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Flashcards in Drugs- Cancer Deck (38):
1

CCS

Cell cycle specific drugs- antimetabolites, topoisomerase inhibitors, microtubule poisons

2

CCNS

Cell cycle non specific- alkylating agents, antitumor abx
Most effective against rapidly cycling cells

3

Myelosuppression

Delayed effect; leukopenia, neutropenia, thrombocytopenia; risk of infxn; tx with G-csf, gm-csf, platelet transfusion

4

Alkylating agents

covalently bind to/modify biological molecules
-DNA key target
-Must be reactive
CCNS
-Target rapidly growing cells
-Monitor pts with CBC and hematocrit
-Can cause secondary malignancy

5

Mechlorethamine


-Alkylating agents
IV (in arterial supply to tumor), short half life. Subq causes necrosis.
-Highly reactive
-Primary use in hodgkin's lymphoma

6

Cyclophosphamide

-Alkylating agents
Oral or IV
-Activated by host metabolism
-Used in leukemias and lymphomas and mor e
-BM depression, alopecia, hemorrhagic cystitis (sterile)

7

Ifosfamide

Alkylating agents
-Analog of cyclophosphamide
-IV only
-Hodgkin's and non-hodgkin's
-BM depression (more than cyclophosphamide)
-PN, UT toxicity, CNS effects

8

Melphalan

Alkylating agents
-Highly reactive
-Primarily IV
-Renal excretion
-Marked myelosuppression
-Multiple myeloma, myeloablation

9

Chlorambucil

Alkylating agents
-1.5 hr 1/2 life
-Primary used for CLL, now not used much

10

Busulfan

Alkylating agents
-Alkylsulfonate
-Oral, IV for high dose
-Prior to imatinib, busulfan was key for CML
-Profound myelosuppression, PF, hepatic veno-occlusive disease

11

Bendamustine

Alkylating agents
-Alkylates DNA and inhibits mitotic chekcpts
-CLL, B-cell non-hodgkin's lymphoma
-Typical alkylating agent AE: nausea, vomiting, myelosuppression

12

Dacarbazine

Alkylating agents
-IV, hepatic metabolism, delayed myelosuppression
-Hodgkin's lymphoma, MM

13

Procarbazine

Alkylating agents
-Oral, inhibits DNA, RNA, proteins synthesis by causing strand breaks
-HIgher potential for secondary malignancy than with other alkylating agets
-Hodgkins and non-hodgkins

14

Antimetabolites

-analog of normal component of target cell
-Blocks metabolic pathway after entering
-Folate analogs, purine analogs, pyrimidine analogs

15

Methotrexate

-Antimetabolite
-DHFR substrate and inhibitor
-Tumor cells more sensitive
-Blocks production of bases for DNA synthesis
-IV, oral, intrathecal
-High dose followed by rescue with folinic acid
-Anti folate effects in bone marrow and GI
-Resistance- amplified DHFR, altered DHFR

16

6- MP, 6-TG

-Purine analogs
-Oral
-Bone marrow depression at high doses
-Blocks DNA and RNA synthesis (6MP inh AMP and GMP synthesis, 6TG incorporated into RNA and DNA)
-Resistance from dec hprt activity or dec in alk phos

17

Fludarabine

-Purine analog
-IV or oral as monophosphate
-Triphosphoate inh DNA polymerases and ligase, inc into RNA and DNA
-CLL
-Myelosuppression, nausea, vomiting

18

Cladribine

-Purine analog
-IV
-Activated by deoxycytidine kinase and triphosphate inc into DNA causing strand breaks
-Hairy Cell leukemia, CLL, low grade lymphoma
- Bone marrow suppression is dose limited toxicity

19

Cytarabine

-Pyrimidine analog
-IV or intrathecal
-Activated by deoxycytidine kinase
-Triphosphate incorportated into DNA
-AML, ALL
-Far more toxic than purines

20

Antitumor abx

-Produced by microbes (streptomyces)
-Intercalate with DNA and or RNA and block access to/function of
-IV

21

Doxorubicin, Daunorubicin, idarubicin

-Anthracyclines
-Intercalate into DNA
-Block topoisomerase II, inh DNA and RNA synth, cause strand breaks
-IV, metabolized in liver
-BM suppression, alopecia
-Cardiotoxicity (cumulative dose)
-Idarubicin less cardiotoxic
-Minimize by adminstering dexrazoxane

22

Bleomycin

-abx
-Binds DNA, generates radicals and causes strand breaks
-Active in G2 (CCS)
-HSN, cutaenous rxn, pulm tox, fibrosis

23

MT poisons- Vinca

inhibits, reverses tubulin polymerization, causes metaphase arrest
-IV
-BIliary excretion

24

Vinblastine

-MT poisin
-Nausea, vomiting, aloopecia, bone marrow depression

25

Vincristine

-MT oison
-Same as vinblastine, but less toxic to BM, no nausea and vomiting
-Peripheral neuropathy

26

Etoposide

Topoisomerase inh
-CCS
-Arrests cells in S-G2 stage
-Oral and IV
-Nausea, alopecia, bm sup

27

Asparaginase

-biologic antineoplastics
-break down of asparagine
-inh growth of ALL cells
-Allergic response, enhances coag

28

Rituximab

-Mab blocks CD20
-IV, 1/2 life 22 days
-B cell lymphomas- CLL, non-hodgkin's

29

Dexamethasone, prednisone

-Adrenocorticosteroids
-Suppress prolif of immune cells
-Oral
-Leukemias and lymphomas
-Fluid retention, immunosuppression, diabetes

30

Imatibin

-TKI
-Inh bcr-abl and c-kit
-Blocks GF signaling in CML
-Myelosuppressive
-Edema, fluid retention, hepatotox

31

Dasatinib, nilotinib

-Newer TKI
-Turns cancer from curable to managable disease
Tx cont until resistance or death

32

Ibrutinib

-Inhibits bruton's tyrosine kinase
-Metabolized by CYP3A4 to become more potent
-Mantle cell lymphoma, relapsed/refractor CLL
-AE: GI, thrombocytopenia, neutropenia, infxn, fatigue

33

Idelalisib

-TKI
-PI3K inhibitor
-Relapsed CLL/SLL, relapsed follicular B cell non-hodgkin's lymphoma
-Hepatotoxicity, diarrhea, pneumonitis, intestinal perforation

34

Bortezimib

-Proteasome inh
-Leads to apoptosis
-IV
-MM, mantle cell lymphoma
-Thrombocytopenia, fatigue, peripheral neuropathy
-Hypotension upon infusion

35

ATRA

-Differentiating agent, end proliferation
-Binds to RAR-a receptor
-APL
-Resistance through enhanced clearance or loss of expression of fusion gene

36

Arsenic trioxide

-Differentiating agent
-Promotes modification and degradation of APL fusion protein
-CYtotoxic

37

Lenalidomide

-CLL, MM
-Lacks teratogenic effects of thalidomide
-May inh effects of rituximab

38

Mesna

-Given to diminish or lower AE of cyclophosphamide to prevent hemorrhagic cystitis