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Chemotherapy Viruses > Chemotherapy V > Flashcards

Chemotherapy V Flashcards

1
Q

Define targeted therapy

A

Refers to a new generation of cancer drugs designed to interfere with a specific molecular target (typically a protein) that is believed to have a critical role in tumor growth or progression

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2
Q

Main target of targeted therapy

A

Main target of targeted therapy Tyrosine kinase

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3
Q

Two types of Tyrosine Kinase

A
  • Transmembrane protein with a ligand brining extracellular domain and a catalytic intracellular kinase domain (receptor)
  • Non membrane tyrosine domain (non-receptor)
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4
Q

Dysregulation of Tyrosine Kinase

A
  • Common mechanism of TK activation is the fusion of a partner protein with TK due to chromosomal translocation causing TK oligomerization in the absence of ligand binding or other signals
  • Mutation that disrupts autoregulation
  • increased or aberrant expression of a receptor TK
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5
Q

How is pharmacologic inhibition of tyrosine kinase achieved

A
  1. Small molecule inhibition of the catalytic activity of the kinase
  2. Antibodies against the receptor tyrosine kinases or a ligand of the receptor tyrosine kinase
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6
Q

Class of Imatinib mesylate

A

Tyrosine kinase inhibitor

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7
Q

Macromolecular target of Imatinib mesylate

A

Bcr-Abl fusion protein (9,22 translocation)

c-kit (constitutive phosphorylation)

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8
Q

MOA of Imatinib mesylate

A

Inhibits critical signaling pathways in the cancer cell that are constitutively active
-Binds in the Bcr-Abl ATP pocket to shut down proliferation

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9
Q

Metabolism of Imatinib mesylate

A

Metabolized in the liver by the CYP3A4 system and excreted into the feces by the hepatobiliary system

Avoid coadministration with inducers (St. John’s Wort) and inhibitors of the pathway-other drugs and grapefruit juice

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10
Q

SEs of Imatinib mesylate

A

Superficial edema, nausea, muscle cramps, abdominal pain, musculoskeletal pain, rash, diarrhea, anemia, neutropenia, thrombocytopenia
Rarely, CHF

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11
Q

Administration of Imatinib mesylate

A

Oral administration

Chronic, daily

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12
Q

Consideration of patients with hypothyroid taking Imatinib mesylate

A

Monitor thyroid function

Imatinib may increase the clearance of thyroid hormone and the dose of thyroid medication may have to be increased

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13
Q

Uses of Imatinib mesylate

A

Chronic myelogenous leukemia (Bcr-Abl oncogene addiction dependence for cell survival)
GI stromal tumor (c-kit)

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14
Q

Outcome of Imatinib therapy

A

Resistance will develop and therapy is not known to be curative at the present time
Eradicate Bcr-Abl cells from detection

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15
Q

Other compounds in the same class as Imatinib mesylate

A

Dasatinib and nilotinib (useful in imatinib resistant disease)

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16
Q

Class of Cetuximab

A

Epidermal growth factor receptor (EGFR) inhibitor

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17
Q

Macromolecular target of Cetuximab

A

EGFR

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18
Q

MOA of Cetuximab

A

Overexpression of EGFR receptors leads to increased signaling and affects cell growth and division and metastases and invasion
Also can sensitize cell to effect of chemotherapy and can be used as a radiation therapy sensitizer

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19
Q

SEs of Cetuximab

A 
Hypersensitivity reactions
Rash (seen in most targeted therapy) 
Diarrhea
Hypomagnesemia
Infusion reactions 
Tichomegaly: long eye lashes
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20
Q

Administration of Cetuximab

A

Chimeric monoclonal antibody administered IV weekly or every other week usually in combination with chemotherapy

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21
Q

Uses of Cetuximab

A
  1. Lung CA and head and neck CA (patients not selected based on EGFR expression or kras mutational status)
  2. Colo-rectal cancer (metastatic): perform k-ras mutational analysis on tumor (wildtype responds)
    If k-ras/ n-ras is mutated (independent of EGFR), patient will not respond to cetuximab
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22
Q

Class of Panitumumab

A 
Fully humanized monoclonal antibody
In same class as Cetuximab
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23
Q

Class of Erlotinib

A

Small molecule inhibitor of the tyrosine kinase domain associated with EGFR

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24
Q

Macromolecular target of Erlotinib

A

Tyrosine kinase domain associated with EGFR

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25
Q

MOA of Erlotinib

A

Inhibition of critical cell signaling pathways

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26
Q

Metabolism of Erlotinib

A

Metabolized by CYP3A4- avoid coadministration with inducers

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27
Q

SEs of Erlotinib

A

Rash, nausea, anorexia and fatigue, nail changes

28
Q

Administration of Erlotinib

A

Oral

29
Q

In what case must mutational analysis be done on the tumor before using Erlotinib

A

Non-small cell lung cancer should have mutational analysis done on the tumor - if there are activating mutations observed the treatment of choice is ertolinib

30
Q

Uses of Erlotinib

A

Lung CA (esp adenocarcinomas non-small cell with EGFR activating mutations), head and neck CA, pancreas cancer (in combo with gemcitabine)

