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Spring '14 Pharmacology > Oncology Pharmacology > Flashcards

Oncology Pharmacology Flashcards

1
Q

What is the 2 part definition of cancer?

A

A term for diseases in which abnormal cells divide without any control AND can invade nearby tissue.

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2
Q

How are cancers categorized?

A

By origin vs. mutational status.

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3
Q

Why do we catergorize cancer by mutations as opposed to site of origin?

A

This helps us target therapy better

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4
Q

Define benign tumor.

A

Non-cancerous, non-malignant. Benign tumors grow larger but do not spread to other parts of the body.

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5
Q

Can benign tumors be life-threatening?

A

Yes. Depending on where they are. For example, even benign tumors in the head can cause increases in ICP that are life-threatening.

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6
Q

Define malignancy.

A

A term for diseases in which abnormal cells divide without control and can invade nearby tissues.

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7
Q

Malignant tumors are referred to as:

A

cancer

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8
Q

Define metastasis.

A

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

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9
Q

What are the 6 hallmarks of cancer

A
  1. Evading apoptosis
  2. Self-sufficiency in growth signals
  3. Insensitivity to anti-growth signals
  4. tissue invasion and metastasis
  5. Limitless replicative potential
  6. Sustained angiogenesis
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10
Q

What is apoptosis?

A

It is programmed suicide. If a cell is damaged it will signal itself or respond to signals from other cells to die.

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11
Q

By avoiding apoptosis, cancer cells can ___________.

A

proliferate

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12
Q

How do cells normally receive growth signals?

A

Cells normally receive growth signals from other cells surrounding it.

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13
Q

Do cancer cells need to receive growth signals from the cells surrounding them?

A

No, they can provide their own growth signals, this leads to hyperplasia.

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14
Q

How do cancer cells send themselves growth signals? Use glutamate as an example.

A

The cancer cell will release glutamate into the space outside the cell, so the glutamate is free to react with the glutamate receptor on the cell membrane, triggering growth. (this glutamate example is specific for melanoma)

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15
Q

What is contact inhibition?

A

As cells grow, divide, and spread out, they reach a limit, a border, like the edges of an agar plate. Once the cell touches the border it sends a signal to the other cells to stop replicating.

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16
Q

Are cancer cells sensitive to contact inhibition?

A

No. Cancer cells do not respond to anti-growth signals.

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17
Q

_____________ is what makes cancer so dangerous.

A

Metastasis

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18
Q

Most cells only grow in one part of the body, how?

A

Cells will grow in areas with like cells and they exchange growth information and start/ stop information from their neighbor cells. Usually if a cell breaks free and travels to another part of the body, it will not proliferate because it is not near its neighbor cells that give it growth information. The cell then dies without having produced offspring.

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19
Q

What are telomeres?

A

Telomeres are the like the aglets on shoelaces. They indicate the end of the line. They protect the end of the chromosome from deterioration and from fusing with other chromosomes.

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20
Q

What happens to telomeres with each cell division?

A

They shorten, so the DNA is limited in how many times it can replicate.

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21
Q

What is telomerase?

A

An enzyme that can extend telomeres. Telomerase is normally turned ‘off’ in healthy cells.

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22
Q

What happens to telomeres in a cancer state?

A

Telomerase is turned on, allowing for multiple replications of the cell to no end.

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23
Q

As cancer cells bulk up into a tumor, how do they get their blood supply?

A

By angiogenesis. Cancer cells can trigger new blood vessel formation to feed itself.

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24
Q

What does a tumor suppressor do?

A

It inhibits cell proliferation or stimulates apoptosis when needed.

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25
Q

Why would you want to stimulate apoptosis in one of your cells.

A

If there is DNA damage, you don’t want those cells to replicate

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26
Q

Tumor suppressor genes are genes that ________ a cell from progressing toward cancer.

A

protects

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27
Q

What if there is a mutation to a tumor suppressor gene?

A

Then cancer can grow. However, you need two damaged tumor suppressor genes for cancer to proliferate. If only one of the genes is damaged, the healthy one will override it and maintain function.

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28
Q

One of the most important things that protects people from cancer is?

A

p53

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29
Q

What is the classic role of p53?

A

it prevents cells with damaged DNA from proliferating. It is the guardian of the genome.

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30
Q

Is there any evidence that p53 affects cancer?

