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SBL 2 > Cancer Pharmacology > Flashcards

Cancer Pharmacology Flashcards

1
Q

What phase does the synthesis of the components needed for DNA syntesis occur?

A

G1

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2
Q

What stage does synthesis of DNA occur?

A

S

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3
Q

Where are the components that are needed for mitosis made?

A

G2

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4
Q

What are cell cycle specific agent examples?

A
  • Antimetabolites (S)
  • Epipodophyllotoxins (S-G2)
  • Antitumor Ab’s (G2-M)
  • Taxanes (M)
  • Vinca alkaloids (M)
  • Camptothecins (S)
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5
Q

What are the classes of cell cycle nonspecific agents?

A
  • Alkylating agents
  • Antimetabolites
  • Anthracyclines
  • Antitumor Abx
  • Platinum analogs
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6
Q

What are good examples of cancers that are curable in a small subset of patients?

A
  • Hodgkins
  • NHL
  • Choriocarcinoma
  • Germ cell cancer
  • AML
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7
Q

What are the curable childhood cancers?

A
  • Burkitt’s
  • Wilms’
  • Embryonal rhabdomyosarcoma
  • ALL
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8
Q

What is a growth fraction?

A
  • ratio of proliferating cells to G0 cells
  • Major determinant of responsiveness to chemotherapy
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9
Q

What does a high growth fraction indicate?

A
  • Very high rate of replication
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10
Q

What is the log cell kill hypothesis?

A
  • Antineoplastic therapy follows first order kinetics which means that a dose of a drug will destroy a constant fraction of cells
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11
Q

What does PGP do? How does it relate to drug resistance?

A
  • pharmacological barrier site, it “kicks” drugs out of the cell
  • High baseline experssion correlates with primary inherent resistance to natural productions
  • It can also be overexpressed leading to acquired drug resistance
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12
Q

What are the common AE that occur with nearly all classic antineoplastic agents?

A
  • Nausea
  • Vomit
  • Fatigue
  • Stomatitis
  • Alopecia
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13
Q

What are three pharmacological rescue agents that decrease adverse effects of cancer treatments?

A
  • Hematopoietic agents for neutropenia, thrombocytopenia, and anemia
  • Serotonin receptor antagonist ((Zofran)ondansetron) and other drugs for emetogenic effects
  • Bisphosphates to delay skeletal skeletal complications
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14
Q

What are two ex of Nitrogen mustard alkylating agents?

A
  • Cyclophosphamide
  • Ifosfamide
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15
Q

What are the five major types of alklyating agents?

A
  • Nitrogen mustards
    • cyclophosphamide
  • Nitrosureas
    • carmustine
  • Alkyl sulfonates
    • busulfan
  • Methylhydrazine derivatives
    • procarbazine
  • Triazines
    • dacarbazine
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16
Q

MOA for alkylating agents?

A

forms covalent linkages with DNA

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17
Q

What adverse effect does Acrolein cause and what inactivtes this drug?

A
  • Hemorrhagic cystitis
  • Mesna inactivates it and is used for prophylaxis of chemo iinduced cystitis
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18
Q

What adverse effects does Cyclophosphamide have?

A

Hemorrhagic cystitis

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19
Q

What AE does cisplatin (alkylating agent) have?

A
  • Renal tubular damage
  • Ototoxicity
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20
Q

What AE does Busulfan (alkylating agent) have?

A
  • Primalry fibrosis
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21
Q

What are the main categories of antimetabolites?

A
  • Folic acid analogs (methortrexate)
  • Pyrimidine analogs (5-fluorouracil)
  • Purine analongs ( 6-mercaptopurine)
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22
Q

Antimetabolite MOA?

A
  • Block pathways that lead to cell replication
  • Cell cycle specific
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23
Q

How does methotraxate work?

A
  • Looks like folic acid and when it comes in contact with dihydrogolate reductase it blocks it so we can’t form dTMP to help make DNA
    *
24
Q

Methotrexate AE? What is the rescue drug?

A
  • Mucosal ulceration
  • Leucovorin
    • doesn’t rescue cancer cells at high does methotrexate but does rescue healthy cells
25
Q

What is Fluorouracil?

A
  • Prodrug
  • FdUMP Covalently binds thymidylate synthetase and blocks de novo synthesis of thymidylate
26
Q

What is Mercaptopurine?

A
  • Metabolized by HGPRT to form monophosphate nucleotide 6-thioinosinic acid
  • Inactivated by xanthine oxidase in the first pass effect
  • Allopurinol inhibits xanthine oxidase, this is used as a supportive care in tx of acute leukemis to prevent hyperuricemia due to tumor cell lysis
    • This blocks the first pass effect
    • Reduce amount of 6-MP if giving Allopurinol
27
Q

What are the common toxicities of antimetabolites?

A
  • Diarrhea
  • Myelosuppression
  • N/V
  • immunosuppression
  • Thrombocytopenia
  • Leukopenia
  • Hepatotoxicity

Relatively little toxicity after initial dose

28
Q

What are the examples of natural antineoplastic agents?

A
  • Vinca alkaloids
    • vinblastine
    • vincristine
  • Taxane
    • paclitaxel
  • Epipodophyllotoxins
    • etoposide
  • Abx
    • doxorubicin
  • Antrhacenedione
    • Bleomycin
  • Enzyme
    • L-Asparaginase
29
Q

How do Vinblastine and Vincristine (vinca alkaloids) work?

A
  • Binds tubulin diners and inhibits microtubule assembly
  • Cell cycle specific to M phase
30
Q

AE of vinca alkaloids?

