Onco Flashcards
pathologic description of Call–Exner bodies
Microfollicular pattern with numerous small cavities that may contain eosinophilic fluid
pathologic description of immature teratomas
Immature neural tissue with rosettes and tubules
pathologic description of dysgerminomas
Cytoplasmic glycogen demonstrated with periodic acid-Schiff stain
pathologic description of Schiller–Duval bodies
A central capillary surrounded by connective tissue and a peripheral layer of columnar cells
Schiller–Duval bodies are seen in
yolk sac tumors (germ cell variant)
“hobnail” cells on microscopy indicate
Clear cell carcinoma
Pelvic endometriosis linked to what cancer
clear cell carcinoma
Complete mole karyotype
46XX, 46XY
(All paternal)
Partial mole karyotype
69xxx, 69xxy, 69xyy
(Extra set is paternal)
What size simple cyst needs f/up?
- > 5 and <7 cm, almost certainly benign; yearly follow-up with ultrasound recommended
- > 7 cm, consider MRI vs. surgical evaluation to further characterize the mass
What size simple cyst doesnt need f/up?
- ≤3 cm, physiologic finding
- > 3 and ≤5 cm, almost certainly benign; does not need follow-up
lifetime risk for development of ovarian cancer (no risk factors)
1 in 75
Carrier of BRCA1 risk of ovarian CA
39–46%
Carrier of BRCA1 risk of breast CA
57%
Carrier of BRCA2 risk of ovarian CA
10–27%
Carrier of BRCA2 risk of breast CA
49%
When to perform risk reducing BSO for BRCA1 carrier
age 35–40
When to perform risk reducing BSO for BRCA2 carrier
age 40–45
Histologic feature of Uterine papillary serous carcinomas
Psammoma body
is characterized microscopically by a round central area with surrounding collections of calcium
Histologic feature of Ovarian granulosa cell tumor
Call-Exner bodies
Tumor cells are arranged in sheets punctuated by small follicle-like structures and coffee-bean nuclei (Call-Exner bodies)
Histologic feature of Yolk sac, Endodermal sinus tumor
Schiller-Duval bodies
Invaginated papillary structures with a central vessel
Histologic feature of Clear cell carcinoma
Hobnail cells
Histologic feature of Dysgerminoma
Sheets of lymphocytes / germ cells
Histologic feature of Brenner tumor
Walthard nests
Histologic feature of Krukenberg tumor
Signet cells
Name for pathologic description:
Invaginated papillary structures with a central vessel
Schiller-Duvall bodies
Name for pathologic description:
small follicle-like structures and coffee-bean nuclei
Call-Exner bodies
Name for pathologic description:
round central area with surrounding collections of calcium
Psammoma body
Histologic feature of Immature teratoma
Immature neuroepithelium
Histologic feature of Choriocarcinoma, Embryonal carcinoma
Malignant cytotrophoblasts/syncytiotrophooblasts
GTN FIGO dx criteria
one of:
- 4 or more B-hCG plateau over at least 3k
- increase in B-hCG of 10% or more for 3 or more values over at least 3wks
- histologic choriocarcinoma
- persistence of beta-hcg 6mo after molar evacuation
GTN Staging
GTN Risk Scoring
BRCA2 higher risk for which CA
breast
BRCA1 higher risk for which CA
ovarian
Lynch genes
MLH1, MSH2, MSH6, PMS2
Cowden
breast and thyroid cancer
PTEN mutation
Li Fraumeni
soft tissue sarcomas and breast cancer
p53 mutation
Tumor marker: inhibin
granulosa-cell tumor
inhibiting calls from your grandma
Tumor marker: CA 125
epithelial ovarian CA
Tumor marker: CEA
pancreatic and colon cancers
Tumor marker: AFP
germ cell tumors
Tumor marker: CA 19-9
pancreatric
Tumor marker: B-hCG
germ cell tumors
mural nodularity indicates which CA
Ovarian CA
Tumor marker: LDH
germ cell tumors
CA 125 level requiring onco referral
> 200 PREMENO
35 POSTMENO
risk of progression of endometrial hyperplasia to cancer
1% simple without atypia
3% complex without atypia
8% simple with atypia
29% complex with atypia
- penny, nickle, dime, quarter
CA associated with DES exposure
