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Ovarian Epithelial Tumours: Morphologic Types, New Developments and Pathogenesis

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Ovarian Epithelial Tumours: Morphologic Types, New Developments and Pathogenesis OVARIAN EPITHELIAL TUMOURS: MORPHOLOGIC TYPES, NEW DEVELOPMENTS AND PATHOGENESIS W Glenn McCluggage Royal Group Of Hospitals Belfast OVARIAN CARCINOMA • second commonest female genital tract malignancy in developed countries • most cases advanced (stage 3-4) at diagnosis • overall prognosis is poor (approximately 35% 5 year survival) OVARIAN CARCINOMA • heterogeneous group of neoplasms • clinically often considered as one disease • pathogenesis until recently largely unknown • different morphological types have different underlying pathogenesis, molecular events, natural behaviour and prognosis • many studies/clinical trials lump all types together • studies/clinical trials must include good pathological review TO DISCUSS • morphological types of ovarian carcinoma • pathogenesis of different types • grading • problematic areas in typing • proposed new classification of ovarian carcinomas • theory of origin of high grade pelvic serous carcinoma from fallopian tube WHO CLASSIFICATION (2003) OF OVARIAN CARCINOMAS • serous • mucinous • endometrioid • clear cell • transitional • squamous • undifferentiated • mixed (10% rule) TYPING OF OVARIAN CARCINOMA • at present of limited therapeutic significance • treatment more dependent on stage and grade • NEW ERA OF DIFFERENT THERAPY FOR DIFFERENT OVARIAN CANCER TYPES (surgery, traditional chemotherapy, targetted therapies) • ongoing trials regarding alternative therapeutic agents in clear cell, mucinous and low grade serous carcinoma (chemoresistant neoplasms) OTHER REASONS FOR TYPING • carcinoma grading (differs between different types) • personal and family history risk • clear cell and mucinous histology (although rare) are independent predictors of poor outcome in advanced stage • ? need for lymphadenectomy in stage 1 ovarian carcinoma RECENT POPULATION BASED (WASHINGTON / BRITISH COLUMBIA) • 68-71% serous • 3% MUCINOUS • 9-11% endometrioid • 12-13% clear cell • 1% transitional • 6% mixed DIFFERENCES FROM PREVIOUS STUDIES • increase in serous • marked decrease in mucinous • reversal of endometrioid and clear cell ratio LOW STAGE (I/II) VERSUS HIGH STAGE (III/IV) I/II III/IV serous 36% 88% clear cell 26% 5% endometrioid 27% 3% mucinous 8% 1% POST-CHEMOTHERAPY • up-front chemotherapy sometimes administered (poor operative risk, miliary disease etc) • CHORUS study in UK • MAY BE DIFFICULT TO TYPE UNLESS MINIMAL OR NO RESPONSE • require pre-chemotherapy biopsy (not just ascitic fluid) for typing of carcinoma and to have tissue available for studies/targetted and personalised treatments (recent NICE guidelines in UK) POST CHEMO WT1 p16 GRADING OF OVARIAN CARCINOMA • no universal grading system • several in use (FIGO, WHO, Shimizu/Silverberg) but inconsistently applied • some systems are universal; some apply different criteria for different types OVARIAN SEROUS CARCINOMA (OSC) • most common ovarian carcinoma • often advanced stage at diagnosis • traditionally graded as grade 1, 2, 3 (well, moderately, poorly differentiated) • several grading systems in use OVARIAN SEROUS CARCINOMA (OSC) – RECENT DEVELOPMENTS • two distinct tumour types (called low grade and high grade OSC) • not two grades of same neoplasm • different neoplasms with different underlying pathogenesis, molecular events, behaviour, prognosis • high grade much more common than low grade • use instead of traditional grading schemes PATHOGENESIS (LOW GRADE SEROUS) • low grade arise from pre-existing benign and borderline tumour (? not all cases) • micropapillary variant of borderline may be intermediate stage in development of low grade serous carcinoma • sometimes called invasive micropapillary serous carcinoma (poor term) • well-defined adenoma-carcinoma sequence PATHOGENESIS (HIGH GRADE SEROUS) • thought to arise directly from ovarian surface epithelium or epithelium of cortical inclusion cysts or epithelium of distal fallopian tube • no well-defined precursor lesion (postulated to be serous tubal intraepithelial carcinoma)-rapid development • doesn’t arise from borderline tumour DEVELOPMENT OF LOW-GRADE AND HIGH-GRADE OVARIAN SEROUS CARCINOMA fimbria of fallopian tube ovarian surface epithelium benign serous cystadenoma serous tubal ovarian cortical usual serous borderline intraepithelial intraepithelial inclusion neoplasm carcinoma neoplasia cysts micropapillary variant of serous borderline neoplasm high grade low grade serous carcinoma serous carcinoma MORPHOLOGY • classification as high grade or low grade serous is reproducible (MD Anderson system) • distinction based mainly on nuclear atypia (not on architecture) in worst area of tumour • low grade serous – uniform nuclei with mild atypia; < 12 