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Pathology and MuscSkel > Antineoplastics and angiogenesis > Flashcards

Antineoplastics and angiogenesis Flashcards

1
Q

What are the rationale for anti-neoplastic drugs?

A

kill all tumor cells
suppress growth of tumor cells but not normal cells
improve ability of normal cells

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2
Q

Cancer stem cells are what?

A 
small compartment of tumor
often quiescent
resistant to chemo and radiation
can regenerate tumor
one mechanism for drug resistance
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3
Q

At what size is a tumor visible on X-ray?

A

at 1 cm in diameter

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4
Q

When is a tumor first palpiable?

A

at 1 gram; when first become symptomatic

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5
Q

What type of kinetics does killing tumor follow?

A

first-order kinetics; so a constant dose of drug kills a constant fraction of tumor cells

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6
Q

Tumor size predicts what with respect to chemotherapy use?

A

not hte dose but duration of treatment

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7
Q

What must the chemotherapy regimen must be like to be curative?

A

have a 2-4 log kill efficiency and be repeated 4-12 times

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8
Q

Class II drugs target what type of tumor/cell?

A

target cells in specific stage of cell cycle

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9
Q

What do class III drugs target what type of tumor/cell?

A

targets cells in cell cycle relatively specific for cancer cells

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10
Q

What do class I drugs target?

A

target and kill all cells regardless of what sage they are at

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11
Q

What are targets-target therapies for antineoplastics?

A

targeting molecular targets taht are more specific for the cancer cells

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12
Q

What is angiogenesis?

A

extension of capillaries or blood vessels from existing blood supplies

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13
Q

What is vasculogensis?

A

formation of capillaries or blood vessels independently of old blood vessels and eventually join

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14
Q

What is the difference between vessels in tumor vs normal vessels?

A

tumor vessels lack smooth muscle all the way around them; and much more chaotic, holes used for mestasis

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15
Q

Why is it difficult for drugs to enter tumor?

A

itnratumor pressure due to damaged lymphatic vessels

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16
Q

What is the role of VEGF in permeability of vessels?

A

50,000 times more potent than histamine

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17
Q

What is NOTCH?

A

when it is cleaved and enters nucleus it is important in early angiogenisis by transcription increase

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18
Q

What are the benefits of anti-angiogenic therapy?

A

target genetically stable population
naturally occuring-high tolerance low side effects
ease accessibility
**this is the ideal

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19
Q

What is tumor doubling timea function of?

A

cell cycle time
growth faction
cell loss

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20
Q

What are are the four principles of tumor growth curve?

A

tumor mass generally first detectable at 10^9 cells
as a tumor grwos more cells enter G0
tumor cells are generally mores sensitivie to chemo agents during early growth periods
a palable tumor is large enought to have metastasized

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21
Q

What are the four stages of tumor growht?

A

I: tumor contained in organ of orgin
II: tumor metastasized regionally but is totally removable
III: metastasized regionally but no longer totally removable
IV: tumor is metastasized beyond local area

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22
Q

What log-kill rate is needed to double the expected lifespan of a patient?

A

2-4 log-kill

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23
Q

What is the total-kill concept?

A

one surviving cell can regenerate the tumor

the lifespan of the host is inversely related to the number of cells that survive therapeutic measures

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24
Q

What are two antineoplastic drugs that are class I?