vaginal clear cell
(can be ovarian)
also have T shaped uterus
highest risk factor for breast CA
age
most deadly GYN malignancy
ovarian CA
ovarian CA most common stage at dx
Stage III, IV
most common ovarian CA
epithelial type:
High grade serous
Endometrioid
Clear cell
Mucinous
Low grade serous
Most common sex-cord stromal tumor
granulosa cell tumor
types of germ cell tumors
DEEP CT
Dysgerminoma (most common)
Endodermal sinus (yolk sac)
Embryonal
Polyembryonal
Choriocarcinoma
Immature teratoma
endometriosis associated with which CA
clear cell
ovarian CA risk reduction from tubal ligation
24-28%
ovarian CA risk reduction from salpingectomy
65%
ovarian CA risk reduction from oophorectomy
97% (still have risk of primary peritoneal carcinoma)
type 1 epithelial ovarian CA
Papillary serous histology
High grade
P53 mutations in >95%
BRCA abnormalities
type 2 epithelial ovarian CA
Endometrioid, clear cell
May originate from endometriosis
PTEN, KRAS/BRAF, MMR mutations
LMP and low grade serous
BRCA1 chromosome
17q
- tumor suppressor gene
BRCA1 inheritance
autosomal dominant
when do to risk reducing BSO (+/- hyst) for BRCA1
age 35-40
BRCA2 chromosome
13q
BRCA2 inheritance
autosomal dominant
when to do risk reducing BSO (+/- hyst) for BRCA2
age 40-45
non-gyn associated malignancies with BRCA mutations
pancreatic cancer and prostate cancer
also melanoma for BRCA2
when to start breast CA screening in BRCA+
annual MRIs & clinical exams age 25-29
annual mmg and breast mri age 30-75
Lynch syndrome (HNPCC) inheritance
autosomal dominant
Lynch syndrome (HNPCC) gene defects
- mismatch repair genes
MSH2, MSH6, PMS2, and MLH1
Lynch syndrome (HNPCC) when to do hyst/BSO
when completed child bearing / early mid 40s
screening/surveillance for Lynch syndrome pts
- colonoscopy q1-2y starting at 20-25yo or 2-5y prior to earliest CA dx in family
- EMB q1-2y starting at 30-35yo
- monitor VB
when to refer to gyn onc for elevated CA-125: postmenopausal
> 35 u/mL
when to refer to gyn onc for elevated CA-125: premenopausal
> 200 u/mL
Most common chemo regimen for GYN CA
Carbo / Taxol
borderline tumors precursor to
low-grade epithelial ovarian CA
most common germ cell tumor
dysgerminoma
dysgerminoma markers
LDH & low BHCG
immature teratoma markers
AFP, CA125
endodermal sinus tumor marker
AFP
Schiller-duval bodies characteristic for
endodermal sinus tumor (aka yolk sac)
bleomycin toxicity
pulmonary fibrosis
granulosa cell tumor markers
Inhibin A/B, AMH
granulosa cell tumors can produce
estrogen - can see endometrial path
sertoli-leydig tumors can produce
testosterone
most common GYN malignancy in US
endometrial CA
endometrial cancer type associated with estrogen excess
Type 1
characteristics of Type 1 endometrial CA
Obesity, estrogen excess
Loss of PTEN function, MSI (microsatelite instability), and K-ras alterations
Arises from endometrial hyperplasia
Androstenedione converted to estrone by aromatase in adipose tissue
85% 5 year survival rate
Histology- grade 1-2, endometrioid
characteristics of type 2 endometrial CA
Estrogen independent
Background of atrophy, may see polyp
High grade, advanced stage, aggressive cell types
Overexpression of P53
Poor prognosis: 58% 5 year survival
Histology: serous, clear cell, mucinous, squamous, transitional cell, undifferentiated and carcinosarcoma
p53 associated with what type of cancer
serous (ovarian or endometrial)
Risks of Tamoxifen use
endometrial proliferation, hyperplasia, cancer, polyps
Endometrial intraepithelial neoplasia (EIN) categories
Benign (benign endometrial hyperplasia)
Premalignant (EIN - have nuclear atypia)
Malignant (endometrial adenocarcinoma, endometrioid type, well differentiated)
management endometrial hyperplasia without atypia
progesterone
- repeat sampling in 3mo
management endometrial hyperplasia with atypia (EIN)
