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Therapeutics Fall Semester P3 > Cumulative Final-Oncology (Mabe/Dykhuizen) > Flashcards

Cumulative Final-Oncology (Mabe/Dykhuizen) Flashcards

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1
Q

3 requirements for cancer

A
  1. Uncontrolled cell growth
  2. Tissue invasion
  3. Metastases (spreading to other parts of body)
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2
Q

Hallmarks of cancer

A
  1. Sustaining proliferative signaling
  2. Resisting cell death
  3. Genome instability and mutation
  4. Inducing or accessing vasculature
  5. Activating invasion and metastasis
  6. Enabling replicative immortality
  7. Avoiding immune destruction
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3
Q

Carcinoma definition

A

Squamous epithelial origin

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4
Q

Adenocarcinoma definition

A

Glandular epithelial origin

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5
Q

Sarcoma definition

A

Mesenchymal origin (bone, fat, muscle)

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6
Q

Lymphoma/leukemia definition

A

Hematopoietic origin

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7
Q

Melanoma

A

Pigment-producing cell origin

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8
Q

Blastoma

A

Precursor cells (mainly in children)

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9
Q

Teratoma

A

Germ cell

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10
Q

Oncogene

A

-Contributes to cancer development
-Activation of proto-oncogenes is DOMINANT allele

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11
Q

Examples of oncogenes

A

-Scr
-HER2
-EGFR

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12
Q

Tumor suppressor

A

-Normally prevents cancer
-Heterozygous mutation often transmitted as germ-line mutations (associated with heritable forms of cancer)
-Loss of function mutations are RECESSIVE

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13
Q

Examples of tumor supressors

A

-Retinoblastoma (Rb)
-BRCA

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14
Q

Importance of genomics in cancer

A

-Some cancers run in families (BRCA, Rb)
-Genetic profiling of individual cancers may predict effective tx
-Tumor suppression mutations (BRCA) can indicate tumor/cancer, but does NOT guarantee it!

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15
Q

Explain the roles of BRCA and PARP and how mutations may impact these

A

-BRCA and PARP are tumor suppressors that repair DNA
-To inhibit a cell from replicating, BRCA and PARP must be inhibited
-1 mutant mutation with BRCA indicates a high correlation of breast cancer
-Many times, a natural mutation will inhibit BRCA, so we use PARP inhibitors must be used

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16
Q

Specific drug used for BRCA mutations

A

**Remember, we want to inhibit PARP so both, BRCA and PARP, are inhibited to prevent proliferation and replication
-Olaparib (PARP inhibitor)

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17
Q

Importance of mitogenic signals in cancer

A

May enable tumor growth

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18
Q

Importance of cell cycle in cancer

A

DNA damage/mitosis may lead to cancer and cause a cell to continue to proliferate uncontrollably

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19
Q

What is ALWAYS a problem in drug tx?

A

RESISTANCE

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20
Q

Major mechanisms of resistance

A
  1. Change in binding pocket – drug no longer fits (decreased pro-drug activation)
  2. Upregulation of protein that the drug is targeting
  3. Target amplification and mutation (increased detoxification of drug)
  4. Multi-drug resistant transporters (pump drugs out of cell)
  5. Reduced transport into cell
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21
Q

What substrates did we learn that are NOT substrates for multi-drug resistant transporters?

A
  1. Resistance to gefitinib: Osimertinib
  2. Resistance to BCR-Abl T315I: Ponatinib
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22
Q

Dose-limiting toxicities

A
  1. Hematopoietic – infections
  2. Platelets – hemostasis
  3. RBC – anemia
  4. GI – N/V; loss of appetite
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23
Q

Combination chemotherapy

A

-Want differing MOA + differing toxicities
-Common combo tx
1. Cyclophosphamide (alkylating agent)
2. Doxorubicin (topo inhibitor)
3. Vincristine (microtubule inhibitor)
4. Prednisone (steroid)

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24
Q

What is the most common side effect for patients receiving chemotherapy?

