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Pharm > Antieoplastic agents > Flashcards

Antieoplastic agents Flashcards

1
Q

What are carcinomas?

A

Malignant cells that arise from epithelial tissues (ectoderm or endoderm)

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2
Q

What are Sarcomas?

A

Malignant cells that arise from CT (mesoderm)

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3
Q

What are neoplasms that involve the bone marrow and peripheral blood called?

A

Leukemias

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4
Q

What are neoplasms that arise from B or T lymphocytes, and commonly present as masses within lymph nodes or othe soft tissues?

A

Lymphomas

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5
Q

What are myelomas?

A

Plasma cell diseases

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6
Q

What is the role of p53?

A

intracellular signal that induces apoptosis

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7
Q

What is the mutation in tumors that allows for sustained proliferation?

A

Telomerase

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8
Q

What are the enzymes that allow tumors to metastisize?

A

metalloproteases

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9
Q

What are the five main types of lymphoid malignancies?

A
  1. Acute lymphoid leukemia
  2. Chronic lymphoid leukemia
  3. non-Hodgkines
  4. Hodgkins
  5. Plasma cell diseases
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10
Q

What is the philidelphia chromosome? What disease does this cause?

A

Translocation between chromosome 9 and 22, causing a fusion of the BCR-ABL genes

Chronic myeloid leukemia

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11
Q

What is the purpose of the ABL gene?

A

Makes a Y kinase that stimulates cellular growth

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12
Q

What are the common changes that protooncogenes undergo to facilitate cellular growth? (3)

A

Constitutive activity
Resist degradation
Increase expression

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13
Q

What is the Ras/Raf kinase cascade used for, generally?

A

Growth signal

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14
Q

What is the receptor in breast CA that trastuzima inhibits?

A

Her2/neu

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15
Q

What is curative intent when describing antineoplastic drugs?

A

Drugs that are used to cure CA

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16
Q

What does it mean for a drug to be an adjuvant therapy?

A

Drug that is used to decrease the changes that a CA will return

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17
Q

What does it mean for a drug to be a neo-adjuvant therapy?

A

Drug that is used to shrink the tumor before primary treatment

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18
Q

True or false: ras is mutated in about 30% of all cancers

A

True

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19
Q

c-myc is upregulated in what types of CA?

A

Colorectal cancers

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20
Q

What is Hodgkin’s lymphoma?

A

B cell CA

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21
Q

Mutations in the IGF pathway lead to what?

A

Prostate, breast, and colorectal CA

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22
Q

What are the three major points in the cell cycle, where there are checkpoitns?

A

G1/S
G2/M
metaphase/anaphase

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23
Q

What are the two things that are checked at the G2/M checkpoint?

A

Is all DNA intact

Are all chromosomes attached to the mitotic spindle

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24
Q

What is the thing that is checked at the G2/M check point?

A

Is the DNA completely replicated

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25
Q

What are the two things that are checked at the G1/S check point?

A

Cell size/nutrition good?

DNA intact?

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26
Q

What is the general target of chemotherapy?

A

Highly proliferative cells

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27
Q

Is the therapeudic index high or low with chemo?

A

Low

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28
Q

True or false: in general, the longer the cell doubling time of the tumor, the easier it is to treat

A

False- the shorter the doubling time

29
Q

Why do we use combinatiion therapies?

A

Avoid evolution/selection of the tumor cell

30
Q

What is the cell kill hypothesis?

A

Chemo kills via first order kinetics

31
Q

Since chemo kills via first order kinetics, there must be repeated doses of a drug. What is the limit to these doses?

A

Adverse side effects

32
Q

Why a tumor cells fast to evolve?

A

Really unstable DNA

33
Q

What is the specific protein that, when upregulated in a tumor cell, allows it to survive?

A

MDR transporter

34
Q

Why don’t all cells within a tumor die at the same rate?

A

Not all have equal acess to blood supply

35
Q

Most chemotherapeutic drugs ultimately kill cell through what mechanism?