A

non-specific cytotoxicity:
mechlorethamine
carmustine

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25
What drug is a class II that focuses on cells in the G1 phase?
prednisone
26
What drugs are pyrimidine analogs that kill cells in the S phase greatest activity, class II?
Cytarabine, fluorouracil
27
What drug is an antimetabolite that is a folic acid analog that kills cells in the S phase? Class II
methotrexate
28
What drug is an antimetabolite, purine analog, class II, S phase ?
mercaptopurine
29
What drug is a class II, substituted urea, kill cells S phase?
hydroxyurea
30
What drugs are antibiotics, that are class II drugs, G 2 phase?
bleomycin, etoposide
31
What are the taxane, G2 phase, Class II?
Paclitaxel
32
What drug is Class II, m phase focused, a mitotic nhibitor?
vinblastine, vincristine
33
What drug is a class III alkylating agent?
cyclophosphamide
34
What drug is a miscellaneous metal salt, class III drug?
cisplatin
35
What drug is an antibitoic, class III drug?
doxorubicin
36
What is the dosing frequency for one cycle of treatment of class I agents?
given as a single dose for each cycle of therapy?
37
What is the dosing frequency for one cycle of treatment of class III agents?
given as a single dose for each cycle of therapy?
38
What is the dosing frequency for one cycle of treatment of class II agents?
given by continuous infusion or frequent small doses
39
What are the optimal intervals for cycles of treatments?
optimal intervals are those which deliver the next cycle of treatment when there is the greatest difference between recovery of normal tissue and recovery of tumor
40
What are the toxic effects of the alkylating agen mechlorethamine?
nausea vommiting, myelosuppression
41
What is the mechanism of action of alkylating agents as anti-neoplastic rugs?
introduce alkylgroups into DNA | cause DNA crosslinks, strandbreaks
42
What are the toxic effects of cyclophosphamide, an alkylating agen?
nasuea and vomitting limited myelosuppression alopecia
43
What are the toxic effects of carmustine?
nasuea and vommitting | delayed myelo suppression
44
What is mechlorethamine used to treat?
hodgkin's and non-hodgkins lymphoma* | breast, lung and ovarian
45
What is cyclophosphamide used to treat?
``` very broad spectrum, mostly widely used Hodgkins and non-hodgkins lymphoma multiple myeloma neuroblastoma leukemias carcinoma of endometrium, breast lung ```
46
What is a unique side effect of cyclophosphamide?
may cause sterile hemorrhagic cytitis
47
What are the properties of carmustine?
alkylating agent, extensively metabolized in liver | highly lipophilic, rapidly crosses blood brain barreir
48
What is carmustine used to treat?
treatment of brain tumors, multiple myeloma, melanoma
49
What is the mechanism of action of methotrexate?
metabolized to polyglutamates which binds to dihydrofoloate reductase and prevent formation of tetrahydrofolate
50
What does methotrexate bind to?
serum albumin
51
What are the toxicities associated with methotrexate?
intestinal epithelium, bone marrow suppression | renal tubular necrosis
52
What is methotrexate used to treat?
acute lymphocytic leukemia; choriocarcinoma
53
What si teh mechanism of action of fluorouracil?
activated in cells to FUTP which inhbiits RNA synthesis and FdUMP whihc interferes with DNA synthesis
54
What is flurouracil used to treat?
carcinoma of the stomach, colon, pancreas, ovary, head and neck, breast, bladder topical cream for basal cell carcinoma
55
What is the toxicity of fluorouracil?
nausea, anorexia, diarrhea, delayed myelosuppression
56
What is the mechanism of action of cytarabine?
cytidine analog competes with cytidine for all 3 phosphorylation steps to dCTP cytarabine tri-phosphate competes with dCTP for incorporation into DNA and causes DNA chain termination
57
What is the toxicity of cytarabine?
marked myelosuppression and neurotoxicity
58
What is cytarabine used to treat?
acute leukemia
59
What is the mechanism of mercaptopurine?
purine analog that is converted in cells to ribonucleotide that inhibits RNA and DNA synthesis
60
What is mercaptopurine used to treat?
acute leukemia and chronic granulocytic leukemia
61
What is mercaptopurine toxicity?
``` gradual bone marrow depression vomiting nausea anorexia jaundice ```
62
What is the mechanism of action of hydroxyurea?
substituted urea that inhbiits ribonucleotide reductase blocking DNA synthesis; arrest at G1 to S pahse
63
What is hydroxyurea used to treat?
granulocytic leukemia, head and neck cancer
64
What is the toxicity associated with hydroxyurea?
hematopoietic depression, GI disturbances
65
What are the mechanism of action of vina alkaloids?
binds to tubuline, inhibiting proper formation of microtubules and miotic spindle, arresting cellls in metaphase M phase-specific
66
What is Vinblastine used to treat?
hodgkins and non-hodgkins lymphoma | breast cancer
67
What is vinblastine toxicity?
strongly myelosuppressive epithelial uclerations neurological disturbance and bronchospasm
68
What is vincristine used to treat?
acute lymphocytic leukemia, hodgkins and non-hodgkins lymphomas, wilms tumor, neuroblastoma and rhabdomyosarcoma
69
What is the toxicity of vincristine?
alopecia neuromuscular abnoramlities (peripheral neuropathy incl) significantly less bone marrow suppression than vinblastine
70
What is the mechanism of action of taxanes?
blocks late in G2 phase; enhances assembly and stability of microtubules by binding to Beta0subunit of tubulin
