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550 Pharm > Cancer > Flashcards

Cancer Flashcards

0
Q

Malignancy;

A

abnormal cells divide without control and can invade nearby tissue; referred to as cancer

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1
Q

Benign

A

cancerous; do not spread to other parts of the body

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2
Q

Metastasis

A

the spread of cancer from one part of the body to another

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3
Q

What are the six hallmark signs of cancer?

A
  • evading apoptosis
  • self-sufficiency in growth signals
  • insensitivity to anti-growth signals
  • tissue invasion and metastasis
  • limitless replicative potential
  • sustained angiogenesis
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4
Q

What is a tumor suppressor gene?

A
  • inhibit cell proliferation or stimulate apoptosis when needed
  • gene that protects a cell from progressing towards cancer
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5
Q

T/F: Mutations of tumor suppressor genes cause loss or reduction in function.

A

True

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6
Q

What is a class role of p53?

A

prevents cells with damaged DNA from proliferating

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7
Q

T/F: About half of all people with cancer have p53 mutations.

A

True

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8
Q

Germ-line mutations

A

inheritable variations in all of your cells

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9
Q

Somatic mutations

A

not heritable, variations often due to environment

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10
Q

Proto-oncogene

A

normally stimulates cell proliferation

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11
Q

What are some examples of proto-oncogenes?

A

growth factors, growth factor receptors, signal transducing proteins

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12
Q

T/F: Most chemotherapeutic drugs are non-specific and lead to toxicity.

A

True

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13
Q

What are chemotherapy goals?

A
  1. ) inhibit synthesis of new DNA strands to stop cells from replicating them (methotrexate)
  2. ) Damage DNA of the affected cancer cells (alkylating agent)
  3. ) stop mitosis and therefore stop cell division
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14
Q

Doxorubicin inhibits __________. How does it work?

A
  • topoisomerase II

- doxorubicin intercalates in the DNA, cuts the DNA and doesn’t allow the DNA to reseal

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15
Q

Alkylating agents attach ______ groups to the ______ DNA base.

A

alkyl; guanine

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16
Q

What are spindles used for and where are they made?

A

used in mitosis and made of microtubules

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17
Q

Vinca alkaloids

A

prevent tubulin from forming into microtubules

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18
Q

What are the new targeted therpies?

A
  • hormone therapy
  • monoclonal antibodies
  • tyrosine kinase inhibitors
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19
Q

What is an example of hormone therapy?

A

tamoxifen - active metabolite is an antagonist at the estrogen receptor

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20
Q

Alkylating agents directly damage the _____ in the nucleus of the cell preventing replication.

A

DNA

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21
Q

What is the idea behind self-sufficiency in growth signals?

A

provide their own growth signals by an auto-loop

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22
Q

T/F: Cancer cells have contact inhibition?

A

False; cancer cells have loss of inhibition

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23
Q

In part cancer cells are able to invade and metastasis due to what hallmarks?

A

self-sufficiency in growth signals and insensitivity to anti-growth signals

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24
Q

With each DNA replication the telomere gets ________.

A

shorter

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25
Q

What is the purpose of telomerase

A
  • an enzyme that adds DNA sequence

- can be activated by mutations

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26
Q

T/F: Is most healthy cells telomerase is not active.

A

True, it is not active

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27
Q

Why is it important not to active telomerase activated?

A

if the DNA becomes mutated, you don’t want it to endlessly replicate.

28
Q

What gene is an example of a tumor suppressor gene?

A

p53

29
Q

p53 activation

A

certain type of DNA damage that activate p53 - once activated, its able to determine whether its reparable or irreparable -

30
Q

p53 - Reparable

A

reparable - a specific signaling cascade that will lead to cell cycle arrest -> DNA repair

31
Q

p53 - irreparable

A

apoptosis

32
Q

Where in the cell cycle is p53 activated if there is DNA damage?

A

G1 & S

33
Q

What is the order of the cell cycle?

A

G1 > S > G2 > mitotic phase (mitosis & cytokinesis)

34
Q

Are tumor suppressor mutations dominant or recessive?

A

recessive

35
Q

T/F: One wild-type gene usually produces enough protein to protect the cells.

A

true

36
Q

T/F: If the first hit is a germline mutation, second somatic mutation is more likely to enable cancer.

A

true

37
Q

Oncogenes

A
  • in healthy cells we have a lot of proto-oncogenes, once there is a certain type of damage and they get mutated -> oncogenes
  • have altered cellular functions and can lead to spontaneous abnormal types of growth (begin or malignant
38
Q

Typical signal transduction

A

ligand binds to the receptor -> leads to activation of RAS > RAF > MEK > ERK > activates transcription factors > proliferation and survival

39
Q

Mutation in RAF

A
  • cascade is always on regardless of ligand binding to a receptor - can lead to cancer
40
Q

Are mutations of proto-oncogenes dominant or recessive?

