Border line ovarian tumours
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Transcript of Border line ovarian tumours
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◙ Are BOTs considered malignant ??
◙ What is the mean age for BOTs ??
◙ Can BOTs be associated with ascites ??
◙ Can BOTs cause lymphadenopathy or peritoneal deposits ??
◙ Do we have a staging system for BOTs ??
◙ Can we use chemo-Rx for BOTs ??
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◙ Tumours of borderline malignancy,
◙ Tumours of low malignant potential,
◙ Atypical proliferative tumours.
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◙ In 1929, Howard C. Taylor, was the 1st to use of the term“(semi-malignant tumours)” for
a subset of large ovarian tumours that had an indolent clinical course with relatively
favourable outcome despite the presence of peritoneal disease.
◙ However, BOTs were not considered a distinct entity until 1971, when the FIGO& WHO
established a separate borderline category of tumours.
◙ Since then, a considerable controversy has surrounded the definition & management of
BOTs, because of their enigmatic pathogenesis & confusing biologic behaviour.
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◙ BOTs are relatively un-common, (incidence = 1.5-–2.5 / 100,000 people / year).
◙ BOTs = 15-–20% of ovarian epithelial neoplasms.
◙ Most commonly they affect white women of reproductive age typically during the 4th
decade. Up to 27% of patients with BOTs are < 40 years.
◙ The mean age of presentation is ≈ 10-20 years earlier than that of invasive ovarian
carcinomas.
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◙ BOTs are histologically characterized as epithelial tumours with a stratified
growth pattern but without destructive stromal invasion.
◙ According to the 2003 WHO classification, BOTs are classified into serous,
mucinous, endometrioid, clear cell, & transitional (Brenner) subtypes.
◙ Serous & mucinous neoplasms constitute the majority of BOTs (65% & 32%
respectively).
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◙ Unclear because of the small number of cases & the lack of RCSs.
◙ Risk factors linked with BOTs are as invasive ovarian cancer.
◙ As epithelial ovarian tumours, BOTs, originate from tubal or ovarian surface
epithelium or epithelial inclusion cysts
◙ Rarely seen in women with BRCA mutations.
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◙ It was postulated that specific genetic changes contribute to the pathogenesis &
stepwise progression of BOTs to low-grade invasive ovarian carcinomas.
◙ Unlike high-grade serous carcinomas (ch.ch. by p53 mutations in > 50%),
◙ serous BOTs are ch.ch. by KRAS & BRAF mutations in 2/3 of cases,
◙ mucinous BOTs are characterized by KRAS mutations, &
◙ β-catenin & PTEN mutations are commonly seen with endometrioid BOTs.
◙ In addition, endometriosis is an important precursor of endometrioid & clear cell BOTs.
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◙ Ch.Ch. of BOTs:
◙ Stratification of papillae
◙ Microscopic papillary projections or tufts (arising from the epith. lining of the
papillae.
◙ Epith. pleomorphism
◙ Atypicality
◙ Mitotic activity
◙ NO stromal invasion
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◙ Compared to benign serous tumours, BOTs have more abundant papillary
projection, & shows more inc. of bilaterality..
◙ Divided into 2 types:
◙ Typical serous borderline tumours (90%), &
◙ Borderline tumours with micropapillary patterns (5-–10%)
◙ Unlike high-grade serous carcinomas, they are resistant to platinum-based
chemotherapy. However, prognosis is generally excellent.
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invasive25%
non-invasive
75%
Peritoneal Implants ◙ Because women with extra-ovarian spread
of disease have a very good prognosis, the
peritoneal lesions are classified as implants
instead of metastases, & LN involvement is
not named metastases, they may be:
1. non-invasive = just stuck on the peritoneal
surfaces, or
2. Invasive = invaded the underlying tissue such as
omentum & bowel wall.
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L.N.s27%
Regional L.N.s◙ LN involvement has no prognostic value,
they may serve as sites of recurrence &
progression to carcinoma.
