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Malignant Mixed Mullerian Tumours of the Uterus

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Malignant Mixed Mullerian Tumours of the Uterus MALIGNANT MIXED MULLERIAN TUMOURS OF THE UTERUS - AN IMMUNOHISTOCHEMICAL STUDY By Ellen Bolding Town Cape of Dissertation submitted in fulfilment of Part III M.Med(Anat.Path). University of CapeUniversity Town, October, 1989. Supervisor : Professor A J Tiltman Department of Anatomical Pathology The University of Ciipe Town has been given the right to repr..,,::·.,cc t:,i.; ::,t,Si::; in whole or In part. Copyright is heiJ by the a~thor j L.~ "-----~·"r.!1~·~:.Jlr:;":"'.' \..,.., . .J.1"'",11,'""'W1""........ V. The copyright of this thesis vests in the author. No quotation from it or information derived from it is to be published without full acknowledgement of the source. The thesis is to be used for private study or non- commercial research purposes only. Published by the University of Cape Town (UCT) in terms of the non-exclusive license granted to UCT by the author. University of Cape Town To my husband Derck Smits, for his constant support and encouragement, for laughing and not laughing in the right places, and for tolerating the many "take-away" dinners. 11 ACKNOWLEDGEMENTS I am indebted, and extremely grateful to the following persons: Firstly, my supervisor, Andrew Tiltman, for his enthusiasm, critical advice and crucial encouragement in the early stages of this project. Secondly, to Susan Ford for her excellent technical assistance, particularly for performing the immunohistochemistry. Thirdly, to Val Dunn, for her invaluable secretarial assistance in prepara­ tion of this manuscript. This work was partially sponsored by the National Cancer Association. lll I, Ellen Bolding, hereby declare that the work on which this thesis is based is original ( except where acknowledgements indicate otherwise) and that nei­ ther the whole work nor any part of it has been, is being, or is to be submitted for another degree in this or any other University. I empower the University to reproduce for the purpose of research either the whole or any portion of the contents in any manner whatsoever. (Date) IV INDEX Page Introduction .................. ........... 1 Materials and Methods ............ ........ 20 Results ................................... 25 . DlSCUSSlOn .......... ........... ......... 38 Illustrations 47 References 69 V INTRODUCTION Malignant Mixed Mullerian tumours (MMMTs) of the uterus account for 1-2% of all endometrial malignancies and have been a problem, in terms of both subclassification and diagnosis for many years. The entity was first de­ scribed in 1864 by Virchow (92) who described -a mixed form of sarcoma and carcinoma of the uterus, but the first well documented uterine carcinosar- coma was reported by Weber in 1867 (96), and again by Babl-Ruckhard in 1872 (6). .Between the early 1900s and 1950s most papers on the subject consisted of single case reports with or without a review of the literature, which at that stage was still rather scanty and poorly understood. Tumours masqueraded under a variety of different names in an attempt to fit a name to the histologic pattern as well as trying to explain the histogenesis. The number of terms designated to this tumour entity became astronomical and included primary chondrosarcoma, adenoliposarcoma, sarcoma hydropicum polyposum uteri embryoides, dysontogenic tumour, mesenchymal sarcoma, carcinosarcoma, mixed tumour and malignant mixed mesodermal tumour. In 1935 McFarland (55), in a literature survey of utero-vaginal neoplasms with a list of 516 references, found 119 different names given to the entity. In 1941 Liebow and Tennant ( 45) attempted to summarise the anatomical and clinical data in these mixed uterine sarcomas. The diagnosis of malignant mixed tumour was based on the presence of heterologous elements such as 1 striated muscle, osteoid, cartilage and osteoid. The term carcinosarcoma was reserved for those tumours with epithelioid and spindle cell elements. Whether these were true biphasic tumours or carcinomas with spindle cell dedifferentiation was uncertain. There was much speculation as to the origin of these tumours. Many considered them to be malignant growths of metaplastic origin, while others considered the possibility that they might arise from benign tumours de­ veloping in heterotopic uterine tissue. However, because of the multiplicity of tissue types seen, most pathologists favoured the theory that the devel­ opment of these tumours came from a multipotential stem cell. Another viewpoint favoured atypical connections between embryonal and mesenchy­ mal cells from the inguinal area or misplaced ectopic rests as the primary site. In 1954, Sternberg (87), who believed these tumours to be of Mullerian duct origin, proposed that the term malignant Mullerian tumour be used. His studies indicated that this tumour arose from specialised mesodermal tissue and that the carcinomatous components were limited by the epithelial po­ tentialities of the Mullerian tract. Sa.rcoma.tous elements of these neoplasms were not rigidly limited in type by their Mullerian ancestry, and in com­ mon with mesenchymal cells elsewhere, retained the ability to differentiate into many mesenchymal derivations such as chondrosarcoma, fibrosarcoma, rhabdomyosarcoma and leiomyosarcoma. 