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Pharmacology > Cancer > Flashcards

Cancer Flashcards

1
Q

What are the 6 phases of the cell cycle?

A

1) G1
2) S
3) G2
4) Mitosis
5) Cytokinesis
6) G0

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2
Q

What is the G1/gap phase?

A

Decision to reenter cycle is made –> Cell grows and prepares to synthesize DNA (cell contents, except chromosomes, are duplicated)

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3
Q

What is the S/synthesize phase?

A

Cell synthesizes DNA (each of the 46 chromosomes is duplicated by the cell)

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4
Q

What is the G2/second gap phase?

A

The cell prepares to divide (cell double checks the duplicated chromosomes for errors and make needed repairs)

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5
Q

What is the M/mitosis phase?

A

Cell division

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6
Q

What is the G0/arrest/quiescent phase?

A

Cell is in resting state (decision to exit cycle)

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7
Q

What are the 3 cell cycle checkpoints?

A

1) G1/S checkpoint
2) G2/M checkpoint
3) M checkpoint

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8
Q

What does the G1/S checkpoint monitor?

A

Cell monitors size and DNA integrity

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9
Q

What does the G2/M checkpoint monitor?

A

Cell monitors DNA synthesis and damage

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10
Q

What does the M checkpoint monitor?

A

Cell monitors spindle formation and attachment to kinetochores

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11
Q

What protein complex is involved in the cell cycle?

A

Cyclins + Cyclin dependent kinases, Cdks (CCdks)

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12
Q

What is the role of CCdks?

A

CDKs must bind correct C –>
CCdks act as kinases to turn them ‘on’ –>
Cascade of kinases is activated –>
Gene transcription (allows cells to drive through the checkpoint)

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13
Q

What are the levels of C and Cdk throughout the cell cycle?

A

Cdk levels are stable

C levels change throughout cycle

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14
Q

What happens when an oncogene becomes mutated?

A
  • gains a function

- expressed at abnormally high levels/activity

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15
Q

What happens when a tumour suppressor gene becomes mutated?

A

Encodes for a protein that is involved in suppressing cell division - mutation rate increases

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16
Q

What is the normal function of an ACTIVATED oncogene?

A
  • Cell growth

- Gene transcription

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17
Q

What is the normal function of an INACTIVATED tumour suppressor gene?

A
  • DNA repair
  • Cell cycle control (maintains genomic integrity)
  • Cell death
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18
Q

What are 2 types of tumour suppressors?

A

p53, Rb

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19
Q

What is the role of p53?

A

Senses genomic damage via ATM –> stops cell cycle to initiate DNA repair –> if DNA is irreparable, p53 will initiate cell death process

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20
Q

____% of all cancers incur p53/ pathway mutations

A

50

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21
Q

What is the role of Rb?

A

Inactivates G1/S cycle transition by binding + inactivating protein E2F1

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22
Q

What are 2 types of oncogenes?

A

HER2/neu, Ras

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23
Q

What is HER2/neu?

A

An amplified oncogene, growth factor receptor (higher ratio, more aggressive cancer)

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24
Q

What is the tx for over-expression of HER2/neu breast cancers?

A

Herceptin

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25
Q

What is Ras?

A
  • Frequently mutated gene

- Growth factor receptor responsive to small GTPase to transduce multiple cell signals

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26
Q

What does mutation in Ras lead to?

A

Signal-independent expression hyper activation, cell proliferation, anti-apoptic signaling

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27
Q

What are 2 types of genomic instability (GI)?

A

1) Chromosomal instability

2) Enhanced by dysfunctional DNA repair

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28
Q

What is chromosomal instability?

A
  • Translocations –> aneuploidy –> tumour suppression function loss, oncogenic function gain
  • Detectable cytogenetic abnormalities
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29
Q

Describe tumour growth in the early stages:

A

high growth fraction, short doubling time

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30
Q

Describe tumour growth in the late stages:

A

low growth fraction, long doubling times (bc tumour is larger and is starting to compete for space)

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31
Q

In which stage is chemotx most effective?

A

early stage (high growth fraction)

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32
Q

What are the 4 stages of tumour progression?

