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BIOL 3321 - cell and molecular bio > cancer + genetic basis of cancer > Flashcards

cancer + genetic basis of cancer Flashcards

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1
Q

how many canadians will develop cancer in their lifetime

A

1 in 2

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2
Q

how many canadians will die of cancer

A

1 in 4

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3
Q

list the 4 most common types of cancer in order

A

lung, breast, colorectal, prostate

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4
Q

list 3 things that may influence cancer development

A

genetics, environmental influences, lifestyle choices

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5
Q

15% of colorectal cancers are due to inhertied mutations in the ___ gene

A

APC

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6
Q

women who inherit a mutant ____ allele have a ___ change of developing breast cancer by the age of 50 (vs __%)

A

mutant BRCA-1 allele, 60% chance, vs 2%

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7
Q

women who have a heterozygous mutation in the ____ allele have an increased chance in developing ovarian cancer (__% vs __%)

A

BRCA-1 allele, 15-40% vs 2%

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8
Q

list 4 environmental influences of cancer

A

chemical carcinogens, X rays, UV radiation, exposure to certain viruses

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9
Q

T or F: when you move somewhere new, you adopt that country’s common cancer types and lose the common ones where you came from

A

true

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10
Q

list some lifestyle choices that may influence cancer development

A

smoking, diet/being overweight/obesity, lack of exercise, viruses, alcohol

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11
Q

___% of all cancers could be eliminated by lifestyle choices

A

50%

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12
Q

the process by which cancer forms is called ____ or ____

A

oncogenesis or tumorigenesis

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13
Q

how many independent mutations are required to make a cancer cell

A

5-6

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14
Q

describe the multi hit model

A

mutations in genes that control cell growth and division lead to a mutant cell that does not follow the normal rules. Multiple mutations occur to develop cancer

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15
Q

what observation supports the multi hit model

A

most cancers occur later in life

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16
Q

describe the steps in tumor formation

A

an accidental mutation occurs within an epithelial cell. This cell proliferates = more mutated cells. Continued proliferation = tumor development

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17
Q

what two features define a cancer cell

A

it reproduces uncontrollably and it invades/colonizes areas where it’s not normally located

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18
Q

T or F: an abnormal cell that proliferates uncontrollably will ultimately give rise to a tumor

A

true

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19
Q

describe a benign tumor

A

small and localized, noninvasive, only become a medical problem if it gets too big that it interferes with normal processes or if it secretes an excessive amount of a biological substance

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20
Q

describe a malignant tumor

A

composed of cells that can invade nearby tissue (thereby causing secondary tumors to form at new sites = metastasis)

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21
Q

what is a carcinoma

A

from epithelial cells

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22
Q

what is a sarcoma

A

from connective tissue/muscle cells

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23
Q

what is a myeloma/leukemia/lymphoma

A

from WBCs or their precursors

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24
Q

what is the most common form of a malignant tumor + why

A

carcinoma: epithelial cells have the highest cell turnover rate, and these cells are most likely to be exposed to cancer causing agents

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25
Q

describe how cancer cells look different from normal cells

A

cancer cells have large + invariably shaped nuclei, often many dividing cells with disorganized arrangement, variation in size and shape, loss of normal features

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26
Q

how do cancerous cells look in culture?

A

changes to cell morphology, they can grow unattached, loss of contact inhibition

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27
Q

how do cancer cells differ from normal cells in regards to energy metabolism

A

cancer cells undergo aerobic glycolysis: they make use of glycolysis alone to produce energy whether oxygen is present or not

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28
Q

what is another term for cancer cells undergoing aerobic glycolysis

A

the Warburg Effect

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29
Q

how do cancer cells differ from normal cells in regards to genetic makeip

A

tumor cells are almost all aneuploidy (more or less chromosomes than normal)

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30
Q

mutations in which two main classes of genes have been implicated in the onset of cancer?

A

proto-oncogenes
tumor-suppressor genes

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31
Q

what is a proto-oncogene

A

a normal cellular gene that promotes cell survival or cell proliferation

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32
Q

what occurs when a PO gene undergoes a mutation

A

it becomes an oncogene

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33
Q

what is an oncogene + what does it do

A

it’s a mutated PO gene and it produces an overexpressed/overactive product of the PO gene

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34
Q

what type of mutation does a PO gene undergo to become an oncogene

A

gain of function mutation

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35
Q

describe the 4 mechanisms that convert PO to oncogene + the result of these mutations

A
  1. deletion or point mutation in the coding sequence = hyperactive protein in normal amounts
  2. regulatory mutation = normal protein that’s overproduced
  3. gene amplification = normal protein that’s overproduced
  4. chromosome rearrangement = normal protein overproduced OR hyperactive fusion protein
36
Q

what type of fashion do PO mutations act in

A

dominant

37
Q

what does it mean that PO mutations act in a dominant fashion

A

a mutation in a single copy of a gene can push the gene towards a cancer phenotype

38
Q

list 3 things that an oncogene may encode

A

a protein that causes uncontrolled or excessive progression through the cell cycle, a receptor that leads to altered signaling, or anti-apoptotic proteins

39
Q

what does the c-fos gene encode + what proteins is it requires to amke

A

encodes a transcription factor, required to make proteins involved in cell cycle progression

40
Q

increased transcription of the c-fos gene = ___

A

cell division

41
Q

T or F: Ras is a PO gene

A

true

42
Q

result of Ras undergoing mutations to become an oncogene?