A

Yes, about half of all patients with cancer have a p53 mutation.

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31
Q

During interphase of cell replication, there is a series of steps. Growth step 1, S- DNA synthesis, then Growth step 2. Where does the p53 checkpoint fall?

A

Bewtween Growth phase 1 and S Dna synthesis phase. If there is damage to the DNA that is not reparable at the p53 checkpoint, it will signal the cell to die by apoptosis.

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32
Q

Does p53 activation alway give a kill signal to the cell.

A

No, if the DNA is damaged but reparable, it will halt the progress until the DNA can be repaired. If it is not reparable, it will signal the cell to die by apoptosis.

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33
Q

Tumor suppressor genes are usually _______ (recessive/ dominant)

A

recessive

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34
Q

If one of your tumor suppressor genes is defective, will you develop a tumor?

A

No, the other gene (healthy tumor suppressor gene) of the pair, will ovverule and continue to suppress tumors. One wild type gene usually produces enough protein to protect the cells.

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35
Q

Define germline mutation.

A

Inherited variations found in all of our cells. We pass these on to our offspring.

36
Q

Define somatic mutations.

A

These are not inherited. They are variations often due to the environment. These will not be passed on to our offspring. Ex. if we get a sunburn, we get a somatic mutation. But not all somatic mutations cause cancer.

37
Q

What is meant by the 2-hit hypothesis of cancer development?

A

It is thought that a germline mutation makes you more prone to cancer, and a somatic insult enables it.

38
Q

What do proto-oncogenes normally do?

A

They normally stimulate cell proliferation

39
Q

Do we have proto-oncogenes in healthy cells?

A

Yes

40
Q

What happens if an proto-oncogene is exposed to a mutagen, carcinogen, virus, irradiation, or genetic mutation?

A

It can change into a transforming oncogene which creates a cellular oncogene which causes altered cellular functions and spontaneous neoplasm.

41
Q

Proto-oncogenes are genes that have ___________ to cause cancer.

A

the potential

42
Q

Some examples of proto-oncogenes are:

A

growth factors, growth factor receptors, and signal tranducing proteins. Other proto-oncogenes are RAS, RAF, WNT, MYC, ERK, and TRK. (proto-oncogenes are usually genes that regulate growth and differentiation).

43
Q

If a proto-oncogene converts to an oncogene, what will happen?

A

the oncogene has a potential to cause cancer.

44
Q

If you have a defect in RAF (for example), what can happen?

A

The signal for DNA replication will be turned on and will stay on even if there is not ligand activating the process.

45
Q

Are mutations to proto-oncogenes dominant or recessive?

A

Dominant. You only need one to really screw the whole system up.

46
Q

What are the 3 goals of chemotherapy?

A
  1. Inhibit synthesis of new DNA strands to stop cells from replicating
  2. Damage DNA of the affected cancer cells
  3. Stop mitosis and therefore stop cell division
47
Q

Unfortunately most chemotherapy drugs are ________ and can lead to _________.

A

non-specific and can lead to toxicities

48
Q

One approach of chemotherapy is to affect ___ DNA molecule building blocks.

A

pre

49
Q

What is the role of folate in the formation of nucelosides?

A

Folate is taken up by the cell and must be reduced to FH2 and then FH4 by dihyrdrofolate reductase (DHFR) for the formation of thymidine and other nucleosides.

50
Q

What does methotrexate do?

A

Methotrexate has a higher affinity for DHFR than FH2 and therefore prevents the reduction of FH2 to FH4 and thereby depletes intracellular FH4.

51
Q

What does fluorouracil do?

A

It prevents thymidylate synthetase which is needed for DNA production.

52
Q

What do cytotoxic antibiotics do?

A

they interfere with DNA replication and transcription

53
Q

Name a cytotoxic antibiotic

A

Doxorubicin

54
Q

What does doxorubicin do?

A

It inhibits topoisomerase II

55
Q

What does toposoimerase do?

A

it is an enzyme that regulates the overwinding and unwinding of DNA

56
Q

What happens to the cell if topoisomerase is inhibited?

A

The DNA that has split to replicate will not be able to reattach and wind back together. This leads to cell death.

57
Q

As DNA is unwound, it causes ________ further downstream.

A

supercoils

58
Q

What do alkylating agents do?

