Gyne Flashcards
Gross and micro features of polycystic overian disease
Gross - rounded and enlarged ovaries, usually bilateral
- multiple small subcortical follicles, typically similar in size
Micro - fibrous and thick ovarian capsule
- Hyperplastic ovarian stroma
- No stigmata of prior ovulation
Nonneoplastic cysts of ovary and histology of each
Epithelial inclusion cyst - single layer of flat to columnar epithelium +/- cilitated. <1cm (if >1cm, then called serous cystadenoma)
Follicular cyst - uniloculated with inner layer composed of granulosa cells and outer layer theca cells
Corpus luteum cyst - luteinized granulosa cells with outer layers of luteinized theca cells
Endometriotic cyst - lined by endometrial glandular epithelium, underlying endometrial stroma, hemosiderin laden macs
Polycystic ovarian disease - fibrous and thick capsule, hyperplasia ovarian stroma
Hyperreactio luteinalis - multiple follicular cysts with luteinized theca and granulosa layers, edema, luteinized stroma
Histologic types of epithelial neoplasms of the ovary
Serous - benign, borderline, low grade, high grade
Endometrioid - benign, borderline, malignant
Clear cell - benign, borderline, malignant
Mucinous - benign, borderline, malignant
Seroumucinous - benign, borderline, malignant
Brenner - benign, borderline, malignant
Others: mesonephric-like adenocarcinoma, undifferentiated and dediff CA, carcinosarcoma, mixed carcinoma
Diagnosis of mixed carcinoma
Essential: presence of at least 2 ovarian carcinoma histological types with components showing distinct and unequivocal differences by histomorphology
Desirable: differences between the two areas based on ancillary studies
Importance of accurate classification of epithelial tumors of the ovary
Present at different stages
Require different treatment/adjuvant therapy
Respond differently to chemo
Different prognosis and survival
Different molecular
CAP protocol requirements for ovarian/fallopian tube resections
History
Procedure
Specimen integrity
Tumor site
Tumor size
Histologic type, grade
Ovarian surface involvement
Fallopian tube surface involvement
Implants
Other tissue involvement
Largest extrapelvic peritoneal focus
Peritoneal/ascitic fluid involvement
Chemotherapy response scpre
Regional LN status
Distant sites involved
Importance of ovarian integrity and rupture
Rupture may spill malignant cells into abdominal cavity, which may influence treatment
There may be small surface carcinomas
Important to note, in cases when there are benign/borderline/malignant areas, which has ruptured
Omentum grossing
If tumor identifiable, submit representative sections
For borderline or immature teratoma with grossly apparent implants, submit multiple sections
Take 1 per 2cm of normal omentum
Importance of LVI in ovarian carcinomas
Does not impact staging
No prognostic significance
May raise suspicion for metastatic disease to the ovary in cases such as mucinous CA
AJCC T staging for ovary, fallopian tube, primary peritoneal CA
pT1: Limited to ovaries
pT1a: limited to 1 ovary
pT1b: limited to both ovaries
pT1c: Limited to one or both ovaries with any of the following: surgical spill, capsule rupture, surface involvement, malignant ascites
pT2: Tumor involves 1-2 ovaries/FTs with pelvic extension below pelvic brim or primary peritoneal CA
pT3: Essentially pT2 with mets outside the pelvis/retroperitoneal LNs
AJCC N staging for ovary, fallopian tube, primary peritoneal CA
pN0(i+): ITCs </=0.2mm
pN1: Pos retroperitoneal nodes only
pN1a: met up to 10mm
pN1b: met greater than 10mm
AJCC M staging for ovary, fallopian tube, primary peritoneal CA
pM1a: Pleural effusion with + cytology
