Exam 1 Oncology - Mabe Flashcards

(39 cards)

1
Q

Hyperplasia

A

an increase in organ or tissue size due to an increase in number of cells

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2
Q

Metaplasia

A

an adaptive substitution of one type of adult tissue to another type

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3
Q

Dysplasia

A

an abnormal cellular proliferation where there is loss of normal architecture

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4
Q

Anaplasia

A

A loss of structural differentiation
Cells de-differentiate

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5
Q

Carcinoma

A

malignant neoplasm of squamous epithelial cell origin

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6
Q

Adenocarcinoma

A

malignant neoplasm derived from glandular tissue

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7
Q

Sarcoma

A

malignant neoplasm with origin in mesenchymal tissues (bone, muscle, fat)

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8
Q

Lymphoma and Leukemia

A

malignant neoplasm of hematopoietic tissues (blood, white blood cells)

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9
Q

Melanoma

A

type of cancer of pigment producing cells (melanocytes) in the skin or eye

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10
Q

Blastoma

A

malignancies in precursor cells (blasts) which are more common in children

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11
Q

Teratoma

A

A germ cell neoplasm made of several different differentiated cell/tissue types

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12
Q

Define TX, NX, and MX

A

TX: primary tumor cannot be evaluated
NX: regional lymph nodes cannot be evaluated
MX: distant metastasis cannot be evaluated

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13
Q

Define T0, N0, and M0

A

T0: no evidence of primary tumor
N0: no regional lymph node involvement
M0: no distant metastasis

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14
Q

T/F: A well-differentiated tumor is spreads slower than a poorly differentiated tumor

A

True

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15
Q

What is the difference between a benign tumor and cancer?

A

A benign tumor and cancer both involve uncontrolled cellular growth, but cancer also indicates tissue invasion and metastasis

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16
Q

If a tumor in the brain originates from the breast, is it considered a brain or breast cancer?

A

Breast cancer

17
Q

Define proto-oncogene

A

Any gene in a healthy cell capable of promoting tumor growth

18
Q

T/F: Carcinogen-induced cancers have very high mutation rates.

19
Q

Do tumors of the same classification have a unifying genetic “driver”?

A

They can but often do not

20
Q

What type of gene is BRCA1/BRCA2?

A

Tumor suppressor genes - they encode for proteins involved in DNA repair

21
Q

BRCA mutations in breast cancer ________ susceptibility to PARP inhibitors
(hint: PARP inhibitors are primarily used in cancers with BRCA1/2 mutations)

22
Q

How do PARP inhibitors work?

A

They trap PARP in the DNA so it’s unable to uncouple from the DNA and therefore leads to cell death

23
Q

Olaparib drug class

A

PARP inhibitor

24
Q

The cell cycle clock is driven by what?

A

Cyclins paired with cyclin-dependent kinases (CDKs)

25
What is the R point?
time when cells decide whether or not to enter the cell cycle after G1
26
Cyclin __ and CDK ____/_____ are master regulators of cell cycle initiation
Cyclin D CDK 4/6
27
Palbociclib drug class
CDK 4/6 kinase inhibitor
28
Hormonal therapies are primarily targeting _________ in breast and endometrial cancer and ____________________ in prostate cancer.
estradiol dihydrotestosterone
29
What are the two major strategies of anti-endocrine therapy?
1. stop steroid receptor function 2. decrease production of steroids
30
What are the four subtypes of breast cancer?
1. Luminal A (ER+, PR+) 2. Luminal B (ER+) 3. HER2+ 4. Triple negative
31
What type of therapy will most likely be used for a luminal A breast cancer?
Endocrine therapy
32
What is the most common reason for resistance to multiple chemotherapies at once?
Drug transport out of cell
33
Tamoxifen is a prodrug that is metabolized to ________________ by CYP __________
4-hydroxy tamoxifen CYP2D6
34
T/F: SERMs (i.e. tamoxifen) are effective in both pre- and postmenopausal women.
True
35
Which drug has both agonist and antagonist effects: tamoxifen or fulvestrant?
Tamoxifen
36
Where does tamoxifen exhibit antagonist effects?
Brain
37
Where does tamoxifen exhibit agonist effects?
Bone, endometrium
38
What is the primary indication for tamoxifen?
resected and metastatic ER+/PR+ breast cancer
39
Treatment options for postmenopausal women with ER+ disease:
1. Tamoxifen 2. Aromatase inhibitors 3. Estrogen antagonists