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Y3 PPNP Finals > Onco Drugs > Flashcards

Onco Drugs Flashcards

1
Q

What are the 3 basic concepts of chemo?

A
  1. Skipper Schabel Model of Tumor Growth
  2. Gomportzian Model of Tumor Growth
  3. Goldie-Coleman Hypothesis
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2
Q

What does Skipper Schabel Model of Tumor Growth believe in?

A
  1. Chemo agents shd kill all abnormal cell but spare host - (x) exhibit AE to host
  2. % of in vivo leukemia cell population of various sizes killed by given dose of a given drug is reportedly constant/directly proportional
    • every 5mg drug given = 20% cells killed
    • every 10mg drug given = 40% cells killed
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3
Q

What does Gomportzian Model of Tumour Growth believe in?

A
  1. Growth rate decreases with time
  2. Maximal response for chemo is during rapid growth stage
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4
Q

What does Goldie-Coldman Hypothesis believe in?

A
  1. A fraction of tumor cells will develop resistance after tx
  2. Clone will continue to grow even tho pt appears to respond
  3. Key feature: Alternating combi of chemo agents early in tx with non overlapping MOA
    • necessary to prevent development of resistant clones
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5
Q

What are the different kinds of groups of medications is for chemo?

A
  1. Cell cycle specific agents
  2. Cell cycle non-specific agents
  3. Molecular targeted therapy
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6
Q

What are some examples of cell cycle non specific agents?

A
  1. Alkalyting agents
  2. Anthracycline antibiotics
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7
Q

What are the examples of alkaylating agents

A
  1. Cyclophosphamide
  2. Thiotepa
  3. Busulfan
  4. Carmustine
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8
Q

What is the MOA of alkylating agents

A

Alkylate within DNA @ nitrogen 7 position of guanine
|
Miscode through
1. Abnormal base pairing with thymine
2. Depurination by excision of guanine residues
(Miscoding of genes and production of defective genes)
|
Strand breakage
(Cross linking of DNA and ring cleavage may also occur)

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9
Q

What are the examples of anthracycline abx

A

Anything that ends with rubicin

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10
Q

What is the MOA of anthracycline abx

A
  1. Inhibit DNA & RNA synthesis by intercalating between base pairs of DNA/RNA strand
    • prevent replication of rapidly growing/dividing Ca cell
  2. Inhibiting topoisomerase II enzyme
    • prevent relaxing of supercoiled DNA
    • inhibit DNA transcription and replication
  3. Create free O2 radical
    • damage DNA and cell membrane
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11
Q

What are the side effects of anthracycline abx

A
  1. Cardiotoxicity
  2. Alopecia
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12
Q

What are some examples of cell cycle specific agents?

A
  1. Plant alkaloids
    a) Vinca alkaloids
    b) Taxanes
  2. Antimetabolites
    a) Folic acid analogue
    b) Pyrimidine antagonist
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13
Q

What stage of the cell cycle does vinca alkaloids start on

A

M phase

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14
Q

What are some examples of vinca alkaloids

A

Starting with Vin - Vinblastine, Vincristine etc

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15
Q

What is the MOA of Vinca Alkaloids?

A

Bind to microtubular protein tubule in dimetric form
|
drug-tubulin complex binds to forming end of micro tubules = terminate assembling
|
Deploymerisation of microtubule
|
Mitotic arrest at metaphase + dissolution of mitosis spindle + interfere with chromosome segregation

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16
Q

What are some examples of taxanes

A
  1. Paclitaxel
  2. Docetaxel

Anything that ends with taxel

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17
Q

What is the MOA of taxane

A

Interfere with normal function of microtubule breakdown
|
Hyperstabilise microtubule structure

Specifically binds to Beta subunit of tubulin
|
Result in microtubule/paclitaxel complex = (x) ability to disassemble

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18
Q

Why does plant alkaloids like vinca alkaloids and taxanes adversely affect cell function

A

Shortening/assembling and lengthening/disassembling of microtubules (DYNAMIC INSTABILITY) is needed for functions as a mechanism to transport other cellular compounds

