Treatment and Follow Up
Twelve patients underwent a TAH and BSO; two underwent a USO; and one underwent a BSO. All patients underwent surgical staging. All 15 tumors were confined to one ovary (stage I). Two tumors had involvement of the surface of the ovary and one ruptured intraoperatively. Detailed treatment information was available for five patients, of whom two received systemic chemotherapy and three did not. Clinical follow up was available for seven patients, six of whom had no evidence of disease, with a mean follow up of 44 months (Table 3). One patient had recurrent carcinoma involving the bowel 46 months after undergoing a TAH and BSO for a unilateral mass that had reportedly ruptured. The primary tumor was predominantly glandular and had diffuse grade 3 nuclear atypia. The diagnosis of carcinoma was based on the finding of large areas of confluent glandular growth. The serosal bowel recurrence was resected and was histologically similar to the ovarian primary tumor. The patient was alive 40 months after this recurrence but was lost to further clinical follow up.
In the WHO classification, endometrioid ovarian tumors are divided into benign, borderline, and malignant (carcinoma) categories, with a diagnosis of carcinoma based on the identification of destructive infiltrative stromal invasion, but the criteria for the identification of stromal invasion are not described in detail in the WHO classification. 48 In contrast, the criteria for the identification of stromal invasion in the endometrium, which separates complex atypical hyperplasia from well-differentiated carcinoma, are well established and include altered desmoplastic stroma, confluent glandular growth, and papillary growth pattern. 32 We reasoned that the same criteria for recognizing stromal invasion in the endometrium could be applied to ovarian endometrioid tumors. Application of these criteria to ovarian tumors, however, has limitations because the frequent adenofibromatous architecture of the ovarian tumors makes identification of a desmoplastic stromal reaction difficult. In addition, the tendency for many ovarian neoplasms to show a papillary architecture limits the interpretation of papillary growth as evidence of stromal invasion in the ovary. In most cases in this series, the diagnosis of carcinoma was based only on a complex glandular proliferation with confluent growth. This also has been the experience of Scully et al. 50 Confluent glandular growth was the only pattern of invasion seen in the tumor from the one patient who had a recurrence. Accordingly, confluent glandular growth appears to be the most common and reliable indicator of stromal invasion in endometrioid tumors. In the two carcinomas in this series that showed destructive infiltrative growth by virtue of haphazard glands infiltrating the stroma, recognition of an unequivocal stromal reaction was difficult because of the adenofibromatous nature of endometrioid tumors in the ovary. Thus, relying on the presence of this pattern as the sole diagnostic criterion for carcinoma would have resulted in an underdiagnosis of carcinoma, because only 13[percnt] of the carcinomas in our series had this type of invasion.
Although the criteria for the diagnosis of APTs vary among studies, a review of the literature identified 92 cases with available clinical follow up, which appear to correspond to what we have designated APT, APT with microinvasion, or intraepithelial carcinoma. 2,11,23,24,33,41,53 The data from these seven studies and the 14 patients with clinical follow up from the current series are summarized in Table 4. All 106 tumors were stage I at the time of diagnosis, and 105 (99[percnt]) of 106 patients had no evidence of recurrence or died of other causes, with a mean follow up ranging from 28 to 96 months. Among these 106 patients, there was one who was found to have recurrent disease 6 weeks after initial surgery. The tumor was histologically identical to her ovarian lesion and involved the vagina. 24 The vaginal tumor was not resected and the patient was alive with disease 6.4 years later. The stable clinical course suggests that the tumor was implanted or incompletely resected at the time of surgery rather than representing a true metastasis. Another patient who had an unusual clinical course was reported by Bell et al. 2 This patient underwent a USO for an atypical endometrioid adenofibroma and had an endometrioid carcinoma in her opposite ovary 3 years later. At the time of the study, she was currently free of disease 6 months after resection of the carcinoma. In view of the apparent absence of disease elsewhere, it is likely that this case represents a new independent carcinoma developing in the opposite ovary.