surgery (have to be prepared to perform pelvic LN sampling)
- only progesterone for fertility sparing purposes
Lifestyle modifications
when to do EMB based on US
PMB + endometrial thickness >4mm
or persistent PMB
no sampling for PMB and endometrial thickness 4mm or less (NPV >99%)
CA stage with omental mets
ovarian CA - III
endometrial CA - IV
when to include omentectomy and upper abdominal biopsies and washings in surgical staging
serous histology
where does uterine sarcoma met to
lung & liver
mole type where fetal tissue present
partial mole
karyotype of partial mole
Triploidy
XXX, XXY, XYY
karyotype of complete mole
46 XX (90%)
46 XY (10%)
risk of progression to GTN higher for which type of mole
complete
theca-lutein cysts associated with which type of mole
complete
HCG f/up for molar pregnancy
HCG 48 hrs after evacuation,
every 1-2 weeks while elevated,
then monthly for 6 months
GTN common met sites
Lung (80%), vagina (30%), liver (10%), and brain (10%)
GTN prognostic score low vs high risk criteria
score
low risk <7
high risk >= 7
highest risk criteria for WHO prognostic score GTN
4 points each for:
>12mo from preg
pre-tx HCG >= 10^5
mets to brain, liver
>8 mets
previously failed 2 or more chemo
tx for nonmestastatic GTN
Single agent chemo: MTX or Actinomycin-D
tx for low risk GTN
1st therapy single agent MTX or Acti-D.
If elevated HCGs continue, swith to other single agent, consider TAH for local disease, combo chemo therapy
tx for high risk GTN
EMA-CO
Etoposide, Methotrexate, Actinomycin-D, Cyclophosphamide, Vincristine (Oncovorin)
or MAC
Methotrexate, Actinomycin-D, Cyclophosphamide
Brain or liver metastases require XRT
most common vulvar CA
SCC
tx for Bartholin’s cyst in woman >40
excision recommended to rule out adenocarcinoma
surgical margin for excision of vulvar CA
2cm wide
depth down to level coplanar with fascia over the pubic symphysis
want >8mm for good local control
how to age out of cervical CA screening for gen pop
65yo with 2 consecutive, negative primary HPV tests, or 2 negative contests, or 3 negative cytology tests within the past 10 years, with the most recent test occurring within the past 3-5 years, depending on the test used
how to age out of cervical CA screening s/p hyst
if hyst for CIN 2-3:
3 consecutive annual HPV based tests before entering long term surveillance
Incidence of abnormal vaginal cytology is 14%
Incidence of vaginal dysplasia is 1.7%
If no prior then screening not recommended
cervical CA surveillance after tx for CIN 2-3, AIS
HPV based testing at 3 year intervals for 25 years
Regardless of whether hysterectomy has been performed during hte surveillance period
HPV+ test should always
reflex to cytology, regardless of age
HR HPV strains
HPV 16 and 18 in >70% of cervical cancer
HPV-associated cancers
oropharyngeal, anal, vaginal, vulvar, penile, non-melanoma skin cancers
cervical CA tx: when to do surgery
Stage IB2-IIA1
- all depends on tumor size and extension
cervical CA tx: when to do chemo/rad
Stage IB3, IIA2, IIB, III, IVA
- all depends on tumor size and extension
characteristics of Phase specific chemo drugs
Work on a specified phase
Most effective in rapidly growing cells
characteristics of phase nonspecific chemo drugs
Work on multiple phases
Most effective in rapidly growing cells
chemotherapy induction
initial treatment of disease with chemotherapy
chemotherapy Consolidation
drug therapy used as follow up after remission from induction
Adjuvant chemotherapy
drug therapy after initial surgery or radiation therapy
Neoadjuvant chemotherapy
drug therapy given prior to surgery or radiation that is itself insufficient for cure
Salvage chemotherapy
drug therapy after failure of primary therapy
palliative chemotherapy
treatment given to reduce symptoms of disease without curative intent
chemo complete response