A

1) Hyperplasia: initial abnormal growth
2) Dysplasia: different sized cells are not ordered
3) Carcinoma in situ
4) Cancer (malignant tumours): metastasis

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33
Q

Differentiate bw benign and malignant:

A

Benign (non-invasive):

  • well-defined borders
  • well differentiated
  • regular nuclei
  • rare mitoses

Malignant (invasive):

  • irregular borders
  • poorly differentiated
  • irregular/larger nuclei
  • more frequent/abnormal mitoses
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34
Q

What are 2 predictors of cancer behaviour?

A

Grade

Stage: Tumour, Lymph Nodes, Metastases

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35
Q

Describe Grade 1 Cancer

A

Well differentiated cells

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36
Q

Describe Grade 2 Cancer

A

Moderately differentiated cells

37
Q

Describe Grade 3 Cancer

A

Poorly differentiated cells

38
Q

Describe Grade 4 Cancer

A

Anasplastic (lost all differentiation, mitotic bodies are present)

39
Q

What are 3 ways cancer can spread?

A
  • Seeding body cavities
  • Lymphatic drainage to lymph nodes
  • Hematogenous via blood vessels
40
Q

Name 5 methods of cancer detection

A
  • Blood work
  • Palpation
  • Symptomatic
  • Coincidental
  • Image based (CT scan, PET/CT, MRI)
41
Q

What does cancer treatment depend on?

A
  • Tumour type
  • Location and amt of disease
  • Pt’s health status
42
Q

What are 3 objectives of cancer tx?

A
  • Kill cancer cells
  • Lead to cancer cell apoptosis
  • Contain/limit cell growth
43
Q

What are 6 cells affected by toxicity?

A
  • Cancer cells
  • Bone marrow (most common dose-limiting complication)
  • GI mucosa (N/V)
  • Hair follicles
  • Taste buds
  • Redness and skin peeling (radiation recall reaction)
  • Fetus (absolute CI)
44
Q

What cancers respond to curative tx: chemo?

A
  • Non Hodgkin’s lymphoma
  • Hodgkin’s disease
  • Choriocarcinoma
  • Lympoblastic leukemia
  • Burkitt’s lymphoma
  • Wilms tumour
  • Rhabdomyosarcoma
45
Q

What cancers respond to curative tx: chemo + radiation + surgery?

A
  • Breast
  • Bladder
  • Prostate
  • Rectal
46
Q

What cancers require palliative tx?

A
  • Lung
  • Esophageal
  • Pancreatic
  • Most brain tumours
47
Q

What is radiation tx?

A

Ionization and excitation of atoms that kill cells

48
Q

What are 4 types of radiation tx?

A
  • External beam radiation (gamma photons, neutron beams)
  • Radioimmunoconjugates (AB targeted radiation)
  • Radioconjugates (isotope tagged to bone seeking material)
  • Free isotopes
49
Q

What are 4 purposes of chemo tx?

A

1) Primary: shrink/eliminate tumour
2) Neoadjuvant: make tumour more amenable to other tx
3) Adjuvant: get rid of micro metastasis
4) Palliation: sx control

50
Q

What are 4 responses to chemotx?

A

1) CR: complete disappearance for at least 1 month
2) PR: >50% reduction in tumour size or markers + no new disease for 1 month
3) SD: no reduction
4) Progression: 25% increase in tumour size

51
Q

Cancer drugs can be divided in two classes:

A

1) Cell cycle specific drugs

2) Non cell cycle specific drugs

52
Q

What cancers are CCS drugs least effective in tx?

A

Cancers with low growth fractions

53
Q

CCS MOA:

A

Kills proliferating cells (prefers high growth factor tumours):

  • Plant alkaloids target cells at G2/M phase
  • DNA synthesis inhibitors target cells at S phase
54
Q

What is CCS tx dependent on?

A

Schedule: give in divided doses at repeated intervals

55
Q

NCCS MOA:

A

Kills proliferating and non-proliferating cells (+ high/low growth tumours)
- Kill can happen at any phase

56
Q

What is NCCS tx dependent on?

A

Dose or concentration

57
Q

Tx Factors

A

Refer to slide 61-62

58
Q

Why is cancer chemotherapeutics given in cycles?

A

To allow normal cells time to recover. Also allows remaining cancer cells to recover and develop resistance :(

59
Q

What are 3 principles used in tx to reduce resistance problem?