A

Nausea/Vomiting

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25
Most common dose-limiting effect of chemo
Myelosuppression (blood is constantly dividing, so the blood cells get damaged by chemo since chemo targets rapidly dividing cells)
26
If you find a specific target for cancer, you can use ______ to program the immune system to attack the specific target
CAR-T -Chimeric receptors combine all the different parts that a T cell would normally need into 1 spot (CD-19 is most successful)
27
Endocrine therapy is driven by
Hormone receptors
28
Which hormones are produced in the pituitary gland?
LH and FSH
29
Which hormone is produced in the hypothalamus?
GnRH
30
The estrogen receptor primarily binds estrogen where in the cell?
In the cytoplasm and then moves to the nucleus
31
Which enzyme converts androstenedione to estrone?
Aromatase (CYP19)
32
ER+ tumors will be treated with _____
Endocrine therapy
33
Tamoxifen is a prodrug that MUST be metabolized by ____
CYP2D6
34
What is unique about the action of tamoxifen as compared to Fulvestrant?
It activates ER in the bone
35
Which of the following is not a hormone responsive cancer type?
Ovarian Cancer
36
Which compound acts directly on AR?
Enzalutamide
37
Cell signaling is largely driven by the transfer of ____
phosphates (ATP is the major source of phosphate groups that will be transferred by a kinase to a target protein.
38
Amino acids that are targets for phosphorylation
Serine Threonine Tyrosine Lipids
39
Which compounds inhibit EGFR?
-Gefitinib -Osimertinib -Afatinib -Lapatinib
40
What mutation in EGFR confers resistance to 1st and 2nd generation EGFR inhibitors?
T790M
41
Which kinase inhibitors target EGFR?
-Gefitinib -Erlotinib -Dacomitinib -Afatinib -Osimertinib
42
Most common SE with kinase inhibitors
Rash-It is a good thing with these bc it means pt is responding to tx
43
Which kinase inhibitor targets RAF?
Dabrafenib
44
Which kinase inhibitor targets EGFR + HER2?
Lapatinib
45
Which kinase inhibitor preferentially binds HER2?
Tucatinib
46
Which kinase inhibitors are used for BCR-Abl (philadelphia chromosome)?
Imatinib Ponatinib (specifically T315I)
47
Which kinase inhibitor targets EML4-ALK translocation?
Alectinib
48
Which kinase inhibitor targets BRAF V600?
Dabrafenib + Trametinib
49
Which kinase inhibitor targets BTK?
Acalabrutinib
50
Which kinase inhibitor targets mTORC1?
Everolimus
51
Which drug primarily interferes with purine biosynthesis?
6-MP
52
What rescues a 5-FU overdose?
Thymidine
53
What enhances 5-FU effect?
Leucovorin
54
Which antimetabolite should not be given to a patient being treated for gout?
6-MP; it interacts with allopurinol and can cause 6-MP to not be broken down
55
Which antimetabolite does NOT directly inhibit DNA synthesis?
MTX
56
Alkylating agents are potent
Electrophiles
57
Which alkylating agent is a prodrug?
Cyclophosphamide
58
Which agent do you have to give with Mesna and why?
Cyclophosphamide because the by-product, acrolein, can accumulate in the urine leading to hemorrhagic cystitis
59
T/F: All alkylators and platinum compounds are cross-linkers.
True
60
Topoisomerase 1 inhibitors primarily halt cells in which phase of the cell cycle?
S phase
61
Topo 1 cuts ____ strands of DNA
1; inhibitors will covalently attach to Topo 1
62
Which drugs are Topo 1 inhibitors?
Irinotecan and Topotecan
63
What is special about Irinotecan?
It is a prodrug converted to SN-38 (active); SN-38 is metabolized by UGT1A1. Must test pts for UGT1A1 polymorphism bc irinotecan would be toxic for those pts.
64