A

-dominant - only need one to be bad

41
Q

How is folate ultimately used for DNA production?

A

folate is taken up and converted into FH2 by DHFR and the FH4 by DHFR. Fh4 is then used with DUMP. DUMP is methylated by thymidylate synthetase into DTMP. DTMP is needed for DNA production

42
Q

T/F: Methotrexate has a higher affinity for DHFR than FH2 and therefore depletes intracellular FH4.

A

true

43
Q

How was topoisomerase work?

A

DNA is double stranded - as replication and transcription machinery are coming along - it needs to unwind this DNA in order for polymerase to work - as its unwinding its causing super coils downstream - topoisomerase II would go to the coil, cut it unwind it and reseal it back together

44
Q

What is an example of an alkylating agent? And how does it work?

A

cyclophosphamide; attaches an alkyl group to guanine DNA base
-two Cl- very reactive, can either bind to two guanine on the same side (intra-strand crosslinking) or bind on different strands (inter-strand crosslinking)

45
Q

How do vinca alkaloids work?

A

microtubules are put together and polymerize, however vincas block the polymerization by binding to microtubules - cannot pull sister chromatins apart

46
Q

Targeted therapy can reduce ______ and increase ______.

A

toxicity; efficacy

47
Q

Tamoxifen is a ________. What does this mean?

A

prodrug; its not active, once it is metabolized the metabolite is active

48
Q

How does tamoxifen work?

A

if estrogen receptors are leading to large amount of proliferation - its needs to be stopped- tamoxifen metabolite binds to estrogen receptor and will cause a confirmation change (different than a normal estrogen binds) - cannot recruit coactivators - so these cells are no longer growing

49
Q

What are the two ways monoclonal antibodies work?

A
  1. block growth signals

2. stop new blood vessel from forming

50
Q

What hallmark is monoclonal antibodies preventing?

A

angiogenesis

51
Q

How does it block growth signals?

A

EGFR binds - activates K-RAS > RAF > MEK > ERK/MAPK

52
Q

T/F: RAF is a tumor supressor gene.

A

False, its a proto-oncogene

53
Q

When is cetuximab used?

A

when there is an overexpression in EGFR

54
Q

Where does cetuximab bind?

A

to the EGFR receptor and blocks it

55
Q

If someone has a mutation in K-RAS, would you give this patient ceruximab?

A

no; upstream targeting will have no effect

56
Q

What does bevacuzimab do?

A
  • angiogenesis inhibitor
  • binds to VEGF and prevents it from binding to the receptor - prevents the auto phosphorylation and prevents angiogenesis
57
Q

Explain the cascade leading to angiogenesis.

A

VEGF - binds to VEGF receptor - leads to cross phosphorylation can activate a down stream signal transduction - angiogenesis

59
Q

What is an example of a tyrosine kinase inhibitor?

A

vemurafenib or PLX4032

60
Q

What is the most common B-RAF mutation?

A

B-RAF V600E - present in 60% or more melanomas

  • causes constitutive activation of B-RAF
  • tightly regulated
61
Q

T/F: Vemurafenib (PLX4032) treats only patients with BRAFV600E mutations.

A

True

62
Q

How come in the progression-free graft, patients treated with Vermurafenib, will have a decrease in their survival rate?

A

another mutation can activate the MEK cascade further downstream

63
Q

Combination therapies

A

you can prevent an alternate pathway from activating

64
Q

Where is the ABL gene normally located?

A

chromosome 9

65
Q

Where is the BCR gene normally located?

A

chromosome 22

66
Q

What happens in CML

A

philadelphia chromosome is made, part of chromosome 9 breaks and part of chromosome 22 breaks - a fusion protein is created and BCR-ABL is formed

67
Q

What is BCR-ABL? How does it normally function?

A
  • tyrosine kinase - not tightly regulated
  • normally when BCR-ABL comes in contact with a substrate - it hydrolyzes ATP-ADP and phosphorylates the substrate making it active
68
Q

What is gleevac (imatinib) and how does it work?

A

-tyrosine kinase inhibitor
competitively binds to ATP binding site of BCR-ABL inhibiting kinase activity - ATP can no longer bind and BCR-ABL tyrosine kinase can no longer phosphorylate the substrate - inhibits progression of CML

550 Pharm (6 decks)

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