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

Cumulative Final-Oncology (Mabe/Dykhuizen) Flashcards

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
Q

Most common dose-limiting effect of chemo

A

Myelosuppression (blood is constantly dividing, so the blood cells get damaged by chemo since chemo targets rapidly dividing cells)

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26
Q

If you find a specific target for cancer, you can use ______ to program the immune system to attack the specific target

A

CAR-T
-Chimeric receptors combine all the different parts that a T cell would normally need into 1 spot (CD-19 is most successful)

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27
Q

Endocrine therapy is driven by

A

Hormone receptors

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28
Q

Which hormones are produced in the pituitary gland?

A

LH and FSH

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29
Q

Which hormone is produced in the hypothalamus?

A

GnRH

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30
Q

The estrogen receptor primarily binds estrogen where in the cell?

A

In the cytoplasm and then moves to the nucleus

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31
Q

Which enzyme converts androstenedione to estrone?

A

Aromatase (CYP19)

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32
Q

ER+ tumors will be treated with _____

A

Endocrine therapy

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33
Q

Tamoxifen is a prodrug that MUST be metabolized by ____

A

CYP2D6

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34
Q

What is unique about the action of tamoxifen as compared to Fulvestrant?

A

It activates ER in the bone

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35
Q

Which of the following is not a hormone responsive cancer type?

A

Ovarian Cancer

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36
Q

Which compound acts directly on AR?

A

Enzalutamide

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37
Q

Cell signaling is largely driven by the transfer of ____

A

phosphates (ATP is the major source of phosphate groups that will be transferred by a kinase to a target protein.

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38
Q

Amino acids that are targets for phosphorylation

A

Serine
Threonine
Tyrosine
Lipids

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39
Q

Which compounds inhibit EGFR?

A

-Gefitinib
-Osimertinib
-Afatinib
-Lapatinib

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40
Q

What mutation in EGFR confers resistance to 1st and 2nd generation EGFR inhibitors?

A

T790M

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41
Q

Which kinase inhibitors target EGFR?

A

-Gefitinib
-Erlotinib
-Dacomitinib
-Afatinib
-Osimertinib

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42
Q

Most common SE with kinase inhibitors

A

Rash-It is a good thing with these bc it means pt is responding to tx

43
Q

Which kinase inhibitor targets RAF?

A

Dabrafenib

44
Q

Which kinase inhibitor targets EGFR + HER2?

A

Lapatinib

45
Q

Which kinase inhibitor preferentially binds HER2?

A

Tucatinib

46
Q

Which kinase inhibitors are used for BCR-Abl (philadelphia chromosome)?

A

Imatinib
Ponatinib (specifically T315I)

47
Q

Which kinase inhibitor targets EML4-ALK translocation?

A

Alectinib

48
Q

Which kinase inhibitor targets BRAF V600?

A

Dabrafenib + Trametinib

49
Q

Which kinase inhibitor targets BTK?

A

Acalabrutinib

50
Q

Which kinase inhibitor targets mTORC1?

A

Everolimus

51
Q

Which drug primarily interferes with purine biosynthesis?

A

6-MP

52
Q

What rescues a 5-FU overdose?

A

Thymidine

53
Q

What enhances 5-FU effect?

A

Leucovorin

54
Q

Which antimetabolite should not be given to a patient being treated for gout?

A

6-MP; it interacts with allopurinol and can cause 6-MP to not be broken down

55
Q

Which antimetabolite does NOT directly inhibit DNA synthesis?

A

MTX

56
Q

Alkylating agents are potent

A

Electrophiles

57
Q

Which alkylating agent is a prodrug?

A

Cyclophosphamide

58
Q

Which agent do you have to give with Mesna and why?

A

Cyclophosphamide because the by-product, acrolein, can accumulate in the urine leading to hemorrhagic cystitis

59
Q

T/F: All alkylators and platinum compounds are cross-linkers.

A

True

60
Q

Topoisomerase 1 inhibitors primarily halt cells in which phase of the cell cycle?

A

S phase

61
Q

Topo 1 cuts ____ strands of DNA

A

1; inhibitors will covalently attach to Topo 1

62
Q

Which drugs are Topo 1 inhibitors?

A

Irinotecan and Topotecan

63
Q

What is special about Irinotecan?