pM1b: liver of splenic parenchymal metws, mets to extrabdominal LNs, transmural involvement of bowel
Most common histologic subtype of familial ovarian CA and common mutations associated with it
High grade serous
BRCA1/2
How to submit Ovary and FTs in patients with BRCA mutations or suspected increased risk of HBOT
Ovarian and tubal tissue should be serially sectioned and submitted in toto
FTs submitted according to SEE-FIM protocol
Types of serous neoplasms of ovary and their histologic characteristics
Serous cystadenoma, cystadenofibroma, adenofibroma, surface papilloma : cystic or papillary with broad papillae and/or small glands in prominent fibromatous stroma or as small simple papillae on surface
Serous borderline tumors: Hierarchical branching papillae with variable amounts of stroma in cores, stratified epithelial lining with tufting/cell detachment, mild to moderate atypia
- implant = extraovarian disease, noninvasive
- autoimplant = desmoplastic implant on ovarian surface
- SBT with microinvasion: <5mm
SBT, micropap/cribriform subtypes: area of pure micropap/crib growth >5mm, elongated micropap at least 5x longer than wide, with medusa head appearance. Small punched out crib spaces
LGSC: SBT with extraovarian invasion (invasive implant), variety of patterns (small nests, glands, papillae, micropap, inverted macropap)
- frequently free-floating within unlined clear spaces
- Psammoma bodies, mid-mod atypia, rare necrosis
- Coexisting SBT
HGSC: Heterogenous patterns, significant atypia, markedly increased mits, atypical mits, necrosis and multinucleated cells
Difference in management of various types of serous neoplasms
Benign: unilateral oophorectomy
Borderline: removal of all visible disease with peritoneal and omental sampling, no retroperi LN sampling
LGSC: THBSO, omentectomy, LN dissection, resect all visible disease, postoperative chemo depending on stage
HGSC: neoadjuvant therapy as required, surgery, chemo
Prognosis of each type of serous neoplasms
Benign: 100% survival
Borderline: depends on stage
- Stage I: good
- Advanced stage: 4-7% develop LGSC, rarely HGSC
LGSC: depends on stage
- Early: good
- Advanced: poor
HGSC: generally poor
Poor prognostic features in SBT
Micropap/crib subtype
Advanced stage
Bilaterality
Ovarian surface involvement
Residual disease after surgery
Significance of SBT in LNs
1/3 of pts with SBT who have LND
Must exclude: endosalpingiosis, psammomatous calcs with no epithelial cells, nodal mesothelial hyperplasia, metastatic LGSC
More common in subcapsular sinuses
Not considered an adverse prognostic factor
Classification of endometrioid tumors of ovary
Benign: cystadenoma or cystadenofibroma
Borderline
Malignant
Benign finding in ovary associated with endometrioid neoplasms
Endometriosis
Morphologic features of each type of ovarian endometrioid neoplasm
Cystadenoma - cyst lined by endometrial epithelium, no stroma, associated with endometriosis, mucinous metaplasia
Cystadenofibroma - Endometrial epithelium within fibromatous stroma
Borderline tumor - Two growth patterns, adeofibromatous (more common) and intracystic
- Adenofibromatous - background of endometrioid adenofibroma, crowded glands (resembling EAH), mild-mod atypia, squamous metaplasia
- Intracystic - simple papillary architecture protruding into endometriotic cyst
- microinvasion
Carcinoma - morphologic resemblance to endomertioid carcinoma of uterus
- back to back glands, destructive invasion, associated with squamous, mucinous differentation, endometriosis
Grading of endometrioid adenocarcinoma of the ovary
FIGO: same as uterus
Molecular alterations in endometrioid carcinoma
ARID1A
PTEN
PIK3CA
MMR
CTNNB1
