Exam 1 Oncology - Mabe Flashcards
Hyperplasia
an increase in organ or tissue size due to an increase in number of cells
Metaplasia
an adaptive substitution of one type of adult tissue to another type
Dysplasia
an abnormal cellular proliferation where there is loss of normal architecture
Anaplasia
A loss of structural differentiation
Cells de-differentiate
Carcinoma
malignant neoplasm of squamous epithelial cell origin
Adenocarcinoma
malignant neoplasm derived from glandular tissue
Sarcoma
malignant neoplasm with origin in mesenchymal tissues (bone, muscle, fat)
Lymphoma and Leukemia
malignant neoplasm of hematopoietic tissues (blood, white blood cells)
Melanoma
type of cancer of pigment producing cells (melanocytes) in the skin or eye
Blastoma
malignancies in precursor cells (blasts) which are more common in children
Teratoma
A germ cell neoplasm made of several different differentiated cell/tissue types
Define TX, NX, and MX
TX: primary tumor cannot be evaluated
NX: regional lymph nodes cannot be evaluated
MX: distant metastasis cannot be evaluated
Define T0, N0, and M0
T0: no evidence of primary tumor
N0: no regional lymph node involvement
M0: no distant metastasis
T/F: A well-differentiated tumor is spreads slower than a poorly differentiated tumor
True
What is the difference between a benign tumor and cancer?
A benign tumor and cancer both involve uncontrolled cellular growth, but cancer also indicates tissue invasion and metastasis
If a tumor in the brain originates from the breast, is it considered a brain or breast cancer?
Breast cancer
Define proto-oncogene
Any gene in a healthy cell capable of promoting tumor growth
T/F: Carcinogen-induced cancers have very high mutation rates.
True
Do tumors of the same classification have a unifying genetic “driver”?
They can but often do not
What type of gene is BRCA1/BRCA2?
Tumor suppressor genes - they encode for proteins involved in DNA repair
BRCA mutations in breast cancer ________ susceptibility to PARP inhibitors
(hint: PARP inhibitors are primarily used in cancers with BRCA1/2 mutations)
increase
How do PARP inhibitors work?
They trap PARP in the DNA so it’s unable to uncouple from the DNA and therefore leads to cell death
Olaparib drug class
PARP inhibitor
The cell cycle clock is driven by what?
Cyclins paired with cyclin-dependent kinases (CDKs)
What is the R point?
time when cells decide whether or not to enter the cell cycle after G1
Cyclin __ and CDK ____/_____ are master regulators of cell cycle initiation
Cyclin D
CDK 4/6
Palbociclib drug class
CDK 4/6 kinase inhibitor
Hormonal therapies are primarily targeting _________ in breast and endometrial cancer and ____________________ in prostate cancer.
estradiol
dihydrotestosterone
What are the two major strategies of anti-endocrine therapy?
- stop steroid receptor function
- decrease production of steroids
What are the four subtypes of breast cancer?
- Luminal A (ER+, PR+)
- Luminal B (ER+)
- HER2+
- Triple negative
What type of therapy will most likely be used for a luminal A breast cancer?
Endocrine therapy
What is the most common reason for resistance to multiple chemotherapies at once?
Drug transport out of cell
Tamoxifen is a prodrug that is metabolized to ________________ by CYP __________
4-hydroxy tamoxifen
CYP2D6
T/F: SERMs (i.e. tamoxifen) are effective in both pre- and postmenopausal women.
True
Which drug has both agonist and antagonist effects: tamoxifen or fulvestrant?
Tamoxifen
Where does tamoxifen exhibit antagonist effects?
Brain
Where does tamoxifen exhibit agonist effects?
Bone, endometrium
What is the primary indication for tamoxifen?
resected and metastatic ER+/PR+ breast cancer
Treatment options for postmenopausal women with ER+ disease:
- Tamoxifen
- Aromatase inhibitors
- Estrogen antagonists