A

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
Q

A pt has a hx of heart disease and poor cardiac function. Which topoisomerase inhibitor should NOT be prescribed?

A

Doxorubicin

65
Q

What drugs are Topo II inhibitors?

A

Doxorubicin and Etoposide

66
Q

Major SE of doxorubicin

A

Cardiotoxicity

67
Q

How can we reduce some of the cardiotoxicity from doxorubicin?

A

Give Dexrazoxane with the doxorubicin

68
Q

Which topo inhibitor does NOT intercalate?

A

Etoposide

69
Q

Which topo inhibitor creates free radical intermediates that cause single and double strand DNA breaks?

A

Bleomycin

70
Q

What is the dose-limiting toxicity of bleomycin?

A

Pulmonary toxicity from minimal amounts of bleomycin amino hydrase in the skin and lungs

71
Q

Which of the microtubule inhibitors block the polymerization of tubulin?

A

Vincristine

72
Q

Which phase is sensitive to microtubule inhibitors?

A

G2/M

73
Q

Which drugs are vinca alkaloids?

A

Vincristine and Eribulin

74
Q

Major SE of vinca alkaloids

A

Peripheral neuropathy

75
Q

Dose-limiting SE for taxanes

A

Myelosuppression

76
Q

What is unique about paclitaxel?

A

It is linked to albumin to increase circulation and solubility

77
Q

What drugs are considered taxanes?

A

Paclitaxel

78
Q

What drug is considered epothilone and works like taxanes?

A

Ixabepilone

79
Q

Where does trastuzumab bind?

A

HER2 receptor and induces cellular cytotoxicity

80
Q

What does pertuzumab bind?

A

HER2 and inhibitors dimerization

81
Q

What does cetuximab bind to?

A

EGFR; blocks phosphorylation and activation of receptor-associated kinases

82
Q

What is the warning with cetuximab?

A

Severe infusion reaction from non-specific immune response to antibodies

83
Q

What does panitumumab bind to?

A

Extracellular EGFR domain

84
Q

What does bevacizumab bind to?

A

VEGF; blocks new vessel formation; no benefit for monotherapy so use with 5-FU

85
Q

What does rituximab bind to?

A

CD20; inhibits B cell proliferation

86
Q

What does daratumumab bind to?

A

CD38 on plasma B cells

87
Q

What are bispecific T cell engagers (BiTE) used for?

A

To overcome central tolerance

88
Q

What does Blinatumomab bind?

A

CD19 on B cell + CD3 on T cell

89
Q

What does mosunetuzumab bind?

A

CD19 on B cell + CD3 on T cell

90
Q

What does Teclistamab bind?

A

BCMA on multiple myeloma cells + CD3 on T cell

91
Q

What does Taquetamab bind?

A

GPCRC5D on multiple myeloma cells + CD3 on T cell

92
Q

SE of immune therapies

A

Cytokine storm

93
Q

What acts as brakes/checkpoints in the immune system that we target?

A

CTLA-4 and PD-1

94
Q

MOA of ipilimumab

A

Bind CTLA-4 to reverse CTL inhibition so T cell can continue to attack APC

95
Q

MOA of pembrolizumab

A

Bind PD-1 on T cell to prevent binding to PD-L1 and PD-L2
*Use with ipilimumab

96
Q

MOA of atezolizumab

A

Binds PD-L1 to prevent binding to PD-1

97
Q

Exclusions for immune therapies

A

Pts with autoimmune disease and patients with medical conditions requiring immunosuppression

98
Q

MOA of Sipuleucel-T

A

APC collected from pt–activated ex-vivo with
PAP-GM-CSF–reinfused into pt (goal: stimulate pt own immune cells to attack cancer)

99
Q

CAR-T MOA

A

T cell isolated from pt (CD19); pt will never have B cells again, but T cells will live indefinitely

100
Q

MOA of azacitibine + decitibine

A

Incorporates into DNA and covalently binds DNMT enzymes

101
Q

MOA of Bortezomib

A

Inhibits proteasome (will cause a backup in ‘garbage disposal’)

102
Q

MOA of Pamalidomide

A

Binds cereblon to induce it to ubiquitinate + degrade zinc-fingers transcription factors, which are needed in lymphocyte development

103
Q

What is unique about Pamalidomide?

A

MUST complete REMS

104
Q

MOA of Venetoclax

A

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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