TP53 in high grade
KRAS
Prognosis of each type of ovarian endometrioid tumot
Benign: excellent
Borderline: excellent
Malignant: better than serous
Commonly presents as Stage I disease, higher the stage worse the prognosis
Metastatic endometrial endometrioid carcinoma to ovary vs synchronous ovarian and endometrial primaries
Superficial myometrial invasion in synchronous, deep in metastatic
Absent LVI in synchronous, present in metastatic
Endometriosis present in synchronous
Ovarian involvement parenchymal, solitary, unilateral in synchronous
Ovarian involvement surface, small, multinodular, bilatearl in mets
Tumor spread in other locations in metastatic
Clinical sig of metastatic vs synchronous endometrial and ovarian endometrioid CA
Synchronous primary associated with excellent prognosis when tumor limited to endometrium and ovary
Types of clear cell neoplasms of ovary
Clear cell cystadenoma or cystadenofibroma
Clear cell borderline (rare)
Clear cell carcinoma
Associated benign finding for clear cell carcinoma of ovary
Endometriosis
Morphology of clear cell carcinoma of ovary
Varied patterns: solid, papillary, tubulocystic, mixed
Hobnailed cells with relatively uniform hyperchromatic nuclei, prominent nucleoli
Clear or eosinophilic cytoplasm with relatively low mitotic activity
Presence of hyaline globules or psammoma bodies
Hyalinized stroma
DDx of clear cell carcinoma of ovary
Serous CA
Endometrioid CA with clear cell changes
Yolk sac tumor
Dysgerminoma
Metastatic clear cell CA from extraovarian site
Steroid cell tumors
Morphological features of ovarian mucinous borderline tumor
Cysts lined by GI-type mucinous epithelium: stratification, tufting, villous, slender filiform papillae
Mild to mod cytologic atypia
Epithelial prolif >10% tumor volume
Associated with mucinous cystadenoma, brenner, or mature cystic teratoma
Mural nodules
Differentiate primary ovarian tumor from metastatic
Primary: unilateral, single large mass, mainly parenchymal involvement, no hx, IHC compatible with ovary
Mets: bilateral, multiple small foci or single cells, surface and parenchymal involvement, extensive LVI, pools of mucin, hx, dirty necrosis, IHC compatible with extraovarian
Clinical features of adult granulosa cell tumors
Pts middle-aged to postmenopausal
Amenorrhea, postmenopausal bleeding
Frequently estrogen-secreting - associated with endometrial hyperplasia and carcinoma (androgenic changes rare)
Hemoperitoneum
May have elevated serum B-inhibin
Early stage have good prognosis
Gross and microscopic findings of adult granulosa cell tumors
Gross - unilateral, average size 10cm, solid and cystic, soft yellow/tan-hemorrhagic
Micro - varied architectural patterns with granulosa cells (ovoid cells with grooves +/- Call-Exner bodies), low mitotic activity
Molecular of Adult granulosa cell tumor
FOXL2 mutation
DDx of adult granulosa cell tumor
Poorly diff or undiff CA
Endometrioid adenoCA
Smell cell carcinoma
ESS
Thecoma and cellular fibroma
Stromal tumors with minor sex cord elements
Large solitary luteinized follicle cyst of pregnancy
Yolk sac tumor
Adult granulosa cell tumors vs juvenile granulosa cells tumors
AGCTs: perimenopausal women, somatic FOXL2 mutation, solid and cystic, many patterns with prominent grooving, low mitotic rate
- SF1+ WT1+ CD99+ CD56+ inhibin+/-, calretinin+, FOXL2+
- EMA negative
JGCTs: mean pt age 13, rarely associated with Maffucci, Ollier, DICER, TSC
- Nodular or diffuse, widely variable nuclear atypia, hyperchromatic, rarely grooved, rare Call-Exner bodies
- Presence of immature follicles
- variable mitotic rate, higher than AGCTs
- SF1+ WT1+ EMA+ CD99+
What to do with an immature teratoma at frozen section
