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Biochem 4 > Cancer > Flashcards

Cancer Flashcards

1
Q

Antimetabolite drug

A

Methotrexate

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2
Q

Metastasis step by step

A
  1. Somatic mutation
  2. growth factors support expansion
  3. Intravasation
  4. Migration
  5. Adhesion to epithelium
  6. Extravasated
  7. Angiogenesis
  8. Growth in metastatic location
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3
Q

Invasion versus Intravasation

A 
Invasion = cancer cells in the surrounding tissue
Intravasation  = progression into blood and lymph
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4
Q

Most cancers will metastasize in the

A

Lungs

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5
Q

What phase of the cell cycle does Topoisomerase inhibitors target

A

S/G2 phase

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6
Q

Loss of function in BAX results in

A

Evading apoptosis, cancer!

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7
Q

What is an example of a drug used in inhibiting Angiogenesis

A

Avastin

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8
Q

What action do antimetabolite drugs have?

A

Disrupts DNA synthesis as a folic acid analog (review)

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9
Q

What is involved in Targeted Therapy

A

Activity of a deviant protein is selectively blocked/ signal transduction inhibitors

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10
Q

How does an activated capsase promote apoptosis

A

Shuts down cell metabolism, shuts off communication with surrounding cells, signals for phagocytosis

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11
Q

What phase of the cell cycle do miotic inhibitors target?

A

G2/ M phase

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12
Q

Intrinsic Pathway of Apoptosis

A

BCL-2 inhibits extrinsic pathway —> cell survival

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13
Q

Anti-Tumor Antibiotics target which phase of the cell cycle

A

All phases

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14
Q

How does the secretion of MMPs promote mestastasis

A

Remodel extra cellular matrix = stimulates growth
Epithelial mesenchymal transition = decrease adhesion = promote motility
Growth factors = enhance proliferation
Structural reorganization of surface glycoproteins (change oligosaccharide chain)

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15
Q

What favors cell survival?

A

BCL-2

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16
Q

Alkylating Agents mechanism

A

Damages DNA by forming cross bridges.

Platinum based covalent interstrand and intrastrand crosslink with purine bases on DNA forming adduct with DNA

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17
Q

The Warburg Effect:

A

Cancer/fast proliferating cells convert glucose into lactate even in the presence of oxygen to use the byproducts as building blocks for growth.

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18
Q

How does Trastuzumab (Herceptin) work?

A

Used in immunotherapy- binds to HER2 intrinsic tyrosine kinase receptor, blocking downstream signaling pathways

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19
Q

Example of a drug used for Targeted Therapy

A

Imatinib / Gleevec in CML

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20
Q

Example of a drug used for Immunotherapy

A

Trastuzumab (Herceptin)

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21
Q

Immunotherapy consists of:

A

Antibodies as therapeutic agents

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22
Q

How should a multi drug treatment be used

A

Simultaneously, not one after the other

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23
Q

Breast cancer metastasizes in the

A

Bones

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24
Q

Anti-Tumor Antibiotics mechanism

A

Intercelating into DNA

25
The extrinsic pathway for apoptosis involves:
P53 regulated BAX induces cytochrome C release from mitochondria —> capsases are activated —> apoptosis
26
Miotic inhibitor drugs:
Paclitaxel/taxol
27
Cancers of the gut will metastasize in the
Liver
28
How does the drug Avastin function
Blocks angiogenesis by inhibiting VEFG
29
Alkylating Agents drugs
Cisplatin (Carboplatin)
30
What phase of the cell cycle do Alkylating agents target?
G1/S/G2 = interphase
31
What phase of the cell cycle does antimetabolite drugs target
S phase
32
What is meany by “aerobic glycolysis” in the Warburg Effect
Tumor cells will use the anaerobic pathway to convert glucose to lactate however oxygen is present.
33
What is the action of miotic inhibitors?
Binds to microtubules in metaphase inhibiting cell division | Binds to BCL-2 “inhibits the inhibitor” for apoptosis
34
What favors cell death?
BAX, cytochrome C
35
Anti-Tumor Antibiotics Drugs
Doxorubicin, Anthracycline, Daunorubicin
36
When does a tumor become malignant
When cancer cells secrete a matrix that eats through the basal lamina into the underlying tissue
37
Gain of function in BLC-2 would lead to
Favoring cell survival (no apoptosis) = cancer!
38
Cancer cells only need ~_____% growth factor of what normal cells need
10
39
What is activated that makes cancer cells “immortal”
Telemorase
40
Cancer cells can grow on top of each other due to
Loss of contact inhibition
41
Cancer cells have ___________ adhesion molecules
Decreased
42
Why are cancer cells unable to repair DNA
Checkpoints disabled
43
What is the chromosome situation in cancer cells
Deranged chromosome content - aneuploidy/polylploidy
44
The degree of abnormality of cancer chromosomes is dependent on
The stage of cancer
45
Epithelial-mesenchymal transition =
Decreasing adhesion molecules = more motility
46
New blood vessels are produced in response to
Hypoxia
47
Hypoxia stimulates (pathway)
Increase HIF-1 —> increase VEGF —> angiogenesis
48
Inducers of angiogenesis:
VEGF, ANG (angiopoietin), FGF (fibroblast growth factor), TGF-B (transforming growth factor B)
49
Neurofibromin functions as a _________ activating protein, which deactivates ________ Without neurofibromin, ______ remains active longer
GTPase RAS RAS
50
Neurofibromas are tumors in what kind of cell
Schwann cells
51
Usually, MSH2 and MLH1 work together to
Repair mistakes in DNA by removing the incorrect piece | Not working in Hereditary non-polyposis colon cancer
52
Knudsen’s hypothesis
Two-hit model
53
Truncated tyrosine kinase:
Don’t need a ligand to dimerize
54
Amplification of receptors for tyrosine kinase:
Too many normal receptors at the cell surface can bind to too much growth factor binding
55
Three points of receptor-tyrosine kinase (RTK) signaling pathway that can become overactive as a result of mutations:
1. RTK itself 2. Ras GTPase 3. Transcription factor for MYC
56
An increase in RTK, RAS GTPase or transcription factor for MYC ultimately leads to
Increase the levels of cyclin D and allow the cell to cross the restriction point
57
E6 binds to
P53
58
E7 binds to
Rb

Biochem 4 (9 decks)

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