2 Between 1950 and the mid 1970s several articles (16 , 18, 39 , 45, 51 , 54, 72, 79, 81, 87) appeared from various large institutions describing the range of morphologic findings, documenting the clinical disease, presentation, age range, mode of spread and modalities of therapy used. The majority of pa­ tients were postmenopausal women between the ages of 45-85 with a mean age of 65 years. The commonest presentation was that of postmenopausal bleeding, followed by lower abdominal pain/ discomfort and a pelvic mass. There was no significant association between this tumour and obesity, hyper­ tension or diabetes, and the role of prior radiotherapy as a possible aetiologic factor was controversial. Generally, the prognosis was poor. In 1966 Norris and Taylor (61) reviewed :n cases of carcinosarcoma and addressed the problem - "Is carcinosarcoma the same entity as mixed mes­ enchymal tumour?" Their findings showed that the 31 patients with carci­ nosarcoma had an overall better prognosis than those containing mixed or · heterologous elements, and recommended that the terms not be used inter­ changeably, but that they be regarded as separate entities because of their different behavioural patterns. In a follow up study ( 62) of 31 cases of heterol­ ogous mixed mesodermal tumours, they attempted to evaluate the relation­ ship of the morphologic features to the survival of the patients. The presence of cartilaginous elements was found to be associated with a more favourable prognosis, whereas the presence of rhabdomyoblastic cells indicated a worse prognosis. They emphasised, however, that the over.all prognosis of this 3 group was worse than carcinosarcoma. The authors also supported the view that the origin of these tumours was a multipotential stem cell which could differentiate along both carcinomatous and sarcomatous lines, and that the inherent metaplastic potential of the sarcomatous cells accounted for the wide variety of mesenchymal elements. Another clinicopathologic study of 66 cases from the Netherlands (81), evaluated after 5 years of therapy, showed the same trend as found by Norris and Taylor with their carcinosarcomas, i.e. a mean 43, 7% five year survival and a mean 27% five year survival for the mixed mesodermal group. In contrast to this, studies of a large series of patients by Chuang et al (16) and later by Williamson and Christopherson (99), found that there was no significant difference in the biological behaviour of these two groups, i.e. carcinosarcoma and mixed mesodermal tumours, and hence no difference in prognosis. These tumours differed only in their histological appearance and not in their clinical course. The issue remained unresolved. In the following years various reputable institutions once again reported retrospective studies with follow up (22,57, 69,76,82). Little new informa­ tion was added to the clinical and pathologic findings, but issues revolved around modalities of therapy, in particular the "type of surgery". Discussion centered around the use of adjuvant chemotherapy and radiotherapy. It was recognised that this was an aggressive tumour, with a propensity to both vas­ cular and lymphatic invasion, and that an aggressive treatment programme 4 was warranted. Several series reported an improved survival in patients with stage I and II disease when chemotherapy was given prior to surgery and radiotherapy. Studies to determine the most important prognostic indicator were un­ dertaken by Barwick and Livolsi (8) who found that the most important factor was tumour extent, particularly the depth of myometrial invasion. Though their homologous group had a better 5 year survival rate than the heterologous counterpart, the true significance of heterologous elements was uncertain. Most believed that heterologous tumours were more aggressive because of a more rapid growth and, hence, deeper myometrial invasion and metastatic spread. The forty year experience of carcinosarcomas (homol­ ogous tumours) from the State of Missouri, reported by Doss et al (21), emphasised the need for accurate staging - even explorative laparotomy for definite staging to determine the optimal therapeutic modality. In 25% of cases the staging was altered by surgery, and clinical staging was thus con­ sidered inaccurate and inadequate for proper management. Accurate staging included surgical
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