A

Inducing apoptosis

36
Q

What is epithelial-mesenchymal transition?

A

The process by which cells lose adhesive properties and become motile

37
Q

What is the basis for the immune suppression with chemo?

A

Bone marrow toxicity since it divides a lot

38
Q

What is the basis for the GI issues seen with chemo?

A

Attack of fast replicating enterocytes

39
Q

What are the four ways of perturbing normal DNA synthesis in cancer cells?

A
  1. Staving pyrimidine/purines
  2. Incorporation of altered nucleotides
  3. Alkylating, crosslinking etc of DNA
  4. Prevent topoisomersase
40
Q

What are the two ways of perturbing mitosis?

A

Prevent micotrubule formation

Prevent microtule destruction

41
Q

What are the three targeted ways of killing tumors?

A
  1. Pertubing hormone/growth signaling
  2. Inhibiting blood supply
  3. Target activating proteins
42
Q

What part of the cell cycle do DNA alkylating drugs and intercalating drug act?

A

non specfic (all of them)

43
Q

True or false: Drugs that are nonspecific are still going to kill replicating cells more often than slower replicating ones

A

True

44
Q

What are the two purines?

A

Adenosine

Guanine

45
Q

What are the three pyrimidines?

A

Thymidine
Cytiding
Uridine

46
Q

What are nucleosides?

A

Nucleobases with a ribose attached

47
Q

What are nucleotides?

A

Nucleobases with a ribose and a phosphate

48
Q

What is the main process that antimetabolites target?

A

De novo nucleotide biosynthesis

49
Q

What, generally, are the molecules that make up the antimetabolites?

A

analogs of purines and pyrimidines

50
Q

What part of the cell cylce do antimetabolites generally work?

A

S phase

51
Q

What is the role of ribonucleotide reductase?

A

Turns ribonucleotides into deoxyibonucleotides

52
Q

What is the precursor for purines?

A

inosine monophosphate

53
Q

What is the MOA of methotrexate? (hint, two enzymes involved)

A

Blocks dihydrofolate reductase from forming THF, which inhibits thymidylate synthase, which decreases dTMP production

54
Q

Which cancers are methotrexate particularly useful in treating?

A

Acute lymphoblastic leukemia

Osteosarcomas

Choriocarcinomas

55
Q

How can you deliver a high dose of methotrexate? MOA?

A

administer leucovorin, which prevent toxicity via THF derived cofactors

56
Q

What is the MOA of resistance of tumor cells to methotrexate?

A

Impair transport

Change/elevate DHFR

57
Q

What are the adverse effects of methotrexate?

A

Bone marrow suppression

Nephrotoxicities

Hepatic dysfunction

58
Q

What is the MOA of 5FU?

A

fdUMP causes DNA/RNA damage by decreasing thymidylate levels

59
Q

What is the enzymes that 5FU inhibits?

A

Thymidylate synthetase

60
Q

What are the uses of 5FU?

A

GI cancers

Part of breast treament

61
Q

What are the adverse effects of 5FU?

A

Oral and GI ulcers

Bone marrow suppression

62
Q

What is the MOA of resistance to 5FU?

A

Amplification of thymidylate synthetase

63
Q

What is capecitabine?

A

Prodrug of 5FU

64
Q

What is the MOA of cytarabine (Ara-c)?

A

Ara-c is converted by deoxycytidine kinase,

65
Q

What are the cancers that cytarabine is used to treat?

A

Leukemias/hematological tumors

66
Q

What is the enzyme in celll that breaks down cytarabine (ara-c)? What part of the body does not have very much of this enzyme?

A

Cytidine deaminase

CNS

67
Q

What phase of the cell cycle does cytarabine act in?

A

S phase

68
Q

What are the adverse effects of cytarabine?

A

Cerebellar syndrome
(dysarthria, nystagmus, ataxia)

Renal/hepatic dysfunctino

69
Q

What drug causes cerebellar syndrome? Why?

A

Cytarabine d/t lack of cytadine deaminase in the CNS

Pharm (73 decks)

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