Currie JL, Rosenshein NB, et al.: Long-term follow-up of serous ovarian tumors of low malignant potential. Gynecologic Oncology 47(2): 150-158, 1992.

  3. Koern J, Trope CG, Abeler VM: A retrospective study of 370 borderline tumors of the ovary treated at the Norwegian Radium Hospital from 1970 to 1982. Cancer 71(5): 1810-1820, 1993.

  4. Norris HJ: Proliferative endometrioid tumors and endometrioid tumors of low malignant potential of the ovary. International Journal of Gynecological Pathology 12(2): 134-140, 1993.

  5. Trope C, Kaern J, Vergote IB, et al.: Are borderline tumors of the ovary overtreated both surgically and systematically? A review of four prospective randomized trials including 253 patients with borderline tumors. Gynecologic Oncology 51(2): 236-243, 1993.

  6. Lim-Tan SK, HE Cajigas, Scully RE.: Ovarian cystectomy for serous borderline tumors: a follow-up study of 35 cases. Obstetrics and Gynecology 72(5): 775-781, 1988.

  7. Rice LW, Berkowitz RS, Mark SD, et al.: Epithelial ovarian tumors of borderline malignancy. Gynecologic Oncology 39(2): 195-198, 1990.

  8. Piura B, Dganis R, Blicksteins I, et al.: Epithelial ovarian tumors of borderline malignancy: a study of 50 cases. International Journal of Gynecological Cancer 2(2): 189-197, 1992.

  9. Casey AC, Bell DA, Lage JM, et al.: Epithelial ovarian tumors of borderline malignancy: long-term follow-up. Gynecologic Oncology 50(3): 316-322, 1993.

  10. Snider DD, Stuart GC, Nation JG, et al.: Evaluation of surgical staging in stage I low malignant potential ovarian tumors. Gynecologic Oncology 40(2): 129-132, 1991.

  11. Yazigi R, Sandstad J, Munoz AK: Primary staging in ovarian tumors of low malignant potential. Gynecologic Oncology 31(3): 402-408, 1988.

  12. Leake JF, Rader JS, Woodruff JD, et al.: Retroperitoneal lymphatic involvement with epithelial ovarian tumors of low malignant potential. Gynecologic Oncology 42(2): 124-130, 1991.

  13. Barnhill D, Heller P, Brzozowski P, et al.: Epithelial ovarian carcinoma of low malignant potential. Obstetrics and Gynecology 65(1): 53-59, 1985.

  14. Bostwick DG, Tazelaar HD, Ballon SC, et al.: Ovarian epithelial tumors of borderline malignancy: a clinical pathologic study of 109 cases. Cancer 58: 2052-2065, 1986.

  15. Tumors of the ovary: neoplasms derived from coelomic epithelium. In: Morrow CP, Townsend DE: Synopsis of Gynecologic Oncology. New York: John Wiley and Sons, 3rd ed., 1987, pp 257-303.

  16. Sutton GP, Bundy BN, Omura GA, et al.: Stage III ovarian tumors of low malignant potential treated with cisplatin combination therapy (a Gynecologic Oncology Group study). Gynecologic Oncology 41(3): 230-233, 1991.

  17. Tamakoshi K, Kikkawa F, Nakashima N, et al.: Clinical behavior of borderline ovarian tumors: a study of 150 cases. Journal of Surgical Oncology 64(2): 147-152, 1997.

  18. Bell DA, Scully RE: Serous borderline tumors of the peritoneum. American Journal of Surgical Pathology 14: 230-239, 1990.

  19. Michael H, Roth LM: Invasive and noninvasive implants in ovarian serous tumors of low malignant potential. Cancer 57: 1240-1247, 1986.

  20. Friedlander ML, Hedley DW, Swanson C, et al.: Prediction of long-term survival by flow cytometric analysis of cellular DNA content in patients with advanced ovarian cancer. Journal of Clinical Oncology 6(2): 282-290, 1988.

  21. Kaern J, Trope C, Kjorstad KE, et al.: Cellular DNA content as a new prognostic tool in patients with borderline tumors of the ovary. Gynecologic Oncology 38(3): 452-457, 1990.

  22. de Nictolis M, Montironi R, Tommasoni S, et al.: Serous borderline tumors of the ovary. Cancer 70(1): 152-160, 1992.

  23. Eltabbakh GH, Belinson JL, Kennedy AW, et al.: p53 and HER-2/neu overexpression in ovarian borderline tumors. Gynecologic Oncology 65(2): 218-224, 1997.

  24. Fort MG, Pierce VK, Saigo PE, et al: Evidence for the efficacy of adjuvant therapy in epithelial ovarian tumors of low malignant potential. Gynecologic Oncology 32(3): 269-272, 1989.

  25. Gershenson DM, Silva EG: Serous ovarian tumors of low malignant potential with peritoneal implants. Cancer 65(3): 578-585, 1990.

  26. Barnhill DR, Kurman RJ, Brady MF, et al.: Preliminary analysis of the behavior of stage I ovarian serous tumors of low malignant potential: a Gynecologic Oncology Group study. Journal of Clinical Oncology 13(11): 2752-2756, 1995.

Date Last Modified: 05/1999



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