Indicate to surgeon that immature component is seen and grade if possible
Indicate if any other GCT component is present
Most common immature component in an immature teratoma
Immature neuroepithelium
WHO grading of immature teratoma
Graded based on amount of immature neuroepithelium
Grade 1: At most 1 4x field on any slide
Grade 2: 1-3 4x fields
Grade 3: >3 4x fields
Prognosis of immature teratoma
Depends on stage and grade of primary and any metastatic tumor
5 year overall survival >90%
Reporting parameters for immature teratoma
Procedure
Specimen integrity
Primary tumor site
Ovarian surface involvement
Tumor size
Presence of other germ cell components
Presence of other malignancy arising from teratoma
Histologic grade
Implants
Extent of extraovarian involvement
Peritoneal ascitic fluid
Pleural fluid
Regional LNs
Pathologic stage classification
Types of malignancy that can arise from teratomas
Any type of malignancy an arise from the different cell lineages
Most common is SCC
Tumors in female genital tract that can have heterologous elements
Teratoma
Carcinosarcoma
Endometrioid adenocarcinoma
Adenosarcoma
Sertoli-Leydig cell tumor
Gynandroblastoma
Histologic patterns of yolk sac tumors
Microcystic or reticular
Endodermal sinus
Solid
Alveolar-glandular
Polyvesicular vitelline
Myxomatous
Papillary
Microcystic
IHC for ovarian GCTs
Yolk sac tumor: SALL4+ AFP+ CAM5.2+ Glypican-3+
- OCT4- D2-40- CD117+/-
Dysgerminoma: SALL4+ OCT4+_ CD117+ D2-40+
- AFP- CK- (or weak)
Embryonal CA: SALL4+ OCT4+ CAM5.2+ CD30+
- CD117- D2-40-
Choriocarcinoma: SALL4+ B-HCG+
Yolk sac tumor vs clear cell carcinoma of ovary on histology
Both: can be tubulocystic, papillary, solid with clear cytoplasm and hyaline globules
YST: No association with endo, more crazy patterns possible, schiller-duval bodies
CCC: Hobnail, cuboidal cells, stromal hyalinization and myxoid stroma, can have eosinophilic cytoplasm
Common types of salpingitis, their etiology and complications
Acute salpingitis - young females with ascending infection (chlamydia and gonorrhea) or polymicrobial PID. Complications of infertility and ectopic pregnancy
Chronic salpingitis - resolving acute salpingitis, Complicated by hydrosalpinx
Granulomatous salpingitis - TB, fungal, Crohns, Sarcoid. Complications infertility and ectopic preg
Salpingitiis isthmica nodosum - young females, unclear etology. Complications infertility and ectopic preg
Significance of FTs in origin of ovarian CA
FT may be primary source for a significant number of HGSCs involving ovary, FT, peritoneum
50% of cases with pelvic serous CA have STIC lesion
Morphological and IHC features of STIC
Discretely different population of epithelial cells replacing the normal tubal mucosa
Epithelial stratification
Increased NC ratio wtih rounded hyperchromatic nuclei, loss of polarity, prominent nucleoli
Absence of ciliated cells
Increased mits, possibly with abnormal mits
Abnormal p53 and increased Ki67
p53 signature lesion vs tubal intraepithelial lesion and clinical significance
p53 sig lesion has at least 12 consecutive morphologically benign but abnormal p53 IHC with low Ki67
Tubal intraepithelial lesion in transition (TILT) has abnormal p53 IHC with features intermediate between p53 signature and STIC
Pathological changes or complications associated with IUDs
Actinomyces infection
Endometritis
Squamous metaplasia
Uterine perforation or laceration (rare)
Types of endometrial metaplasia
Tubal
Squamous
Eosinophilic
Mucinous
Papillary syncytial
Papillary
Hobnail
Secretory
Nonmalignant causes of uterine bleeding
Pregnancy
Atrophy
Anovulatory cycles
Exogenous hormone use
Benign neoplastic
