Chemotherapy Of Cancer (Pharm Block 1)

Front 1

Three therapeutic modalities used for cancer

Back 1

surgery
chemo
rads

Front 2

Most cancer chemotherapeutics trigger what in cancerous cells?

Back 2

Apoptotic cell death

Front 3

4 macroscopic charactersistics of cancer cells

Back 3

1) unregulated division and growth
2) dedifferentiation
3) invasion
4) metastasis

Front 4

3 microscopic characteristics of cancer

Back 4

1) activation of proto-oncogene
2) inactivation of tumor supressor genes
3) Genetic instability

Front 5

1)What kind if cells are most often hurt by chemo toxicity?
2) give three specific examples

Back 5

1) rapidly growing cells
2) GI mucosa, bone marrow, hair follocles

Front 6

Do traditional chemotherapeutics interfere with invasion and metastasis?

Back 6

no

Front 7

DNA alkylating agents: Mechanism

Back 7

interfere with replication, transcription. DNA cleavage reagents cause single strand breaks. DNA crosslinking agents block replication

Front 8

Antimetabolites: mechanism

Back 8

inhibit synthesis of DNA precursors (Class II reaction), or subvert normal biosynthetic pathways.

Front 9

1)Vinca-alkaloid mechanism?
2) Taxane mechanism?
3) what general class are these drugs in?

Back 9

1) bind B-tubulin and therefore inhibit spindle apparatus.

2)inhibit MT disassembly and therefore growth

3) anti-mitotics

Front 10

How are the anthracyclien antibiotics (Topo-II inhibitors) also anti-cancer drugs?

Back 10

Intercalators

Front 11

Topoisomerase 1 poisons:
1)mechanism
2) example

Back 11

1) stabilize covalent complex of enzyme with cleaved DNA.
2) campthecin

Front 12

DNA crosslinking agents:
1) mechanism
2) class of drugs

Back 12

1) form a heterogenous mixture of DNA lesions, including interstrand DNA crosslinks.
2) -platins

Front 13

Antimetabolites:
Analogs of _1__ and _1__ are metabolized to nucleosides in mamallian cells. ___2___ and ___2___ must be given as nucleosides

Back 13

1) G and C/U
2) A and T

Front 14

6-thiopurines:
1) are in what general class of anti-cancer drugs
2) have what two actions?

Back 14

1) antimetaboliltes
2) inhibit de novo purine synthesis AND are incorporated int DNA

Front 15

Pyrimidine analogs
1) are in what general class of anti-cancer drugs
2) have what two actions?

Back 15

1) antimetabolites
2) block thymidine biosynthesis (block thymidylate synthetase) and incorporate into DNA and RNA

Front 16

Ara-C is an antimetabolite that is phosphorylated and then halts replication by:

Back 16

incorporating into DNA and RNA

Front 17

2' deoxycoformycin:

1) is in what general class?
2) inhibits
3) Can also incorporate into DNA and cause:

Back 17

1) antimetabolite
2)Adenosine Deaminase
3) DSBs

Front 18

THF is needed for the de novo synthesis of?

Back 18

Purines

Front 19

1)Methotrexate is an inhibitor of?
2) how is it specific to cancer cells?

Back 19

1) eukaryotic DHFR
2) cancer cells need more purines because they are dividing faster.

Front 20

Name two classes of anti-mitotic drugs?

Back 20

vinca alkaloids
taxanes

Front 21

1) Vinca alkaloids are under what general class of cancer drug?

2) how do they work?

Back 21

1) anti-mitotic

2)vinca-alkaloids bind Beta-tubulin interfering with spindle formation.

Front 22

1) Taxanes are under what general class of cancer drug?

2) how do they work?

Back 22

1) anti-mitotic
2) taxanes bind MTs interfering with their disassembly

Front 23

mAb cancer-therapeutics target what sort of pathways?

Back 23

Growth factors- VEGF, EGFR

Front 24

1)Describe the unique mechanism of action of Gemtuzumab.
clssical use in what disease?

Back 24

Ab against CD33 which is linked to an antibiotic which cases DNA fragmentaton. CD33 is on most hemopoietic cells.
2) AML

Front 25

WHy do hormonal therapies work?

Back 25

Hormones regulate cell growth and some tumors are strongly suppressed by hormone antagonists, including anti-estrogen therapy (breast cancer) and anti-androgens for prostate carcinoma.

Front 26

Hormones: Why do we use glucocoritid therapy?

Back 26

Glucocorticoids suppress mitosis in lymphocytes and are lympholytic. Thus they are useful in leukemais.

Front 27

1) how do we give androgen blockade?
2) how does this attenuate androgen release?

Back 27

1) GnRH AGONIST and androgen receptor ANTAGONIST
2) Continuous stimulation of GnRH receptor shuts down LH production and androgen release

Front 28

Name three types of antiestrogen therapies.

Back 28

1) Selective Estrogen receptor modulators (SERMs)
2) Selective estrogen receptor down-regulators (SERDs)
3) aromatase inhibitors

Front 29

Describe how SERMs work?

Back 29

1Selective Estrogen receptor modulators (SERMs) competitively inhibit estrogen receptors

Front 30

Describe how SERDs work?

Back 30

Selective estrogen receptor down-regulators (SERDs) bind to the receptor but do not cause activation and cause receptor internalization

Front 31

Describe how aromatase inhibitors work.
1) type I
2) type II

Back 31

1) type I aromatase inhibitors irreversible inactivate aromatase by binding to the active site.

2) Type II aromatase inhibitors bind reversibly to the heme group of aromatase

Front 32

Main problem with current chemotherapetics?

Back 32

toxicity in rapidly growing tissues

Front 33

Why do we care so much about molecular diagnostics in the therapy of cancer?

Back 33

Individual response to treatment is highly variable, perhaps reflecting the genetic heterogeneity of tumor cells and different host constellations of predisposing factors.

Front 34

Does resistance exist in caner chemotherapy?

Back 34

yes

Front 35

Why do we use combination therapy in cancer treatment?

Back 35

Combination therapy can improve killing efficiency, limiting the incidence of resistance.