no clinical evidence of disease/complete resolution of signs and symptoms of disease for at least one month
chemo partial response
greater than 50% reduction in tumor masses without evidence of new lesions/tumor
definition of stable disease after chemo
no change in overall size, number of tumor masses, neither increasing nor decreasing by 25%
definition of dz progression after chemo
enlargement of tumor masses by at lease 25%
S-phase specific drugs
Antimetabolites
Folate antagonists (MTX)
Purine antagonists
Pyrimidine antagonists (fluorouracil)
Mitosis specific drugs
Vinca alkaloids (vincristine, vinblastine)
Types of Chemo Drugs
S-phase specific drugs
Mitosis specific drugs
Taxanes (paclitaxel, docetaxel)
G2 phase specific drugs
Cell cycle non specific
G2 phase specific drugs
Topoisomerase I inhibitors (topotecan)
Topoisomerase II inhibitors (etoposide)
Cell cycle non specific chemo drugs
Alkylating agents
- Cylcophosphamide
Anthracyclines
- Doxorubicin
Antibiotics
- Mitomycin
- Bleomycin
- Dactinomycin
Hormones
- Tamoxifen
- Megace
- Lupron
Biologic agents
- Immunomodulators
Monoclonal antibodies
MOA of alkylating agents
Bind to DNA, cause breaks
Cyclophosphamide toxicities
hemorrhagic cystitis (MESNA antidotes), cardiac necrosis
Ifosfamide toxicity
hemorrhagic cystitis (MESNA), neurologic (confusion, coma)
Platinum Agents MOA
Crosslinks to DNA and RNA
cisplatin toxicity
renal, electrolyte wasting, neuropathy, ototoxicity, nausea, vomiting
carboplatin toxicity
bone marrow suppression, neuropathy (rare)
Anthracylcines MOA
Intercalate DNA pairs
Doxorubicin (adriamycin) toxicity
cardiomyopathy, mucositis, vesicant
Chemo Antibiotics MOA
DNA breaks
Bleomycin toxicities
pulmonary fibrosis, mucositis
Actinomycin-D toxicities
mucositis, alopecia, vesicant
Antimetabolites: Pyrimidine antagonists MOA
Blocks DNA synthesis
5-FU toxicities
cerebellar syndrome, cardiac ischemia, blurry vision (lacrimal duct stenosis)
Gemcitabine toxicities
flu-like symptoms
Antimetabolites: Folate antagonists MOA
Blocks tetrahydrofolic acid production
MTX toxicity
mucositis, elevated LFTs, renal
Vinca Alkaloids MOA
Inhibit spindle formation
Vinca Alkaloids Toxicities
Toxicities include vesicants, neuropathy, alopecia
Vinca Alkaloids meds
vinblastine, vincristine, vinorelbine
Topoisomerase inhibitors drugs
Topotecan - inhibit topo I
Etoposide - inhibit topo II
Topotecan toxicity
causes myelosuppression
Etoposide toxicity
causes myelodysplastic syndrome, mucositis
Taxanes MOA
Stabilize microtubules
Taxane examples
paclitaxel, docetaxel
Taxane Toxicities
neuropathy, myelosuppression, alopecia, allergic reaction
Bevacizumab (Avastin) used in
Ovarian- used in up front or recurrence
Endometrial- mostly in recurrence
Cervix- advanced disease or recurrence
Bevacizumab (Avastin) MOA
VEGF inhibitor (monoclonal antibody)
Bevacizumab (Avastin) side effects
HTN, proteinuria, renal compromise, PRES, bowel perforation
PARP Inhibitors MOA
Inhibit DNA repair
Interaction with PARP inhibitors and BRCA mutant tumors
“Synthetic lethality” in BRCA mutant tumors which are already DNA repair deficient
PARP inhibitors side effects
nausea, lethargy, bone marrow suppression
Pembrolizumab toxicity
related immune system over activation
- typically treated with steroids but can be life threatening
Direct radiation therapy MOA
Damage to DNA directly causes cellular death in ⅓ of reactions
Indirect radiation therapy MOA
- Formation of free radicals via interaction of radiation with water
- Majority of RT effects are via this mechanism
Acute Radiation Toxicities
Diarrhea
Urinary frequency
Abdominal cramps
Dysuria
Hematochezia
Hematuria
Chronic Radiation Toxicities
Proctosigmoiditis
SBO
Fistula- rectovaginal, vesicovaginal, ureterovaginal
Necrosis
Strictures
utility of cisplatin with radiation
Radiosensitizer