Causes of hyperestrogenic state
Exogenous estrogens such as estrogen replacement therapy
Endomgenous hyperestrogenism such as polycystic ovarian syndrome
Obesity (peripheral conversion of androgens to estrogens)
Estrogen secreting tumor, such as ovarian functional granulosa cell tumor
WHO classification of endometrial hyperplasia and risk of developing carcinoma for each
Hyperplasia without atypia: 3-4x increased risk
Atypical hyperplasia: 14x
Endometrial intraepithelial neoplasia: 45x
DDx of endometrial hyperplasia
DDx: well diff adenoCA, secretory endometrium, endometrial polyp, metaplsaia, endometrial gland and stromal breakdown
Endometrial hyperplasia vs well diff CA
Architecture - CA has higher complexity with solid areas, fused glands, cribriform glands, desmoplastric stroma
Cytology - not really helpful
Precursor lesion for endometrial serous carcinoma and its histologic/IHC features
Serous endometrial intraepithelial CA: often on surface of polyp or lining preexisting endometrial glands in background of atrophic endometrium, composed of cwells with marked cytologic atypia
IHC: p53 abnormal, increased Ki67, p16 diffusely pos or completely null
DDx polypoid lesion of endometrial cavity
Benign endometrial polyp
Secretory endometrium
Atypical polypoid adenomyoma
Polyp with atypical hyperplasia or EIN
Adenosarcoma
Polyp with area of carcinoma
Carcinosarcoma
Clinical presentation and implications of diagnosis for atypical polypoid adenomyoma
Occurs in premenopausal and nulliparous females and may be associated with infertility
High recurrence rate if incompletely excised
Risk of developing endometrioid adenocarcinoma similar to AEH
Hereditary syndromes that cause familial endometrial carcinoma
Lynch syndrome
Cowden syndrome
Li-Fraumeni
Why screen for Lynch in pts with endometrial CA and how is screening done
Lifetime risk for endometrial CA up to 60%, may be sentinel cancer that develops before CR
FHx alone has poor predictive value
Pts should be considered for genetic counselling
IHC: MLH1, PMS2, MSH2, MSH6
WHO histologic classification of endometrial CA
Endometrioid adenocarcinoma, NOS
- POLE mutated
- MMRd
- p53 mutated
- NSMP
Mucinous CA, intestinal type
Serous CA
Clear cell adenoCA
Mixed cell carcinoma
Mesonephric-like adenocarcinoma
SCC
Undiff
Carcinosarcoma
Define Mixed carcinoma in endometrial setting
Two or more distinct subtypes of endometrial CAs identified in which at least one component is either serous or clear cell - dediff carcinoma and carcinosarcoma are excluded
Can also apply to any percentage of high grade carcinoma
Major and minor types should be specified
When to classify endometrial tumors as “carcinoma, subtype cannot be determined”
High grade tumor with ambiguous features (histology and IHC)
Reporting criteria for endometrial CA resections
Procedure and specimen integrity
Tumor size, histologic type, grade
Myometrial invasion
Involvement of Uterine serosa, LUS, cervical stroma, other tissues/organs, ascitic fluid
LVI
Margins
Regional LNs
Distant Mets
AJCC stage vs FIGO stage
Importance of reporting procedure and specimen integrity
Some laparoscopic procedures may result in venous tumor emboli that are likely iatrogenic
Unexpected endometrial CA in morcellated specimens can risk spreading tumor cells to pelvis and peritoneal cavity
Different procedures may have different margins
Grading methods for common types of endometrial tumors
Endometrioid uses FIGO
- FIGO 1: at most 5% nonsquamous solid growth
- FIGO 2: 6-50% solid
- FIGO 3: >50% solid
- if severe nuclear atypia, upgrade by 1 though consider serous
Mucinous CA uses FIGO
Serous, clear cell, small cell, large cell NEC, undiff, dediff, carcinosarcoma - high grade by definition