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19
Q

What are the uses for plant alkaloids

A
  1. Lung Ca
  2. Breast Ca
  3. Ovarian Ca
  4. Head Ca
  5. Nexk Ca
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20
Q

What are the adverse effects of plant alkaloids

A
  1. Myelosuppression
  2. Alopecia
  3. Neuropathy
  4. Allergies
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21
Q

What is an example of folic acid analogue

A

Methotrexate (MTX)

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22
Q

What is an example of folic acid analogue

A

Methotrexate (MTX)

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23
Q

What is folate

A

An essential dietary fibre

  • Trihydrofolate (THF) cofactors are formed to provide single carbon groups for synthesis of precursors of DNA & RNA
  • to function as a cofactor folate: need to reduce to THF by dihydrofolate predicate (DHFR)
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24
Q

What is the primary site of action for MTX

A

DHFR

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25
Q

What is the MOA of MTX

A

Prevents formation of DHFR
|
Intracellular deficiency of folate coenzymes + accumulation of toxic inhibitory substrate (DNA polyglutamate)
|
One carbon turf reactions for purine and thymine synthesis cease
|
DNA & RNA synthesis impaired

26
Q

What are the indications for MTX

A
  1. Psoriasis
  2. RA
  3. Acute lymphoid leukemia
  4. Choriocarcinoma
  5. Meningeal leukemia
  6. Osteosarcoma
  7. Myosis fungoids
  8. Burkitts lymphoma
  9. Hodgkin’s lymphoma
  10. Breast Ca
  11. Bladder Ca
  12. Head & Neck Ca
  13. Ovary Ca
27
Q

What are the AE for MTX

A
  1. Bone marrow suppression (leucovorin/folinic acid as rescue)
  2. Nephrotoxic (give NaHCO3 to alkalinise urine)
28
Q

What are the examples of pyrimidine antagonist

A
  1. Fluorouracil/5-FU
  2. Gemcitabine
29
Q

What stage of the cell cycle does fluorouracil/5-FU act on

A

S phase

30
Q

What is the MOA of 5-FU

A

inhibit thymidylate synthase
|
Thymidylate depletion
|
Inhibit DNA synthesis/RNA processing

31
Q

When is 5-FU used

A
  1. Metastatic carcinomas of breast & GIT
  2. Hepatoma
  3. Carcinomas of ovary, cervix, prostate, bladder, pancreas and oropharyngeal areas
32
Q

What are the AE of 5-FU

A
  1. Myelosupression
  2. Mucositis
  3. Dermatitis
  4. Diarrhoea
  5. Cardiac toxicity
33
Q

What type of antimetabolite is gemcitabine

A

Deoxycytidine

34
Q

What does gemcitabine convert to

A

Gemcitabine to Gemcitabine monophosphate with deoxycytidine kinase

Then phospholyated to Gemcitabine diphosphate and Gemcitabine triphospate

35
Q

What is the MOA for Gemcitabine

A

1.
Gemcitabine triphosphate compete with deoxycytidine triphosphate to incorporate into DNA strands
|
Base pair will be added before DNA polymerase stops
|
Inhibit DNA replication and repair
|
Gemcitabine induced apoptosis/cell death

2.
Gemcitabine diphosphate bind to ribonucleotide predicate (RNR)
|
Inactivate RNR reversibly
|
Cell (x) deoxyribonucleotide needed for DNA synthesis
|
Induce apoptosis

36
Q

When is Gemcitabine used

A
  1. Pancreatic cancer
  2. Small cell lung Ca
  3. Carcinoma of bladder, breast, kidney, ovary, head and neck
37
Q

What are the AE of Gemcitabine

A
  1. Neutropenia
  2. N & V
  3. Fever
38
Q

What does molecular targeted therapies do

A
  1. Block growth and spread of Ca - interfere with specific oncogene molecules involved in tumor growth and progression
  2. Focus on molecular and cellular changes specific to Ca
    • may be more effective than other tx + less harmful to normal cells
  3. Can be used alone/in combi with chemo/other targeted therapies
39
Q