A pt has a hx of heart disease and poor cardiac function. Which topoisomerase inhibitor should NOT be prescribed?
Doxorubicin
65
What drugs are Topo II inhibitors?
Doxorubicin and Etoposide
66
Major SE of doxorubicin
Cardiotoxicity
67
How can we reduce some of the cardiotoxicity from doxorubicin?
Give Dexrazoxane with the doxorubicin
68
Which topo inhibitor does NOT intercalate?
Etoposide
69
Which topo inhibitor creates free radical intermediates that cause single and double strand DNA breaks?
Bleomycin
70
What is the dose-limiting toxicity of bleomycin?
Pulmonary toxicity from minimal amounts of bleomycin amino hydrase in the skin and lungs
71
Which of the microtubule inhibitors block the polymerization of tubulin?
Vincristine
72
Which phase is sensitive to microtubule inhibitors?
G2/M
73
Which drugs are vinca alkaloids?
Vincristine and Eribulin
74
Major SE of vinca alkaloids
Peripheral neuropathy
75
Dose-limiting SE for taxanes
Myelosuppression
76
What is unique about paclitaxel?
It is linked to albumin to increase circulation and solubility
77
What drugs are considered taxanes?
Paclitaxel
78
What drug is considered epothilone and works like taxanes?
Ixabepilone
79
Where does trastuzumab bind?
HER2 receptor and induces cellular cytotoxicity
80
What does pertuzumab bind?
HER2 and inhibitors dimerization
81
What does cetuximab bind to?
EGFR; blocks phosphorylation and activation of receptor-associated kinases
82
What is the warning with cetuximab?
Severe infusion reaction from non-specific immune response to antibodies
83
What does panitumumab bind to?
Extracellular EGFR domain
84
What does bevacizumab bind to?
VEGF; blocks new vessel formation; no benefit for monotherapy so use with 5-FU
85
What does rituximab bind to?
CD20; inhibits B cell proliferation
86
What does daratumumab bind to?
CD38 on plasma B cells
87
What are bispecific T cell engagers (BiTE) used for?
To overcome central tolerance
88
What does Blinatumomab bind?
CD19 on B cell + CD3 on T cell
89
What does mosunetuzumab bind?
CD19 on B cell + CD3 on T cell
90
What does Teclistamab bind?
BCMA on multiple myeloma cells + CD3 on T cell
91
What does Taquetamab bind?
GPCRC5D on multiple myeloma cells + CD3 on T cell
92
SE of immune therapies
Cytokine storm
93
What acts as brakes/checkpoints in the immune system that we target?
CTLA-4 and PD-1
94
MOA of ipilimumab
Bind CTLA-4 to reverse CTL inhibition so T cell can continue to attack APC
95
MOA of pembrolizumab
Bind PD-1 on T cell to prevent binding to PD-L1 and PD-L2 *Use with ipilimumab
96
MOA of atezolizumab
Binds PD-L1 to prevent binding to PD-1
97
Exclusions for immune therapies
Pts with autoimmune disease and patients with medical conditions requiring immunosuppression
98
MOA of Sipuleucel-T
APC collected from pt--activated ex-vivo with PAP-GM-CSF--reinfused into pt (goal: stimulate pt own immune cells to attack cancer)
99
CAR-T MOA
T cell isolated from pt (CD19); pt will never have B cells again, but T cells will live indefinitely
100
MOA of azacitibine + decitibine
Incorporates into DNA and covalently binds DNMT enzymes
101
MOA of Bortezomib
Inhibits proteasome (will cause a backup in 'garbage disposal')
102
MOA of Pamalidomide
Binds cereblon to induce it to ubiquitinate + degrade zinc-fingers transcription factors, which are needed in lymphocyte development
103
What is unique about Pamalidomide?
MUST complete REMS
104
MOA of Venetoclax
Inhibits BCL-2 (BCL-2 is usually anti-apoptotic + overexpressed in tumor cells) --> with the inhibition, it will drive cell death via apoptosis

Therapeutics Fall Semester P3 (7 decks)

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