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Antineoplastics Natural Products Flashcards

1
Q

What are your Microtubule-damaging agents(microtubule inhibitors)?

A

Vinca alkaloids and Taxanes, Estramustine, Epothilones

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1
Q

Vinca Alkaloids?

A

Vinblastine, Vincristine, Virnorelbine, Eribulin

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2
Q

Taxanes?

A

Paclitaxel, Docetaxel

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3
Q

Camptothecin Analogues

A

Topetecan, Irinotecan

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4
Q

Epipodophyllotoxins

A

Etoposide, Teniposide

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5
Q

Nature-derived?

A

L-Asparaginase, Hydroxyurea, Retinoids, Arsenic Trioxide, Mitotane

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6
Q

Plant derived drugs?

A

Microtubule damaging agents, Camptothecins, epipdophyllotoxins

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7
Q

In the M phase?

A

cell growth and protein production stops
Division of two daughter cells (chromosome seperation)

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8
Q

What do mitotic inhibitors do?

A

interfere with assembly and disassembly of tubulin into microtubule polymers-> inhibits mitosis->Apoptosis

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9
Q

Which drug class disrupts microtubule polymerization?

A

Vinca alkaloids

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10
Q

Which drug class stabilizes microtubule formation (inhibiting microtubule de-polymerization)

A

Taxanes

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11
Q

Vinca Alkaloids work in which phase of cell cycle?

A

Cell cycle specific for M Phase

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12
Q

Vinca Alkaloids MOA?

A

binds to B-tubulin and blocks polymerization with a-tubulin into microtubules–> prevents mitotic spindle formation –>interrupts chromosome aligning and cell division arrests–>apoptosis

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13
Q

Where are microtubules highest at?

A

The Brain

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14
Q

AE of Vinca alkaloids?

A

Neurotoxicity
Constipation

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15
Q

Increased Pgp?

A

Cancer drug resistance

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16
Q

PgP (P-glycoprotein) known as?

A

MDR1, ABCB1, CD243
-ATP dependent efflux pump: provides cellular defense mechanism against potentially harmful substances

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17
Q

Vinca alkaloids are metabolized?

A

Hepatically
Reduce dose in hepatic dysfunction or elevated billirubin

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18
Q

Vinblastine is part of curative treatment for?

A

Hodgkin disease

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19
Q

Curative treatment for metastatic testicular cancer?

A

Vinblastine with Bleomycin and Cisplatin

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20
Q

For childhood leukemia?

A

Vincristine with glucocorticoids (better tolerated in kids)

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21
Q

What is the CHOP regimen?

A

Cyclophosphamide, Hydroxyrubocin, Oncovin, Prednisolone
-Used in Non-Hodgkin lymphoma

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22
Q

For Wilms tumor, Neuroblatoma, Rhabdomyosarcoma?

A

Vincristine -standard for leukemis and lymphomas especially in pediatrics

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23
Q

Vincristine and Neuro?

A

mostly neurological manifestations that can be reversed once stopped, reduced, or suspended