◙ Commonly involved lymph nodes are:
** Pelvic,
** Omental & mesenteric,
** Para-aortic, &
** Supra-diaphragmatic regions.
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◙ Do not have a clearly defined origin, consist of two histologic subtypes:
- The intestinal (85%), & - The mullerian or endo-cervical-like (15%).
◙ Like serous BOTs, they may be associated with abdominal or pelvic implants,
which may be invasive.
◙ It is important to exclude metastatic adenocarcinoma, most commonly from
the GIT (appendicular or colonic primary).
◙ Immunohistochemistry using a cytokeratin panel is useful in differentiating
metastatic versus primary ovarian tumours.
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◙ Mucinous BOTs are most often stage I at time of diagnosis, & it is unusual
to find extra-ovarian disease.
◙ There is strong evidence that the mucinous BOTs associated with
pseudomyxoma peritonei (ascites with abundant mucoid or gelatinous
material) are actually metastatic rather than an ovarian primary.
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Subtypes Include
1. Endometrioid BOTs:
◙ Resemble endometrioid endometrial adenocarcinoma.
◙ They arise either from the surface ovarian epithelium, or from endometriosis.
2. Clear cell BOTs:
◙ ch.ch. by the presence of clear or hobnail cells.
3. Brenner (transitional) BOTs:
◙ Transitional cell tumours with atypical or malignant features of the epithelium.
All has NO stromal invasion
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Hobnail cells lining the glands. They have bulbous hyperchromatic nuclei that protrude into the gland lumen.
Clear cell BOT
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◙ Approximately 15-23% of patients with BOTs are asymptomatic.
◙ As with other ovarian tumours, BOTs are difficult to detect clinically until
they are advanced in size or stage.
◙ The most common presenting symptoms were:
o abdominal pain,
o increasing girth or abdominal distention, &
o abdominal mass.
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◙ There is no characteristics imaging to distinguish BOTs from other ovarian
tumours using U/S, CT, MRI, or PET scans.
◙ Intra-tumoural blood flow is seen in (90%) of BOTs, as in malignant
neoplasms (92%).
◙ The RI & PI are significantly reduced in carcinoma & BOTs (compared with
benign tumours).
◙ Pre-operative CT scanning should be considered to identify foci of
metastasis. & is also useful for follow-up.
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Serous BOT (transvaginal scan): Multilocular-solid tumour with papillae, rather smooth inner cyst wall, & regular septa & anechoic intra-cystic fluid.
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Exophytic implants on the surface of contralateral ovary (TAS):Hyperechogenic implants surround the contralateral ovary without involvement of ovarian stroma.
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Mucinous BOT of intestinal type (TAS):Large, multilocular tumour with “honeycomb” nodule on the posterior inner wall & intra-cystic fluid of low-level echogenicity.
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Mucinous BOT of endocervical type (TVS):Multilocular-solid tumour with larger number of endophytic & exophytic papillae, high intra-papillary flow density, & intra-cystic fluid with low-level echogenicity.
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◙ CA125 levels are do not aid in diagnosis or follow up care in BOTs.
◙ Calculation of RMI or ROMA is not useful in predicting BOTs.
◙ Static DNA cytometry can be performed on biopsy specimens. (95% of BOTs have
diploid DNA excellent prognosis).
◙ Microarray technology, (for the characterization of the tumour genome) is not
widely studied in BOTs, because of low incidence & good prognosis.
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◙ For unilateral stage I disease, unilat. SO , or careful cystectomy may be
done , with proper examination of the contralateral ovary.
◙ Better to remove the opposite ov. = due to the frequent bilateral
synchronous tumours & the possibility of occult metastases (6-43%).
◙ Hysterectomy is indicated = because of the high prevalence of synchronous
endom carc. + ut serosa & endom are common sites for occult
metastases.
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◙ For more advanced disease, more radical surgery is performed.
◙ As 3-17% of patients are < 40 years, fertility sparing surgery may
be considered.
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◙ Comprehensive staging of BOTs is of significant prognostic value & is
performed surgically.
◙ Another common component of staging is the descri ption of the type
of implants, as these have significant prognostic value.
◙ Frozen section may be used, BOTs are diagnosed by frozen section in
58 - 86% of cases.