What are the example of molecular targeted therapies

A
  1. Small molecule inhibitors (erlotinib, geftinib, bortezumab, sorafenib)
  2. Monoclonal antibodies (cetuximab, bevacizumab)
40
Q

What is erlotinib and geftinib used for

A

Non small cell lung ca

41
Q

What is the classification of erlotinib and geftinib

A

Epithelial growth factor receptor (EGFR) tyrosine kinase inhibitor

42
Q

What is the MOA for erlotinib and geftinib

A

Bind to ATP binding site of EGFR
|
Block activity of EGFR tyrosine kinase
|
Block activation & downstream signalling responsible for cell proliferation and survival

43
Q

What is the class of Bortezomib

A

Proteasome inhibitor

44
Q

What does bortezomib treat

A

Multiple myeloma and mantle cell lymphoma

45
Q

What is the MOA of bortezomib

A

Bind to 26S proteasome in cell
|
Normal homeostatic mechanisms to maintain protein balance and function disrupted
|
Accumulation of protein in cell

46
Q

What is the class of sorafenib

A

Multikinase inhibitor

47
Q

What does sorafenib treat

A

Advanced renal cell carcinoma, hepatocellular carcinoma, thyroid carcinoma

48
Q

What is the MOA of sorafenib

A

Target several receptor tyrosine kinase (RTKs) involved in tumor growth and angiogenesis
- vascular endothelial growth factor receptor (VEGFR-2 & VEGFR-3)
- platelet-derived growth factor receptor (PDGFR-Beta)
|
Block signalling pathway that promote tumor blood vessel formation/angiogenesis

49
Q

What are the examples of monoclonal antibodies

A
  1. Cetuximab
  2. Bevacizumab
50
Q

What is the MOA for cetuximab

A

Bind to extracellular EGFR - inhibit dimerization of EGFR
|
Block binding of receptor natural ligands
|
Prevent receptor from undergoing conformational changes req for activation

51
Q

What is the MOA for bevacizumab

A

Inhibit VEGF
|
Decreased blood supply to tumors
|
Limit growth and ability to spread

52
Q

What are the limitations/challenges to good response to targetted therapy

A
  1. Pathway dependence
  2. Tumor heterogeneity
  3. Resistance
  4. AE
  5. Neutralisation (of biological drugs)
53
Q

What are the treatments for classical Hodgkin lymphoma

A

Brentuximab vedotin, nivolumab & pembrolizumab

54
Q

What class of drug is brentuximab vedotin

A

CD30 antibody-drug conjugate + potent microtubule inhibitor monomethyl auristatin E (MMAE)

55
Q

What is the MOA of brentuximab vedotin

A

Internalised once binded to CD30
|
MMAE released with action of lysozomal enzymes on linker

56
Q

What is the class for nivolumab and pembrolizumab

A

PD1 inhibitor/anti PD1 antibody

57
Q

What is the MOA of nivolumab and pembrolizumab

A

Bind to PD1 on T cell
|
Block PDL1/PD1 mediated immune checkpoint signalling
|
Reactivation of T cell that exert cytotoxic function against HRS cell
+
Release immune cells from pathological immune suppression (NIVOLUMAB) = recognition and counter tumor cell

58
Q

What are the treatment for non Hodgkin lymphoma

A
  1. CHOP therapy
  2. Rituximab
59
Q

What does CHOP therapy consist of

A
  1. Cyclophosphamide (alkalyting agents)
  2. Doxorubicin (anthracycline abx)
  3. Vincristine (Vinca alkaloids)
  4. Prednisone (anti inflammatory)
60
Q

What is the class for rituximab

A

Monoclonal antiCD20 antibody

61
Q

What is the MOA for rituximab

A

Bind to CD20
|
Cell lysis

62
Q

What are the 4 mechanisms responsible for elimination of CD20 cell

A
  1. Antibody dependent cellular cytotoxicity (ADCC)
  2. Antibody dependent cellular phagocytosis (ADCP)
  3. Complement dependent cytotoxicity (CDC)
  4. Direct anti tumor effects (apoptosis/other cell death pathways)

Y3 PPNP Finals (6 decks)

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