31
Q

Effect of EGFR activating mutations

A

Make cancer cell more sensitive to TK inhibitors

32
Q

Prototype patients with EGFR activating mutations

A

Prototype patients with EGFR activating mutations Adenocarcinoma, bronchoalveolar
Women
Asian
Never smokers

33
Q

Class of Bevacizumab

A

Inhibitor of vascular endothelial growth factor (VEGF)

34
Q

Macromolecular target of Bevacizumab

A

Vascular endothelial growth factor ligand

35
Q

MOA of Bevacizumab

A

Binds to VEGF ligand and decreases the growth of primary cancers and metastatic cancers due to impaired vasculature formation in the tumor

36
Q

SEs of Bevacizumab

A

Infusion reactions, proteinuria, HTN, arterial clots, bleeding, perforation of the colon, reversible posterior leukoencephalopathy syndrome is rare (seizures, headache, mental status changes, visual changes and findings on MR of the brain)

37
Q

Administration of Bevacizumab

A

IV

Must be combined

38
Q

Uses of Bevacizumab

A

Lung CA and metastatic colorectal cancer

39
Q

List the VEGF inhibitors

A

Bevacizumab
Sorafenib
Pazopanib
Sunitinib

40
Q

Oral VEGF inhibitors

A

Sorafenib
Pazopanib
Sunitinib

41
Q

SEs of oral VEGF inhibitors

A 
Rash
Hand-foot syndrome
HTN
Reversible posterior leukoencephalopathy syndrome
Perforation of the GI tract
CHF
42
Q

Uses of oral VEGF inhibitors

A

Renal cell cancer (clear cell variety)

43
Q

Use of Sorafenib

A

Renal cell cancer (clear cell variety)

Hepatocellular cancer

44
Q

Use of Sunitinib

A

Renal cell cancer (clear cell variety)
Pancreatic neuroendocrine cancer
GI stromal tumors

45
Q

Effect of VEGF inhibitors

A

None are curative

46
Q

Class of Trastuzumab

A

Monoclonal antibody

47
Q

Macromolecular target of Trastuzumab

A

Extracellular domain of epidermal growth factor receptor

Her-2/neu

48
Q

MOA of Trastuzumab

A

Binds to the extracellular domain of the epidermal growth factor receptor and decreases signaling pathways

49
Q

SEs of Trastuzumab

A
  1. Fever, nausea, vomiting, infusion reactions, diarrhea, cough, headache, fatigue, shortness of breath, back pain, rash and muscle pain; allergic reactions
  2. Heart failure (high if also given doxorubicin) - asymptomatic decline in EF (NOT CUMULATIVE and reversible)
50
Q

Administration of Trastuzumab

A

IV weekly

51
Q

Uses of Trastuzumab

A

Breast cancer in combo with chemo when Her2/neu +

Stomach and gastroesophageal junction cancer in combo with chemo when Her2/neu +

52
Q

MOA of lapatinib

A

Small molecule tyrosine kinase inhibitor of Her-2 family

53
Q

MOA of pertuzumab

A

Monoclonal antibody binds to Her-2

54
Q

Use of Crizotinib

A

Patients with ALK-anaplastic lymphoma kinase rearrangements had adenocarcinoma, tended to be younger and had little or no exposure to smoke

60% response rate
33% stable disease

Perform mutational analysis on lung cancer patients for ALK rearrangement

55
Q

Use of Vemurafenib

A

40-60% of patients with melanoma have an actvating mutation in the gene encoding for BRAF (V600E) -> constitutively active phosphorylation and downstream signaling

Inhibits mutated BRAF

56
Q

MOA of Asparaginase

A
  • Bacterial product

- Hydrolyzes L-asparagine -> tumor cells lack asparagine synthetase and protein synthesis is inhibited

57
Q

Toxicities of Asparaginase

A

Immunologic sensitization and depletion of asparagine pools
Allergic reactions
Clotting and bleeding (conc. of clotting factors and AT II dec.)
Pancreatitis, hyperglycemia and mental status changes
Liver enzyme abnormalities

58
Q

Use of Asparaginase

A

ALL

59
Q

MOA of hydroxyurea

A

Analog of urea that inhibits DNA synthesis by inhibiting ribonucleotide reductase

60
Q

Administration of hydroxyurea

A

Oral

61
Q

Main use of hydroxyurea

A

Treatment of high WBC counts in patients with AML and chronic granulocytic leukemia with blast crisis

62
Q

SEs of hydroxyurea

A

Leukemia blasts in high #s can cause sludging in the vasculature leading to thromboses
Nausea and vomiting
Low blood counts
Rash

63
Q

MOA of All trans retinoic acid (tretinoin)

A

Induces terminal differentiation of the leukemic cells

64
Q

Use of All trans retinoic acid (tretinoin)

A

Combination with chemo for patients with acute promyelocytic leukemia (APL, M3)

65
Q

SEs of All trans retinoic acid (tretinoin)

A

Dry skin and dry mucus membranes

Retinoic acid syndrome consisting of fever, weight gain, pulmonary infiltrates and pleural or pericardial effusions

66
Q

Use of Arsenic Trioxide

A

Treatment of relapsed APL (acute promyelocytic leukemia)

67
Q

SEs of Arsenic Trioxide

A

Fatigue, QT prolongation

Syndrome similar to retinoic acid syndrome

Chemotherapy Viruses (5 decks)

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