Among all the reported cases of atypical proliferative (borderline) endometrioid tumors, only two were described as having advanced stage disease at diagnosis, but clinical follow-up information was unavailable in both cases. 15,43 One of these patients had [ldquo]peritoneal implants[rdquo] of bland endometrioid epithelium outside of the ovary unassociated with hemorrhage or endometrial type stroma. 43 Endometrial stroma, however, is notoriously difficult to identify even in what is otherwise bona fide endometriosis. Accordingly, it seems likely that the bland endometrial tissue in this case was endometriosis rather than a metastasis from the ovarian tumor. The other case of an endometrioid adenofibroma of the ovary associated with endometriosis had a similar tumor involving the omentum. 15 It is likely that the omental tumor, like the ovarian tumor, developed independently from endometriosis. There was one patient in our series with peritoneal implants at the time of diagnosis. It is noteworthy that these implants showed no resemblance to the endometrioid tumor. Instead, the lesions were invasive implants of the type associated with serous borderline tumors. The patient had undergone a TAH and BSO, and no serous ovarian tumor was identified. The patient is known to be alive 76 months after the initial diagnosis, but detailed information regarding her clinical course was unavailable. It is possible that the patient had a primary peritoneal serous neoplasm. We are currently analyzing a group of similar tumors that we have classified as peritoneal micropapillary serous carcinoma (unpublished data). Thus, based on the current analysis and review of the literature, including those rare patients reported with extraovarian disease, there is no well-documented case of an advanced stage endometrioid APT, and no documented case with an adverse prognosis has been reported. Furthermore, in the current series, APTs including those with intraepithelial carcinoma and microinvasion are stage I and are also not associated with an adverse outcome, albeit with relatively short follow up.
A review of the literature of reported cases of endometrioid carcinomas shows that approximately 40[percnt] are stage I (Table 5) and many are low grade. 3,7,9,10,17,18,26,28,31,33,35,37,44,47,55,56,60 It should be noted that careful surgical staging was introduced in the early 1980s so that the stages reported in older studies are likely to be inaccurate. In addition, the criteria for histologic grading vary significantly among studies. We classified tumors that had predominantly glandular pattern with minimal solid areas as well-differentiated, regardless of cytologic atypia. Some reviewers might upgrade these tumors to moderately differentiated because of the cytologic atypia, as could be done in similar tumors arising in the endometrium. The reported 5-year survival for all stages in larger series of endometrioid carcinomas ranges from 38[percnt] to 70[percnt] (Table 6). 1,3,9,18,26,30,31,33[ndash]35,47,49,55,61 It should be emphasized, however, that invasive well-differentiated carcinomas are nearly always stage I and unilateral at presentation and their prognosis is particularly favorable (Table 7). 9[ndash]11,17,18,28,31,33,42,47,55,56,60 Of 29 reported patients with stage I, grade 1 tumors followed up for at least 5 years, only one patient died of disease after 24 months; the clinical details of this case were not reported. 9,17,31,33,42,55,56 Our series included only well-differentiated carcinomas that were all unilateral stage I tumors and six of seven patients with clinical follow up were alive with no evidence of disease at a mean follow up of 47 months. One patient with a stage I carcinoma had recurrent disease 46 months after initial surgery and was currently alive 40 months after this recurrence, but was subsequently lost to follow up. It is possible that the serosal bowel tumor represented a new primary tumor arising from endometriosis. The histologic similarity to the primary tumor, however, and lack of endometriosis in this patient favor a recurrence. Accordingly, based on our study and a review of the literature, stage I, well-differentiated endometrioid carcinomas have an excellent prognosis. Therefore, the important clinical cut-off point for stage I endometrioid tumors is the distinction of low-grade (grade 1) versus high-grade (grades 2 and 3) carcinomas, because the outcome of APTs and stage I, well-differentiated carcinoma is excellent and has a 5-year survival rate of nearly 100[percnt]. Finally, in view of the relatively uncommon occurrence of bilateral APTs and well-differentiated endometrioid carcinoma, the finding of bilateral tumors should raise the suspicion of metastases from the cervix, endometrium, or colon because they can closely simulate a primary ovarian endometrioid neoplasm.
This study also sheds light on the pathogenesis of endometrioid carcinoma of the ovary. In particular, the progression of endometrioid neoplasms appears to closely parallel tumor progression of ovarian mucinous neoplasia rather than serous carcinoma. 40 In the current study, 24[percnt] of the APTs, including tumors with microinvasion and intraepithelial carcinoma, showed evidence of an associated adenofibroma with multifocal areas of increased proliferation and architectural complexity. Similarly, 87[percnt] of the carcinomas also had foci of APT and areas of transition often observed. These observations have been made in previous studies and suggest a model of progression from benign endometriosis through atypical proliferative to malignant tumors similar to that seen with mucinous carcinomas. 2,19,37,59,60 Such transitions result in tumors that architecturally qualify as borderline tumors, but show marked cytologic atypia or foci of stromal invasion, necessitating the addition of diagnostic categories, including APT with intraepithelial carcinoma and APT with microinvasion, to cover the range of histologic appearances. In contrast, serous carcinomas frequently present as advanced stage, poorly differentiated tumors with no discernible evidence of a precursor lesion, suggesting that they develop de novo and only infrequently from a serous borderline tumor.