71
What is paclitaxel usedd to treat?
refactory ovarian cancer; breat cancer
72
What is toxicity associated with Paclitaxel?
dose-limiting leukopenia, peripheral neuropathy, myalgia/arthalgia
73
What is the doxorubicin mechanism of action?
prevents DNA and RNA synthesis by intercalating between DNA base pairs, dostorting DNA helix causes lipid peroxidation and free radical generation binds to DNA and topo II
74
What is the Doxorubicin used to treat?
Hodgkin's and non-hodgkin's lymphoma, breast, ovary, small cell lung and other cancers
75
What toxicity is assoicated with doxorubicin?
cardiomyopathy | bone marrow depression, alopecia, GI disturbance
76
What is the mechanism of bleomycin?
a mixture of glycopeptides that bind to DNA causes oxidative-like damage to DNA which leads to DNA strand breaks phase specific for G2 and M
77
What is bleomycin used to treat?
germ cell tumors of testes and ovaries | head, neck, lung, lymphomas
78
What toxicitiy is associated with Bleomycin?
dose-related pulmonary toxicity vesiculation of the skin, skin hyperpigmentation minimal myelosuppression adn immunosuppresion
79
What is the mechanism of action fo Etoposide?
stabilizes DNA topo II complexes resulting in double strand DNA breaks maximal effect in late G2 phase
80
What is used to treat with etoposide?
lymphomas, acute nonlymphocytic leukemia, small cell carcioma of lung, testicular tumor
81
What is the mechanism of Filgastrim?
stimulates granulocyte production by marow
82
What is Filgastrim used for?
given after myelosuppressive agent to speed neutrophil recovery; bone pain major side effect
83
What is the mechanism of Trastuuzumab?
humanized monoclonal antibody that binds to HER2 receptor
84
Wha is trastuzumab used to treat?
breast cancer that overezpress HER2
85
What is the toxicity of Trastuzumab?
cardiomyopathy hypersensitivity infusion reacctions
86
What is the mechansim of cisplatin?
platinum coordination complex, hydrolysis leads to an activated species which causes DNA crosslinks, also promotes apoptosis
87
What is cisplatin used to treat?
wide antitumor spectrum, testis of cancer, ovary, head, neck bladder, esophoagus small cell lung
88
What is the toxicity associated with cisplatin?
``` nephrotoxicity ototoxicity peripheral neuropathy electrolyte disturbance nausea, vomitting, myelosuppression ```
89
What is procarbazine mechanism of action?
poorly understood, but activated in vivo to a methylating agent which causes chromsomal damage
90
What is procarbazine used to treat?
hodgkins
91
What is the toxicity associated with procarbazine?
myelosuppression, nausea, vomitting
92
What is the mechanism of action of tamoxifen?
nonsteroidal antiestrogen that blocks estrogen receptors thereby reducing tumor cell renewal
93
What is tamoxifen activatedd by?
CYP2D6
94
What is tamoxifen used for?
ajuvant therapy in post-menopausal breast cancer pre-menopausal metastic breast cancer treatment of certain endometrail and ovarian cancers breast cancer prophylaxis***
95
What is tamoxifen toxicity?
hot flashes, fatigue, nausea, bone and other musculoskeletal pain
96
What is letrozole mechanism of action?
non-steroidal aromataase inhibitor, inhibitis conversion of androgens to estrogens
97
What is this treatment for letrozole?
breast carcinoma in post menopausal women
98
What are the side effects of letrozole?
bone paina nd other musculoskeletal pain, hot flashes, nausea, fatigue
99
What is the mechanism of action of leuprolide?
synthetic peptide analog oof gonadotropin-releasing horomone (GnRH) after 2-4 weeks it desensitizes GnRH signaling inhibiting LH/FSH secretion decreasing testosterone synthesis to castration levels
100
What is leuprolide used to treat?
advanced horomonally rsponsive prostate cancer
101
What is leuprolide toxicity?
hot flashes, impotence
102
What is the mechanism of action of Flutamide?
potent nosteroidal antiandrogen that blocks androgen receptors
103
What is flutamide used to treat?
metastatic prostate cancer, often with GnRH analog
104
What is the toxicity of flutamide?
gynecomastia, diarrhea, hepatotoxicity
105
What is the reason for resistance to chemotherapy?
resting cells dose limited by toxic effects on sensitive tissues spontaneous mutations clinical resistance selectiona nd overgrwoth-major cause of chemotherapic failure
106
What is multi-drug resistance medaited by?
ATP-dependent drug efflux pumps pump out a variety of drugs from cells simultaneous resistance to many drugs
107
What are strategies to circumvent resistance?
increase dose multi-drug regimens co-admin agens that defeat resistance recruit cells out of resting phase
108
What is the advantages of combination therapy?
provide maximal cell kill within range of toxicity tolerated by host of each drug provide a braoder range of coverage prevent development of new resistant lines
109
What is sequential blockade?
simultaneousl action of two inhibitors acting on different enzymes of a linera metablic pathway
110
What is concurrent inhibition?
inhibitors block two separate pathways that lead to the same end product
111
What is complementary inhibition?
one of the inhibitors affects the function of an end product the other inhbiitor affects the syntehsis of that end product
112
What is rescue?
rescues teh normal cells from treatment

Pathology and MuscSkel (15 decks)

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