A

directly damage DNA in the nucleus of the cell, preventing replication

59
Q

Alkylating agents attach ________ groups to the ________DNA base.

A

alkyl groups to the guanine DNA base.

60
Q

By adding alkyl groups to the guanine base, what happens to the delicate proteins that form the double helix structure of DNA?

A

It causes the proteins to link in odd ways, like cross linking or intrastrand linking, which prevents the DNA from replicating and causes the cells to die.

61
Q

How does vincristine or other vinca alkaloids work?

A

They prevent tubulin from forming into microtubules.

62
Q

If tubulin cannot transform into microtubules, what will happen to the sister chromatids during mitosis?

A

without the tubules, the sister chromatids cannot be pulled apart and the cells division and replication comes to a screeching halt.

63
Q

Name 3 targetted therapies for cancer.

A
  1. Hormonal therapy
  2. Monoclonal antiboides
  3. Tyrosine kinase inhibitors
64
Q

A popular hormone therapy for certain types of breast cancer is:________.

A

Tamoxifen

65
Q

How does tamoxifen work?

A

In breast cancers where the estrogen receptor is causing the problem, a metabolite of tamoxifen acts as an antagonist at the estrogen receptor, preventing the receptor from activating cooactivators.

66
Q

Is tamoxifen in its active form?

A

No, the tamoxifen is inactive, but its metabolite is

67
Q

What do myoclonal antibodies do?

A
  1. They block growth signals
  2. They stop new blood vessels from forming
68
Q

The first step in growth signal transmission is:

A

a ligand is bound to the epidermal growth factor receptor (EGFR).

69
Q

Once a ligand is bound to the EGFR, what happens next?

A

A signal is conducted to K-RAS to RAF to Mek to ERK then to transcription factors.

70
Q

What happens if you get a cancer causing mutation in RAF?

A

The RAF will no longer require the activation of the ligand or any of the upstream activations to put it in motion. RAF can then trigger the cascade further downstream and causes transcription and replication of DNA.

71
Q

Where do monclonal antibodies act?

A

They act at the EGFR ligand binding site. They prevent the binding of the ligand that activates the transcription cascade.

72
Q

Name a monoclonal antibody.

A

Cetuximab

73
Q

What if you give Cetuximab in a situation where KRAS has been activated, will it stop the formation of transcription factors?

A

No, Cetuximab acts at the ligand site, if the defect is further down the chain, the cell wills still be overactive in producing transcription factors.

74
Q

Name a monoclonal antibody used to stop new blood vesels from forming.

A

Bevacuzimab

75
Q

Bevicuzimab is a____________.

A

angiogenesis inhibitor

76
Q

How do Monoclonal antibodies stop angiogenesis pathways?

A

they prevent the autophorphorylization of the receptor, which prevents the VGEF transmission from passing, which would have caused angiogenesis, progression and metastasis of the cancer.

77
Q

What is tyrosine kinase?

A

enzyme responsible for the activation of many proteins by signal transduction cascades. They are activated by adding a phosphate group to the protein.

78
Q

What do tyrosine kinase inhibitors do?

A

They prevent tyrosine kinase from activating a signal transduction cascade that would lead to cell divison and proliferation of dysplastic cells.

79
Q

B-Raf is mutated in approximately what percent of melanomas?

A

80%

80
Q

The common mutation in melanoma is:

A

BRAF V600E which causes BRAF to be coninually activated

81
Q

How does Vemurafenib work for melanomas?

A

It is a tyrosine kinase inhibitor for BRAF but not the wild kind, it is targetted for defective BRAF

82
Q

What chromosome is affected in chronic myelogenous leukemia?

A

Philadelphia Chromosome.

83
Q

What is the Philadelphia chromosome?

A

A part of chromosome 9 breaks and a part of chromosome 22 breaks and they reform to make the Philadelphia chromosome.

84
Q

What is BCR- ABL?

A

The two broken part of the chromosomes that make up the Philadelphia chrmosome seen in CML. This new chromosome is a tyrosine kinase.

85
Q

What is Gleevec?

A

Imatinib. Used to treat CML. Works by binding to ATP binding site for Bcr-Abl and inhibiting kinase activity. Without tyrosine acitivity, the substrate cannot be phosphorylated, halting CML activity.

Spring '14 Pharmacology (6 decks)

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