Ovarian Serous Tumours

Benign serous tumours (serous cystadenoma) – Unilocular thin walled cysts filled with clear fluid. Smooth inner surface or polypoid excrescences which are firm if fibrous or soft if oedematous. Lined by ciliated columnar epithelium similar to fallopian tube. Serous adenofibromas- hard, white predominantly fibromatous tumours.

Serous borderline tumours – one or more cysts lined by varying amounts of polypoid excrescences and closely packed finer papillae and contain thick mucinous fluid. Also papillary growth that covers the outer surface. No friability, haemorrhage or necrosis (features of malignancy). 1) Arborizing papillae that form increasingly smaller branches ending in clusters of epithelium that appear to be detached from the stroma (hierarchical pattern of branching) 2) varying degrees of nuclear atypia 3) absence of frank stromal invasion.

Main diagnostic problems with SBT:

Pseudoinvasion – similar to stroma elsewhere, glands have an orderly arrangement

Auto-implants – sharply circumscribed desmoplastic plaques usually on the outer surface

Mesothelial hyperplasia – mesothelial cells lack atypia and linear arrangement

Micropapillary pattern – on it’s own not a specific adverse factor, however when assoc with advanced stage, invasive peritoneal implants (esp) and microinvasion increased risk

Microinvasion – stromal invasion with single cells or small clusters. Cells usually have abundant eosinophilic cytoplasm. ?increased risk

Peritoneal implants – in 30-40% of SBT. Invasive and non-invasive may co-exist.

  • Non-invasive – epithelial –  atypical epithelial cells present of surface of peritoneum with well defined margins.  No desmoplasia
  • Non-invasive – desmoplastic –  Stromal reaction greater than epithelial component. With well defined margins. Invaginates through spaces.
  • Invasive – Appears invasive. Greater epithelial component. Desmoplasia. Irregular borders.  Poor prognosis.

*Endosalpingosis – assoc with SBT. Glands lined by flattened tubal-like epithelium found in the parametrium. Benign.

Prognosis: extremely favourable. Stage 1 tumours risk of recurrence or development of a second SBT 5-10%. Good sampling important! To ensure areas of invasion not missed!

SBT with lymph node involvement: uncertainty. Still good prog

SBT of peritoneum: without ovarian involvement identified.

Serous carcinomas: 56 yr old. Well diff: Solid and cystic with soft papillae within cysts. Papillae softer and more confluent. Poorly diff: solid, multinodular masses with necrosis & haemorrhage. Histo: Most are high grade with complex, irregular highly cellular branching, slit like glandular lumens, mitoses, desmoplasia, invasion. IHC: CK7, Cam5.2, AE1/3, EMA, CA125 +. FIGO 5 year survival: stage1 -76%, stage 2 56%, stage 3-25%

Psammocarcinoma: rare form of low grade serous carcinoma. Mild to moderate atypia, >75% psammoma bodies, invasion. Good prog. Behaves like SBT.

x10 psammomatous ca x4 psammomatous ca (2)

High grade serous vs High grade endometrioid carcinoma

Most primary ovarian (as well as primary peritoneal and tubal) serous carcinomas exhibit diffuse nuclear positivity with WT1 while most endometroid adenos are negative. p53 may also be of value in that most ovarian serous carcinomas are diffusely positive whilst most endometrioid adenos are negative although some high grade endometrioid adenos are postitive. p16 is more likely to be diffusely positive in serous than in endometrioid. Vimentin and nuclear beta-catenin postitivity favours an endometrioid adenocarcinoma, although not all cases are positive.

High grade serous ovarian carcinoma and Low grade serous ovarian carcinoma

Should be regarded as two distinct tumour types with different underlying pathogenesis, molecular events, behaviour and prognosis. Low grade OSC is thought to arise in a stepwise manner from a benign cystadenoma through a borderline cystadenoma through a borderline cystadenoma with a micropapillary pattern to an invasive low-grade OSC. In contrast high grade OSC is thought to arise directly from the ovarina surface epithelium with as yet no well defined precursor lesion. The precursor lesion has been speculated to be ovarian intraepithelial neoplasia – which is severe atypia involving the surface epithelium or the epithelium of cortical inclusion cysts. There is now emerging evidence that high grade OSC may actually be derived from the epithelium of hte distal fibrial portion of the fallopian tube.

Diagnostic criteria for HG OSC: mod-marked nuclear atypia & >12 mitoses/10 hpf, necrosis and multinucleate tumour cells. For LG OSC: uniform nuclei with only mild nuclear atypia, <12 mitoses/10 hpf (typically 2), no necrosis or multinucleate giant cells.

LG OSC is associate with either kras or braf mutation but not p53. Whilst HG OSC exhibit significantly higher expression of p53, MIB1, bcl-2, ckit & p16 than LG OSC. Both show WT1 positivity.

LG OSC responds poorly to platinum based therapy and since most stain with ER there is a school of thought that hormonal manipulation may play a role in management.

References:

Robboy’s Pathology of the Female Reproductive System.

McCluggage. My approach to and thoughts on the typing of ovarian carcinomas. bmj. Aug 2007

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One Response to Ovarian Serous Tumours

  1. Asking questions are really nice thing if you are not understanding anything entirely,
    however this piece of writing provides good understanding yet.

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