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24
Vinorelbine AE
Granulocytopenia less neurotoxicity
25
Eribulin is a poor substrate of _____ and is effective in?
Pgp efflux pump and effective in drug resistant tumors that overexpress Pgp
26
Eribulin used in?
drug resistant metastatic breast cancer and liposarcoma
27
Taxanes MOA?
bind to a different site on B-tubulin and promote microtubule formation--->stabalizes tubulin-GDP
28
Paclitaxel MOA?
binds to B-tubulin subunit on the inner surface of microtubules and antagonizes their disassembly-->bundles of microtubules appear-->arrest in mitosis-->cell death
29
Drugs that block cell-cycle progression prior to Mitosis _____ the toxic effects of taxanes
antagonize (Like Cisplatin given before)
30
Increased membrane bound efflux proteins such as MRP1 and Pgp
decrease cellular drug accumulation
31
Cabazitaxel is a
poor substrate for Pgp---->useful for treating multidrug resistant tumors like hormone refractory metastatic prostate cancer previously treated with docetaxel
32
Resistance: increase in a-aurora kinase
promotes completion of mitosis
33
upregulation of BIII-isoform of tubulin lacks
taxane binding capacity or direct alteration of the drug target by mutation
34
Antiapoptotic factor (increases surviving) thus _____
downregulates taxanes
35
Paclitaxel clearance is delayed by drugs that ____
inhibit Pgp (cyclosporine A)
36
Taxanes use in cancers?
metastatic ovarian, breast, lung, GI, Genitourinary, and head and neck cancers
37
Paclitaxel exerts its toxic effects where?
Bone marrow
38
Taxanes AE?
Neutropenia (Docetaxel), peripheral neuropathy, hypersensitivity reactions
39
Etramustine MOA
Binds to B tubulin and microtubule proteins causing dissasembly and antimitotic actions
40
Estramustine use?
Metastatic advanced hormone refractory prostate cancer
41
Estramustine active drug form accumulates where?
prostate
42
Estramustine _____the clearance of taxanes
inhibits
43
Epothilones MOA
bind to a B tubulin site distinct from taxanes__>trigger microtubule nucleation --->dysfunctional microtubule stabilization--->cell-cycle arrest at G2-M interface and apoptosis
44
Cremophor what to give before?
premedicate with H1 and H2 antagonists
45
Camptothecin targets?
Nuclear enzyme topoisomerase I by inhibiting
46
what are Camptothecins?
Irinotecan and topotecan
47
Irnotecan is a _____
Prodrug
48
DNA topoisomerases do what?
reduce torsional stress in supercoiled DNA -allowing to untagle to replicate, repair and transcribe
49
Camptothecins are cell cycle specific where?
S-phase
50
low-dose protracted camptothecins
have less toxicity and greater antitumor activity than short courses
51
Toptecan is a substrate for?
Pgp but poor substrate
52
ABCG2/BCRP overexpression in cancer makes it
resistant to irinotecan
53
Irinotecan -->_____----->
converted by carboxylesterase to active metabolite SN-38
54
if you have decreased carboxylesterase activity then you have ____ to Irinotecan
resistance
55
what organs have sufficient carboxylesterase activity?
liver and red blood cells
56
Topotecan not for
Renal impairment
57
Irinotecan SN38G is a
Inactive metabolite by glucuronidated UGT1A1
58
SN38G Inversely correlates with risk of
diarrhea
59
Irinotecan use first line?
advanced colorectal cancer
60
Bacterial glucuronidase contributes to GI toxicity by
releasing unconjugated SN38
61
What are Epipdophylltoxins
Etoposide and Teniposide
62
Etoposide and Teniposide MOA?
form ternary complexes with topoisomerase II and DNA-->prevents resealing of break -->accumulation of DNA breaks leads to cell death
63
Which cell cycle are most sensitive to Etopside and teniposide?
S and G2 phase
64
Resistance to Etoposide and Teniposide occur when?
Mutations of p53 Mutation or decreased topoisomerase II Amplification of MDR1 gene -->Pgp drug efflux
65
Curative therapy for testicular cancer?
bleomycin and cisplatin
66
pts with decreased albumin in etoposide and Teniposide have
greater risk of toxicity
67
AE of Teniposide and Etoposide?
development of unusual form of acute nonlymphocytic leukemia
68
Monocytic leukemia in infants?
Teniposide
69
L-ASP MOA?
catalyzes hydrolysis of asparagine to aspartic acid and ammonia-->depriving malignant cells of asparagine--->cell death
70
L-ASP 1st line treatment for?
ALL (Acute lymphocytci leukemia)
71
L-ASP AE?
Hypersensitivity reactions lowers serum albumin terminates antitumor activity of MTX
72
Hydroxyurea normal levels?
30-200
73
Hydroxyurea MOA?
inhibits ribonucleotide reductase
74
Hydroxyurea is specific to which cell cycle?
S phase
75
Hyrdoxyurea produces arrest at G1/S phase which
prevents cells from leaving and radiosensitizing activity by maintaining cells in radiation sensitive G1 phase and interfering with DNA repair
76
Hydroxyurea BBW
not to be used in women of childbearing potential
77
hydroxyurea aka
radiosensitizer -->used for CML

Oncology (10 decks)

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