Mixed CA: highest grade should be assigned
Types of endometrial CA associated with poor prognosis
Serous carcinoma
Clear cell carcinoma
Undifferentiated CA
Dediff CA
Carcinosarcoma
Small cell and large cell neuroendocrine CA
Histologic prognostic factors in endometrial CA limited to uterine corpus
Tumor type
Tumor grade
LVI
Depth of myometrial invasion
AJCC T staging for endometrial CA
pT1a: limited to endometrium or invading <1/2 myometrium
pT1b: Involving 1/2 or more of myometrium
pT2: Invading stromal connective tissue of cervix
pT3a: Involving serosa/adnexa
pT3b: Vaginal or parametrial involvement
pT4: Bladder or bowel mucosa
AJCC N staging for endometrial CA
pN0(i+): ITCs </=0.2mm
pN1: mets to pelvic LNs
pN1mi: 0.2 - 2.0 mm
pN1a: >2mm
pN2: mets to paraaortic LNs
pN2mi: 0.2 - 2.0 mm
pN2a: >2mm
Histologic subtypes of leiomyoma
Cellular
Mitotically qactive
Epithelioid
Myxoid
With sympastic change
Lipoleiomyoma
FH-deficient
Hydropic
Apoplectic
Dissecting
Diffuse leiomyomatosis
Gross features of leiomyoma vs leiomyosarcoma of uterus
Leiomyoma - range widely in size, usually multiple, sharply circumscribed and unencapsulated, firm white whorled cut surface, with or without degeneration
Leiomyosarcoma - Larger size, usually single, poorly circumscribed/demarcated, hemorrhagic, soft/necrotic “fish flesh” texture, locally invasive growth
Histologic criteria for spindle cell type leiomyosarcoma
2/3 of:
- Diffuse moderate to severe cytologic atypia
- True tumor cell necrosis (coagulative)
- Increased mits ( at least 10/10 hpf)
Histologic criteria for epithelioid cell type leiomyosarcoma
2/3 of:
- Diffuse moderate to severe cytologic atypia
- True tumor cell necrosis (coagulative)
- Increased mits ( at least 4/10 hpf)
Histologic criteria for myxoid leiomyosarcoma
Predominantly myxoid smooth muscle tumor with significant cytologic atypia or tumor cell necrosis
AND >1 mit/10hpf
Define STUMP
Smooth muscle tumor of uncertain malignant potential
- Uncertainty of type of smooth muscle differentiation
- Uncertainty of benign behaviour due to lack of adequate clinicopathologic information
- Uncertainty of mitotic index
- Uncertainty of presence of type of tumor necrosis
Gross features of endometrial stromal tumors
ESN: well-circumscribed yellow/soft, usually solitary
LGESS: poorly circumscribed/demarcated, diffuse permeative growth, intravascular tumor plugs
HGESS: bulky, intracavitary or intramural, tan-yellow, fleshy masses, often hemorrhage/necrosis
Undiff uterine sarcoma: large intracavitary or intramural, tan-yellow, fleshy masses with hemorrhagic/necrosis
Histologic features of endometrial stromal nodule
Circumscribed
At most 3 fingerlike projections <3mm from margin
Bland round to oval small cells with scant cytoplasm, inconspicuous nucleoli
Histologic features of LGESS
Similar cytology to ESN but >3 fingerlike projections >3mm
Permeative growth with LVI
Can have necrosis
Low mitotic activity
Histologic features of HGESS
Permeative, infiltrative growth, LVI, high mitotic rate, necrosis
Nests of round cells with eosinophilic cytoplasm, high grade nuclei, scant to moderate cytoplasm
Histologic features of undiff uterine sarcoma
Destructive pattern of invasion, sheets of uniform or pleomorphic epithelioid and/or spindled cells
Brisk mitotic activity, easily identified necrosis, LVI
IHC LGESS vs HGESS
LGESS: ER+ PR+ CD10+ SMA+
HGESS: Cyclin D1+ CD117+ CD99+ CD10- ER/PR-
T-staging for uterine sarcoma
pT1: limited to uterus
pT1a: at most 5 cm in greatest dimension
pT1b: >5cm
pT2a: involves adnexa
pT2b: involves other pelvic tissues
pT3a: infiltrates abdominal tissues in one site