A
  • Dose escalation: Use high and increasing dose throughout tx
  • Cell kill hypothesis: minimize recovery intervals
  • Sequential scheduling during combination tx
60
Q

SLIDE 76+77

A

Graphs explaining Fractional Hypothesis

61
Q

Chemotx inhibits what 3 stages of an overactive cell cycle?

A

1) Cell growth (e.g.: growth factor proteins- hormones)
2) DNA duplication
3) Cell division

62
Q

SLIDE 81

A

IS IMPT AND WIL L BE ON THE MIDTERM

63
Q

Describe genotoxic agents’ 3 MOA

A

1) DNA bases alkylation
2) Inter/intra-strand DNA cross-links
3) Nucleotide mispairing
DNA damage leads to apoptosis

64
Q

Explain DNA base alkylation:

A

Base pairing is pushed away –> DNA breakage

65
Q

Explain inter/intra- DNA crosslinks:

A

DNA unwinding is prevented during replication –> double strand breaks

66
Q

Explain nucleotide mispairing:

A

Induce base mispairing –> genetic mutations –> non-functioning gene cells in tumour

67
Q

Explain nucleotide mispairing:

A

Induce base mispairing –> genetic mutations –> non-functioning gene cells in tumour

68
Q

Name a commonly used genotoxic agent class

A

Platinum based: cisplastin, carboplatin, oxaliplatin, doxorubicin analogs

69
Q

Name 4 common AEs of genotoxic agents

A

1) hematopoietic effects
2) GI
3) hair loss
4) increased risk of cancer development

70
Q

What are 3 types of antimetabolites?

A
  • Folate antagonists
  • Purine antagonists
  • Pyrimidine antagonists
71
Q

Methotrexate (folate antagonist) MOA:

A

Inhibits dihydrofolate reductase enzyme: forms purine and pyrimidine nucleotides for DNA synthesis –> without this, cell growth is blocked

72
Q

Pemetrexed (next generation antifolate) MOA:

A

Inhibits DHFR, thymidylate synthase, glycinamide ribonucleotide formyl transferase –> DNA, RNA synthesis is inhibited

73
Q

What can be used as an adjuvant to antifolate tx?

A

Folinic Acid

74
Q

What is the benefit of folinic acid as adjunctive tx?

A
  • Reduces myelosuppresion (dose limiting adverse rxn)

- Some DNA/RNA synthesis can be carried out in normal cells

75
Q

What are purines?

A

Chemicals used to build DNA/RNA nucleotides

76
Q

Purine antagonists MOA:

A

Prevent continued replication of DNA –> cell division

77
Q

What is the result of defects in thiopurine methyltransferase (TMPMT) gene?

A

Decreased metabolism of thiopurine drugs –> increased bone marrow toxicity –> myelosuppression, anemia, bleeding tendency, infection

78
Q

What are the 3 TMPT polymorphisms?

A
  • WT/WT: normal allele, extensive metabolizer
  • WT/MUT: intermediate metabolizer
  • MUT/MUT: poor metabolizer
79
Q

TPMT = deactivation pathway –> more active drug, increased toxicity

A

Has impt implications in leukemia and RA (bc causes IM and PM)

80
Q

Pyrimidine antagonists MOA:

A

Blocks pyramiding containing nucleotides’ synthesis

81
Q

5-FU (pryimidine antagonist) MOA:

A

Blocks thymidylate synthase

82
Q

5-FU Indication:

A

colorectal cancer

83
Q

What is the objective of hormonal therapy (G1 phase)?

A

to starve cancer cells form hormonal signals needed for growth

84
Q

What are 4 indications of hormonal therapy?

A

1) Breast cancer
2) Ovarian cancer
3) Endometrial cancer
4) Prostate cancer

85
Q

What are 3 types of hormonal antagonists?

A

1) Selective estrogen receptor modulators (SERMs)
2) Aromatase inhibitors
3) Selective androgen receptor modulators (SARMs)

86
Q

SERM MOA:

A

Inhibits estrogen’s growth stimulating factor

87
Q

Name 3 drugs that are SERMs

A

1) Tamoxifen
2) Raloxifene
3) Toremifene

88
Q

Which enzyme is responsible for tamoxifen metabolism?

A

cyp2d6

Pharmacology (9 decks)

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