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Oncology > Cancer Pharmacology > Flashcards

Cancer Pharmacology Flashcards

1
Q

Adjuvant therapy

A

Eradicate residual cancer AFTER primary surgery

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2
Q

Neoadjuvant therapy

A

Shrink large, locally advanced disease to enable surgical resection

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3
Q

Induction therapy

A

The first treatment given for a disease
-aims to achieve a rapid reduction in tumor burden or disease activity

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4
Q

Consolidation therapy

A

Post-remission therapy to eradicate any remaining disease

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5
Q

Maintenance therapy

A

Administered to prevent cancer from recurring

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6
Q

Palliative therapy

A

Increase survival and improve quality of life by symptom control for advanced, incurable cancer

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7
Q

Cycle

A

A period of chemotherapy treatment followed by a period of rest (holiday)

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8
Q

What does the length of time between cycles depend on?

A
  • May give therapy more frequently to enhance tumor effects BUT increases toxicity
  • Balance with dose-limiting toxicities
  • Also determined by pharmacokinetics of drugs
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9
Q

Alkylating agents

A
  • MOA: Via crosslinking guanine in DNA double-helix strands
  • DNA damage
  • Ex: Cyclophosphamide
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10
Q

Antitumor Antibodies

A
  • MOA: Via DNA intercalation
  • DNA damage
  • Ex: Anthracyclines (Doxorubicin - lymphoma, leukemia, breast, ovarian & Daunorubicin - leukemia), Bleomycin - lymphoma
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11
Q

Topoisomerase inhibitors

A
  • Blocks DNA strand re-ligation during DNA synthesis
  • DNA synthesis
  • Ex: Irinotecan
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12
Q

Antimetabolites

A
  • MOA: Are incorporated into DNA or RNA and inhibit nucleic acid synthesis
  • DNA synthesis
  • Ex: Folic acid, pyrimidine, or purine analogs - methotrexate, mercaptopurine, 5-FU
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13
Q

Microtubule inhibitors

A
  • MOA: Inhibit tubulin polymerization or function
  • Translation/cell division
  • Ex: Paclitaxel
  • Breast cancer
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14
Q

Nutrient deprivation

A
  • MOA: Inhibition of protein synthesis
  • Translation/cell division
  • Ex: Asparaginase
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15
Q

Hormonal agents

A
  • MOA: Receptor antagonist. Attenuating estrogen/androgen production (growth signal)
  • Targeted therapies (“go” signals)
  • Ex: Tamoxifen, degarelix
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16
Q

Epigenetic agents

A

-MOA:
* HDAC inhibitor - blocks deacetylation by HDAC and restores expression of tumor suppressor genes
* DNMT inhibitor - blocks methylation of promoters and restores expression of tumor suppressor genes
* Targeted signals (“go” signals)
* Ex: Vorinostat, azacitidine

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17
Q

Angiogenesis inhibitors

A
  • Target VGEF secreted by cancer cells or VEGFR
  • Ex: Carfilzomib
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18
Q

CDK4/6 inhibitors

A
  • MOA: Prevents phosphorylation of Rb
  • Ex: Ribociclib
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19
Q

PARP inhibitors

A
  • MOA: Prevents double-stranded DNA damage repair in BRCA-deficient cells
  • Ex: Olaparib
  • Activated by DNA damage
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20
Q

What are the three groups of alkylating antineoplastic agents?

A
  • Nitrogen mustards (cyclophosphamide)
  • Nitrosoureas (carmustine)
  • Non-classic alkylating agents (cisplatin)
21
Q

What is the mechanism of action of Anthracyclines?

A

Topoisomerase inhibitors

22
Q

Chromomycins

A

Binds to DNA and inhibit RNA translation

23
Q

Bleomycin

A

Induces DNA strand breaks

24
Q

Camptothecins

A
  • Topoisomerases I inhibitor
  • Inhibits strand resealing
  • Irinotecan (colorectal, lung) and topotecan (ovarian)
25
Q

Epipodophyllotoxins

A
  • Etoposide (lymphoma, lung, ovarian)
26
Q

What is the more detailed MOA of antimetabolites?

A
  • Induce cell death during the S phase of cell growth when incorporated into RNA and DNA or inhibit enzymes needed for nucleic acid production
  • NOT selective for cancer cells
27
Q

Cytarabine (Ara-C)

A

Leukemias

28
Q

Fluorouracil (5-FU)

A

Colorectal cancer

29
Q

Capecitabine

A

Colorectal

30
Q

Gemcitabine

A

Lung, breast, and ovarian cancers

31
Q

Trifluridine and tipiracil

A

Colorectal cancer

32
Q

What are some microtubule inhibitors?

A
  • Eribulin
  • Taxanes (Paclitaxel, cabazitaxel, docetaxel)
  • Vinca Alkaloids (vincristine)
33
Q

Eribulin

A

Breast cancer

34
Q

Taxanes (Paclitaxel, Cabazitaxel, Docetaxel)

A

Breast, lung, ovarian, and prostate cancer

35
Q

Vinca alkaloids (vincristine)

A

ALL, lymphoma, and lung cancer

36
Q

Epigenetics

A

Changes in gene expression that occur without altering DNA sequence

37
Q

CpG islands

A

CpG island are regions with a high frequency of CpG sites

38
Q

Histone modifications

A

A covalent post-translational modification to histone proteins which includes methylation and acetylation

39
Q

DNA methyltransferase (DNMT)

A

Enzymes that catalyze the transfer of a methyl group to DNA

40
Q

Histone acetyl transferase (HAT)

A

Enzymes that acetylate conserved lysine amino acids on histone proteins

41
Q

Histone deacetylase (HDAC)

A

Enzymes that remove acetyl groups

42
Q

What are the several stages in which signal transduction can be inhibited?

A
  1. mAb against the growth factor receptor
  2. mAb against a growth factor
  3. Targeted drugs that inhibit intracellular kinases and prevent subsequent activation of downstream signals
  4. Targeting downstream signals
  5. Targeted therapies can be designed for mutated or WT protein
43
Q

What are the targeted therapies are available for tumors harboring certain mutations?

A
  • Imatinib
  • Dastinib
  • Nilotinib
  • Ponatinib
  • Dabrafenib
  • Vemurafenib
  • Erlotinib
  • Afatinib
  • Gefitinib
  • Osimertinib
  • Lapatinib
  • Cetuximab
  • Panitumumab
44
Q

What is the G1 phase checkpoint regulated by?

A

Cyclin D1 and CDK4/6

45
Q

-tinib

A

tyrosine kinase inhibitor

46
Q

-zomib

A

proteosome inhibitor

47
Q

-ciclib

A

cyclin-dependent kinase inhibitor

48
Q

-parib

A

poly ADP-ribose polymerase inhibitor

Oncology (14 decks)

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