pT3b: infiltrates abdominal tissues in >1 site
pT4: invades bladder or rectum
Classification of epithelial-mesenchymal uterine neoplasms
Carcinosarcoma - poor prognosis
Adenosarcoma - low malignant potential, poor prognosis if recurrent
Carcinofibroma - uncertain prognosis as uncommon
Adenofibroma - Benign, may recur
Adenomyoma - benign, may recur
Define sarcomatous overgrowth in uterine adenosarcoma
Presence of pure sarcomas, usually high grade and without epithelial component, occupying at least 25% of tumor
Types of GTD
Hydatidiform mole
- Complete
- Partial
- Invasive
Nonmolar lesions
- placental site trophoblastic tumor
- Epithelioid trophoblastic tumor
- Gestational choriocarcinoma
- Benign trophoblastic lesions
– Exaggerated implantation site reaction
– Placental site nodule/atypical placental site nodule
– mixed trophoblastic tumors
Hydatidiform mole complete vs partial
Complete: empty ovum, diploid, markedly increased B-HCG, “snow storm” U/S, large edematous villi with circumferential trophoblastic proliferations, trophoblastic atypia, no fetal parts, p57- in villous cytotrophoblasts and villous stromal cells
Partial - Normal ovum, triploid, normal to mod increased B-HCG, Uterus small for dates, 2 populations of villi (changes lesser than complete), trophoblastic atypia absent, fetal parts present, p57+
Cause of complete mole
Fertilization of empty ovum by 2 sperm or by 1 sperm with duplication
Cause of partial mole
Fertilization of normal haploid ovum by 2 sperm with haploid set of chromosomes or by a sperm with diploid set (diandric)
Treatment and prognosis for molar pregnancy
After evacuation, serial B-HCG to monitor for development of persistent GTD
Risk for persistent GTD: 15-20% complete, 0.5-5% for partial
Risk of chorioCA: 2-3% complete, <0.5% partial
Most common type of persistent GTD after molar pregnancy
Invasive mole
Hydatidiform mole vs hydropic abortus
Clinical presentation, B-HCG, rads
Morphology:
Hydropic abortus - no gross abnormality, smooth villi with nild hydrops, no sig trophoblastic prolif, no atypia, no trophoblastic inclusions
p57 IHC - present in hydropic abortus
Ploidy - diploid
DNA microsatellite marker analysis
Histology and IHC for placental site trophoblastic tumor
Histology - large, pleomorphic implantation-site intermediate trophoblastic cells forming confluent sheets or single cells, with infiltrative growth, scattered multinucleated cells,low mits, vascular invasion, fibrinoid deposits and dissection of smooth muscle
IHC: hPL++, CD10+, MUC4+, p63-, Ki67 10-30%
DDx of placental site trophoblastic tumor
Exaggerated placental site
Choriocarcinoma
SCC, undifferentiated carcinoma
Epithelioid trophoblastic tumors
Epithelioid smooth muscle tumor
Placental site nodule and plaque
Prognosis for placental site trophoblastic tumor
25-30% of pts develop recurrent disease or mets and about half of those may die of disease
Poor prognostic features for placental site trophoblastic tumor
Clear cytoplasm
Deep myometrial invasion
Large tumor size
Necrosis
High mitotic count
Advanced stage
At least 48 months since antecedent pregnancy
Age >40
Placental site trophoblastic tumor vs epithelioid trophoblastic tumor
PSTT: implantation-site intermediate trophoblasts similar to exagerated placental site
ETT: chorionic type intermediate trophoblasts, similar to placental site nodule
Both have similar clinical presentation and patient prognosis
IHC for trophoblastic lesions
Placental site nodule: p63+, low Ki67, focal Cyclin E
placental site trophoblastic tumor: HPL+ mod ki67, CD146+
Epithelioid trophoblastic tumor: p63+ CyclinE+, mod Ki67
Choriocarcinoma: HPL+ HCG+, High Ki67
