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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
Q

The extrinsic pathway for apoptosis involves:

A

P53 regulated BAX induces cytochrome C release from mitochondria —> capsases are activated —> apoptosis

26
Q

Miotic inhibitor drugs:

A

Paclitaxel/taxol

27
Q

Cancers of the gut will metastasize in the

A

Liver

28
Q

How does the drug Avastin function

A

Blocks angiogenesis by inhibiting VEFG

29
Q

Alkylating Agents drugs

A

Cisplatin (Carboplatin)

30
Q

What phase of the cell cycle do Alkylating agents target?

A

G1/S/G2 = interphase

31
Q

What phase of the cell cycle does antimetabolite drugs target

A

S phase

32
Q

What is meany by “aerobic glycolysis” in the Warburg Effect

A

Tumor cells will use the anaerobic pathway to convert glucose to lactate however oxygen is present.

33
Q

What is the action of miotic inhibitors?

A

Binds to microtubules in metaphase inhibiting cell division

Binds to BCL-2 “inhibits the inhibitor” for apoptosis

34
Q

What favors cell death?

A

BAX, cytochrome C

35
Q

Anti-Tumor Antibiotics Drugs

A

Doxorubicin, Anthracycline, Daunorubicin

36
Q

When does a tumor become malignant

A

When cancer cells secrete a matrix that eats through the basal lamina into the underlying tissue

37
Q

Gain of function in BLC-2 would lead to

A

Favoring cell survival (no apoptosis) = cancer!

38
Q

Cancer cells only need ~_____% growth factor of what normal cells need

A

10

39
Q

What is activated that makes cancer cells “immortal”

A

Telemorase

40
Q

Cancer cells can grow on top of each other due to

A

Loss of contact inhibition

41
Q

Cancer cells have ___________ adhesion molecules

A

Decreased

42
Q

Why are cancer cells unable to repair DNA

A

Checkpoints disabled

43
Q

What is the chromosome situation in cancer cells

A

Deranged chromosome content - aneuploidy/polylploidy

44
Q

The degree of abnormality of cancer chromosomes is dependent on

A

The stage of cancer

45
Q

Epithelial-mesenchymal transition =

A

Decreasing adhesion molecules = more motility

46
Q

New blood vessels are produced in response to

A

Hypoxia

47
Q

Hypoxia stimulates (pathway)

A

Increase HIF-1 —> increase VEGF —> angiogenesis

48
Q

Inducers of angiogenesis:

A

VEGF, ANG (angiopoietin), FGF (fibroblast growth factor), TGF-B (transforming growth factor B)

49
Q

Neurofibromin functions as a _________ activating protein, which deactivates ________

Without neurofibromin, ______ remains active longer

A

GTPase
RAS
RAS

50
Q

Neurofibromas are tumors in what kind of cell

A

Schwann cells

51
Q

Usually, MSH2 and MLH1 work together to

A

Repair mistakes in DNA by removing the incorrect piece

Not working in Hereditary non-polyposis colon cancer

52
Q

Knudsen’s hypothesis

A

Two-hit model

53
Q

Truncated tyrosine kinase:

A

Don’t need a ligand to dimerize

54
Q

Amplification of receptors for tyrosine kinase:

A

Too many normal receptors at the cell surface can bind to too much growth factor binding

55
Q

Three points of receptor-tyrosine kinase (RTK) signaling pathway that can become overactive as a result of mutations:

A
  1. RTK itself
  2. Ras GTPase
  3. Transcription factor for MYC
56
Q

An increase in RTK, RAS GTPase or transcription factor for MYC ultimately leads to

A

Increase the levels of cyclin D and allow the cell to cross the restriction point

57
Q

E6 binds to

A

P53

58
Q

E7 binds to

A

Rb

Biochem 4 (9 decks)

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