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◙ Complete staging laparotomy is recommended, this include:
◙ Peritoneal wash, or ascetic fluid sampling for cytology.
◙ Biopsy specimens of the pelvic peritoneum (culdesac, pelvic wall, & bladder
peritoneum),
◙ biopsy specimens of the abdominal peritoneum (paracolic gutters & diaphragmatic
surfaces),
◙ biopsy specimens of the omentum, intestinal serosa & mesentery, and
◙ retroperitoneal lymph nodes (pelvic and para-aortic).
◙ Recurrences are mostly following inadequate staging.
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◙ Laparoscopic management of BOTs is associated with a higher rate of cyst
rupture and incomplete staging.
◙ however, laparoscopy lower morbidity & fewer adhesions ( imp. for
fertility).
◙ It should be performed by oncologic surgeons trained in extensive
laparoscopic procedures (for optimal surgical staging, complete debulking, &
better results).
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◙ Well differentiated.
◙ Young women of low parity.
◙ Otherwise normal pelvis.
◙ Encapsulated & free of adhesions.
◙ No invasion of capsule, lymphatics or mesovarium.
◙ Peritoneal washings negative.
◙ Adequate evaluation of the other ovary & negative omental biopsy result.
◙ Probable close follow up
◙ Excision of residual ovary after completion of childbearing (+/-)
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◙ No clear evidence that chemo-Rx can decrease relapse rates or improve
survival in BOTs.
◙ BOTs treated with adjuvant chemo-Rx or radio-Rx showed high persistent or
recurrent disease (40%).
◙ Poor response rates is explained by the low proliferation rate of BOTs.
◙ > 90% of serous BOTs are oestrogen-receptor positive, but there are only case
reports of major responses to tamoxifen, leuprolide, and anastrazole.
◙ The effect of antiangiogenic or other newer targeted agents on BOTs is not
known.
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Management of BOTs
Stage I
Childbearing desired
YES
Oophorectomy or
Cystectomy
NO
TAH + BSO
(staging)
Stage II-III
Optimal cyto-reduction & Post-operative observation
Minimal growth & no symptoms
Observation
Moderate growth &/or symptomatic
Repeat Cyto-reduction
Rapid growth, ascites, or worsening histology
Chemo-Rx
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◙ Overall prognosis is excellent, as:
◙ 60-75 % of cases are stage I disease when diagnosed.
◙ About 95% of BOTs have di ploid DNA.
◙ The 5 year survival rate for patients with stage I = 95%, &
The 10 year survival rate is 70-95%, depending on histologic findings.
◙ Increased stage worse prognosis.
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◙ Five features are related to poor prognosis (based on transformation
of BOTs to invasive disease):
a) Cell type,
b) Stage,
c) Implant type (for serous borderline tumours),
d) The presence of a micropapillary architecture (for serous borderline
tumours),&
e) Microinvasion
◙ Age at diagnosis also influence prognosis.
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◙ Patients with stage I disease have a recurrence rate of about 15%,
◙ Cystectomy is associated with a higher recurrence rate (up to 31%).
◙ Recurrences were noted only in un-staged stage 1 BOTs.
◙ If the tumour is aneuploid, the recurrence rate is high.
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◙ In some studies of fertility sparing surgery for BOTs, the conception rate was 50% of with no foetal
anomalies.
◙ Surgical treatment of BOTs can postoperative infertility due to adhesions & insufficient residual
ovarian tissue after resection.
◙ Some studies show that women treated with ovarian stimulation for IVF have a two-fold increased
risk of BOTs, especially of serous histo-type
◙ In addition, with a prolonged follow-up 15 or more years after the first IVF treatment, they also
observed the increased risk of primary ovarian carcinomas.
◙ Therefore, all patients with previous history of BOTs should receive detailed counselling regarding the
potential risks associated with ovarian stimulation and should undergo close follow-up during and
after IVF therapy.
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◙ HRT to prevent cardiovascular disease & osteoporosis & to
improve quality of life is an important issue, as many patients
with BOTs are relatively young women. HRT should be offered to
these patients.
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