mitoses per 10 HPFs; usually approximately 2/10 HPFs; no necrosis or multinucleation • high grade serous – moderate to marked atypia; >12 mitoses per 10 HPFs; often necrosis and multinucleate cells LOW GRADE OSC WITH “BIGGER” NUCLEI high grade serous high grade serous CORRELATION BETWEEN GRADING SYSTEMS • almost all grade 2 and 3 in old systems are high grade • grade 1 in old systems may be low grade or high grade MOLECULAR (LOW GRADE SEROUS) • KRAS or BRAF mutations in approx 2/3 (early in evolution – mutations found in benign and borderline tumours; identical mutations in borderline and malignant areas in same tumour) • ERBB2 mutations • KRAS and BRAF mutations are mutually exclusive; equivalent effect on tumorigenesis • no Tp53 mutations/abnormalities • progressive increase in chromosomal instability from benign to borderline to malignant MOLECULAR (HIGH GRADE SEROUS) • Tp53 mutations (early in evolution-seen in early microscopic tumours eg BRCA1/2) (p53 dysfunction found in almost 100% high grade serous using stringent methods) • BRCA1/2 abnormalities (germline or somatic mutations or hypermethylation) • no BRAF and only occasional KRAS mutations • high chromosome instability (even in small early tumours) IMMUNOHISTOCHEMISTRY high grade OSC exhibits significantly higher expression of p53, MIB1, bcl2, C-Kit, HER-neu, p16, HLA-G than low grade OSC WT1 expressed in both p53 • p53 immunohistochemistry- lot of confusion • only consider positive/significant if diffuse strong nuclear immunoreactivity (75-80% cells suggested- associated with missence mutation) • p53 null consistent with serous carcinoma (different type of mutation (nonsense) or deletion resulting in truncated protein which is not detected by immunohistochemistry) • most normal tissues and tumours exhibit focal, weak, heterogenous staining (“wild-type” staining) (usually <50%) • also of relevance in other areas of pathology (eg Barrett’s oesophagus) p53 • most ovarian high grade serous carcinomas diffusely positive or totally (“flat”) negative- aberrant staining • most low grade serous, clear cell, mucinous and endometrioid exhibit “wild- type” staining p53 Wild-type p53 BEHAVIOUR AND PROGNOSIS (LOW GRADE SEROUS) • usually advanced at diagnosis • indolent behaviour (median survival 4.2 years; 5 year survival approx 55%; many cases survive longer eg >20 years) • often eventually fatal • poor response to chemotherapy • ? role of hormone therapy (aromatase inhibitors etc) (ER/PR positive) • possible targetted therapies (MEK inhibitors in tumours with RAS mutations) • rarely coexist with or evolve into high grade serous/undifferentiated carcinoma/carcinosarcoma LOW GRADE SEROUS EVOLVING INTO HIGH GRADE MIB1 MIB1 BEHAVIOUR AND PROGNOSIS (HIGH GRADE SEROUS) • usually advanced at diagnosis • aggressive behaviour • median survival 1.7 years • 5 year survival approx 25-30% • responds well initially to chemotherapy but usually recurs • ? role of PARP inhibitors (especially if BRCA abnormalities) PRIMARY PERITONEAL SEROUS CARCINOMA (PPSC) • usually high grade • now being diagnosed more frequently • post-chemotherapy cases (probably cannot diagnose) • use GOG criteria (adopted by WHO) but often have to diagnose clinically/radiologically GOG CRITERIA FOR PPSC • ovaries normal in size or enlarged by a benign process • tumour must be serous in type • microscopy- no tumour in ovary ; tumour confined to surface; <5mm invasion into stroma of ovary (arbitrary figure) • review slides (if <5 years) and, or, report of previous oophorectomy to document absence of tumour OVARIAN MUCINOUS TUMOURS • general issues • classification • morphology and immunohistochemistry • behaviour PREVALENCE • previously mucinous carcinoma was considered to be second commonest variant of ovarian carcinoma • in most older studies, comprise 6-25% of primary ovarian carcinomas (mean 12%) RECENT POPULATION BASED (WASHINGTON / BRITISH COLUMBIA) • 68-71% serous • 3% MUCINOUS • 9-11% endometrioid • 12-13% clear cell • 1% transitional • 6% mixed REASONS FOR DECLINE IN MUCINOUS CARCINOMAS • exclusion of secondaries • pseudomyxoma peritonei (PMP) - usually appendiceal origin • redefinition of criteria for borderline mucinous (intraepithelial carcinoma) • VARIABILITY STILL EXISTS IN DIAGNOSIS BETWEEN BORDERLINE AT UPPER END OF SPECTRUM AND MUCINOUS CARCINOMA EXHIBITING EXPANSILE INVASION (accounts for variation in prevalence of mucinous carcinomas between different institutions) PROBLEMS WITH OVARIAN MUCINOUS TUMOURS • borderline at upper end of spectrum versus carcinoma with expansile invasion • primary versus secondary (borderline and malignant histology) INTESTINAL VERSUS MULLERIAN MUCINOUS • applies to borderline and malignant • intestinal much more common (don’t need goblet cells) • based on morphology - architecture and cytology • markers may help • intestinal type more akin to pancreatic or gastric rather
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