Although the cell of origin that gives rise to endometrioid neoplasms in the ovary is not known, several investigators have postulated an origin from endometriosis with subsequent neoplastic transformation. 3,9,10,19,21,22,45,46 Previous studies have reported concurrent endometriosis in approximately 20[percnt] of patients with endometrioid carcinoma and in approximately 35[percnt] of patients with borderline endometrioid tumors. 2,6,7,9[ndash]11,16[ndash]18,22,26,28,30,31,35,41[ndash]43,45[ndash]47,49,53,56,60 In approximately half the reported cases, the endometriosis was found in the same ovary containing the endometrioid neoplasm. Rare tumors, including one in this series, have been shown to arise in direct continuity from endometriosis, thereby providing further evidence for an origin from ectopic endometrial tissue. 7,9,10,17,44,46,47 Molecular analysis has also shown a common lineage in some ovarian carcinomas with adjacent endometriosis. 21 The data implicating the development of endometrioid tumors from endometriosis are strongly suggestive and highly provocative but do not completely rule out an origin from the surface epithelium of the ovary through a process of metaplasia and neoplastic transformation.
Another controversial area of investigation in endometrioid tumors of the ovary is the role of unopposed estrogenic stimulation in a manner analogous to that in uterine carcinogenesis. Examination of the endometrium from patients with endometrioid carcinoma of the ovary shows that approximately 10[percnt] to 15[percnt] patients have concurrent carcinoma involving the endometrium. 3,6,7,9,10,17,18,26,28,31,34,35,41,42,44,46,47,49,55,56,60 Based on the limited extent of the uterine tumors and favorable clinical outcome, many of these tumors are thought to represent separate primary lesions. 4,9,28,38,58 Molecular biologic studies have further supported the view that many of these patients have independent primary tumors, and it is conceivable that both neoplasms are related to systemic unopposed estrogenic stimulation. 12,14,52 Many endometrioid ovarian tumors, however, are not associated with concurrent endometrial hyperplasia or carcinoma. To ensure that all tumors in the current study were primary ovarian tumors and not metastatic foci from the uterus, cases with concurrent endometrial carcinoma were excluded. As was found in previous studies, evaluation of the endometrium in our cases showed no specific changes. 2,3,6,7,9[ndash]11,17,18,26,28,31,34,35,41,43,44,47,49,53,55,56,60 A minority of patients had hyperplasia, and the remainder were equally distributed among atrophic, proliferative, and secretory endometrium. Furthermore, none of the patients in this study with known clinical follow up, who did not initially undergo a hysterectomy, developed endometrial carcinoma. Thus, although endometrioid carcinomas of the uterus have been convincingly linked to excessive estrogenic stimulation, the findings in this study and others suggest that excess estrogen, at least systemically, plays a lesser role in endometrioid ovarian carcinogenesis.
In summary, we report the clinicopathologic features of 56 proliferative endometrioid ovarian tumors ranging from APTs to well-differentiated carcinomas. An argument can be made to divide these tumors into APT, APT with intraepithelial carcinoma, APT with microinvasion, and carcinoma because this categorization encompasses the wide range of histologic appearances seen in endometrioid tumors of the ovary and reflects the various stages of endometrioid carcinogenesis. From a managerial standpoint, however, the behavior of APTs, including the limited number of cases with intraepithelial carcinoma and microinvasion that have been studied, is benign after oophorectomy. Even well-differentiated carcinoma, when confined to the ovary, is rarely associated with an adverse outcome. Based on our findings and a review of the literature, we recommend that for clinical management, well-differentiated proliferative endometrioid tumors be classified into two categories[colon] APTs tumors and well-differentiated carcinoma. The terms borderline and low malignant potential are misleading because no well-documented case of such a tumor has been associated with an adverse outcome. The excellent prognosis of well-differentiated carcinomas suggests that surgery alone is adequate for management of these tumors, but closer clinical follow up than for patients with APTs is indicated because these tumors occasionally recur. Future clinicopathologic studies should evaluate criteria for distinguishing low-grade (grade 1) from high-grade (grades 2 and 3) endometrioid carcinoma because the literature suggests a more adverse outcome for patients with high-grade, stage I tumors. Based on current data, endometrioid APTs most likely arise from endometriosis that becomes more proliferative and atypical and results in the development of intraepithelial carcinoma, microinvasion, and eventually frankly invasive carcinoma. Future molecular biologic studies will undoubtedly clarify whether this is a valid model of endometrioid carcinogenesis.
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Keywords:[copy] 2000 Lippincott Williams [amp] Wilkins, Inc.
Endometrioid ovarian carcinoma; Endometrioid ovarian tumor; Borderline ovarian tumor; Atypical proliferative ovarian tumor; Low malignant potential; Endometriosis