A
  • Alopecia and bone marrow depression
  • Vinblastine causes Myelosuppression greeater than vincristine
  • Vincristine causes cumulative neuro toxicities compared to vinblastine
31
Q

How do taxanes work?

A
  • Bind to B tubuline and stabilze microtubule formation
  • cell cycle specific to M phaase
32
Q

What were Paclitaxel and docetaxel used for in the past? AE?

A
  • Breast cancer tx before we knew about biologics
  • Pacitaxel
    • hypersens. rxn in hands and toes, change taste
  • Docetaxel
    • smaller dose and less side effects than pacitaxel
      • hypersens. neutropenia, hair loss
33
Q

Topoisomerase inhibitors?

A
  • Campthothecins such as topotecan and irinotecan inhibit topoisomerase I
  • Epipodophyllotoxins such as etoposide and teniposide, and the antrhacycline abx inhibit toposisomerase II
  • Cell cycle specific S and G1 and G2
34
Q

Why do anthracyclines such as doxorubicin lead to significant cardiotoxicity?

A

Due to production of free radicals

35
Q

MOA of anthracycliens (doxorubicin)?

A
  • Topoisomerase II inhibitor and DNA intercalation
  • Cell cycle non specific
36
Q

What is Bleomycin?

A
  • Antitumor abx
  • causes single and double stranded breaks
  • causes minimal myelosuppression
  • Causes significant pulmonary toxicity and presents as pneumonitis with cough dyspnea and crackles
37
Q

How does asparaginase work?

A
  • Hydrolyzes circulating L asparagine into aspartic acid and ammonia, inhibiting protein synthesis
  • Cell cycle specific to G1
38
Q

What can asparaginase be used to treat?

A
  • targeted therapy for ALL
39
Q

Asparaginase AE?

A
  • acute hypersensitivity rxns such as
    • fever
    • chills
    • N/V
    • skin rash
    • urticaria
  • Delayed:
    • risk of clotting and bleeding
    • pancreatitis
    • CNS toxicity such as lethargy confusion hallucination and coma
40
Q

What does the suffix “nib” indicate?

A
  • protein tyrosine kinase inhibitors that bind intracellulary
41
Q

What is Tretinoin used to treat and how does it work? What are the AE?

A
  • treats t(15;17) fusion protein PML-RARa which inhibits granulocytic maturation in APL
  • This binds the fusion protein and antagonizes the inhibitory effect allowing the neoplastic promyelocytes to differentiate into netrioophils that rapidly die
  • Vitamin A toxicity and retinoic acid syndrome are common AE
42
Q

What is imatinib used for?

A
  • BCR-ABL fusion protein that comes from a t(9;22) which is assoc. with CML
  • Imatinib targets the ABL tyrosine kinase and blocks it
43
Q

What is Erlotinib and gefitinib? AE and use?

A
  • Tyrosine kinase domain inhibitorys of EGFR
  • USed in non small cell lung cancer and pancreatic cancer
  • Produces dermatologic toxicities
44
Q

Ziv-aflibercept MOA?

A
  • Recombinant fusion protein made of extracellular domains of VEGF receptors 1 and 2 fused to the Fc portion of IgG1
  • this makes it a souble receptor for VEGF-A, VEGF-B and PIGF
  • Binding of VEGF ligands prevents interactions with VEGFR leading to inhibitiorn of VEGFR signaling
45
Q

How do tyrosine kinase and growth factor receptor inhibitors work? How are they resisted? What are the AE’s?

A
  • Inhibit GF receptor signaling
  • Inhibits tyrosine kinase activity
  • Point mutaitonss in drug binding sites allows for resistance
  • N/V and skin rash
46
Q

What are the biological response modifiers?

A
  • Agents that act indirectly to mediate their antitumor effects by ehancing immunologic response to neoplastic cells
  • Interferons and Interleukin 2 are examples
47
Q

How do interferons work and what are the AE?

A
  • Inhibits cell growth alters cellular differnetiation and interferes with oncogene expression, alters cell surface Ag expression and increases phagocytic activvity of macrophages
  • Bone marrow depression neutropenia, anemia, renal toxicity, ,edema, and arrhythmia
48
Q

How does interleukin2 work and its AE?

A
  • Increases cytotoxic killing by T and NK cells
  • Capillary leak syndrome
49
Q

Ritximab Ag, cancer, and antigen function?

A
  • CD20
  • NHL
  • Proliferation and differnetiation
50
Q

Alemtuzumab ag cancer and ag function?

A
  • CD52
  • Chronic lymphocytic leukemia
  • unknown ag function
51
Q

Gemtuzumab ag cancer and ag function?

A
  • CD33
  • AML
  • unknown ag function
52
Q

Trastuzumab ag, cancer, and ag function??

A
  • HER2/neu
  • Breast cancer
  • tyrosine kinase
53
Q

Cetuximab, ag, cancerm and ag function?

A
  • EGFR (ErbB-1)
  • Colorectal lung pancreatic and breast cancer
  • Tyrosine kinase
54
Q

Bevacizumab ag, cancer, and ag fxn?

A
  • VEGF
  • Colorectal and lung
  • Angiogenesis
55
Q

Ibritumomab and Tostiumomab ag, cancer and ag function?

A
  • CD20
  • NHL
  • Proliferation and differentaition
56
Q

What cancer are Nivolumab and pembrolizumab used to treat?

A
  • Malignant malanoma that is unresectable or metastatic

SBL 2 (9 decks)

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