A

= production of an overactive Ras oncoprotein. Ras will always be on and will mediate signaling without the presence of a ligand = continuous transcription of c-fos = continuous cell cycle = eventual tumor development

43
Q

T or F: Raf is a PO gene

A

true

44
Q

what do mutations in Raf to form an oncogene produce

A

= overactive oncoprotein

45
Q

Raf oncoproteins have been found in 50% of which cancer type

A

melanomas

46
Q

list two RTKs that are proto-oncogenes

A

EGFR and HER2

47
Q

EGFR and HER2 are part of the ___ subfamily of RTKs

A

ERbB

48
Q

what type of mutation does EGFR undergo to produce an oncogene

A

deletion of the coding sequence

49
Q

what is produced when the EGFR oncogene is expressed

A

it produces a truncated EGFR which lacks the ligand binding region = altered signaling

50
Q

in which type of cancer is the EGFR mutation common in

A

gliomas (brain tumors)

51
Q

T or F: since there are many PO genes that have been identified in the RTK/Ras/MAP kinase pathway, anticancer drugs have been make to target the pathway

A

true

52
Q

give an example of an anticancer drug that targets the RTK/Ras/MAP kinase pathway

A

Gefitinib

53
Q

what is Gefitinib

A

an anticancer drug + RTK inhibitor

54
Q

mode of action of Gefitinib?

A

inhibits tyrosine kinase activity of the EGFR. It’s given to those who have mutations in the EGFR gene

55
Q

what type of mutation does HER2 undergo to produce an oncogene

A

gene amplication

56
Q

what is the result of HER2 undergoing gene amplification

A

overproduction of the HER2 receptor

57
Q

how is HER2 activated

A

not by a ligand, but it’s activated upon heterodimer formation with other ERbB members

58
Q

what occurs when HER2 is overproduced

A

cells with extra copies of HER2 can become activated by homodimerization = cells are more frequently stimulated to proliferate = tumor formation

59
Q

what type of cancer is HER2 oncogenes found in

A

breast cancers

60
Q

which anticancer drug offsets the HER2 mutations

A

Herceptin

61
Q

mode of action of Herceptin?

A

it’s a monoclonal antibody that binds to the HER2 receptor and inhibits its activation

62
Q

what is CLL

A

chronic lymphoblastic leukemia

63
Q

why does CLL occur

A

cells do not die and this accumulate

64
Q

which gene from the Bcl2 family is a proto-oncogene

A

Bcl-2

65
Q

what type of mutation does Bcl2 undergo to become an oncogene

A

chromosomal rearrangement

66
Q

what is the result of Bcl2 undergoing chromosomal rearrangement

A

the Bcl2 oncoprotein is overexpressed

67
Q

what did the Bcl2 mutation result in in B cells

A

an enhancer was found upstream of the gene in B cells = overexpression of Bcl2 oncoprotein in B cells

68
Q

what is the result of Bcl2 overexpression

A

it always inhibits Bak/Bax = no apoptosis = tumor formation

69
Q

describe the number of B cells in CLL

A

there is an overproduction of B cells

70
Q

how do we diagnose CLL

A

WBC count or flow cytometry to look for specific surface markers

71
Q

what is a tumor suppressor gene’s normal function

A

to inhibit cell survival or cell proliferation

72
Q

what type of mutation does a tumor suppressor gene undergo that will inhibit its function

A

a loss of function mutation

73
Q

what is the result of a tumor suppressor gene undergoing a loss of function mutation

A

= uncontrolled cell proliferation + increased survival = tumor formation

74
Q

mutations of tumor suppressor genes act in a _____ manner

A

recessive

75
Q

what does it mean that tumor suppressor gene mutations act in a recessive manner

A

loss of function in both copies of the gene is necessary to push the cell towards a cancerous phenotype

76
Q

proteins encoded by tumor-suppressor genes belong to one of five classes. List the five classes

A
  1. proteins that regulate/inhibit entry into the cell cycle
  2. receptors or signal transducers for secreted hormones that inhibit cell proliferation
  3. checkpoint control proteins that arrest the cell cycle if something isn’t correct
  4. proteins that promote apoptosis
  5. enzymes that participate in DNA repair
77
Q

give an example of a tumor suppressor gene that acts as a checkpoint control protein + promotes apoptosis

A

p53 gene

78
Q

at which cell cycle checkpoint is p53 active? what occurs at this checkpoint?

A

G1 checkpoint: checks for cell size, nutrients, growth factors, DNA damage

79
Q

what does it mean that p53 acts as a cell stress sensor

A

upon sensing stress, the levels of p53 increase

80
Q

list 4 types of stress that p53 can detect

A

hyperproliferative signals, DNA damage, telomere shortening, hypoxia

81
Q

what 3 things may occur when p53 levels increase due to stress

A

cell-cycle arrest, senescence, apoptosis

82
Q

describe how p53 causes cell cycle arrest

A

p53 aids in the productions of protein that will halt progression through the cell cycle. Upon sensing DNA damage, cells are arrested in G1, an this allows time for the cell to fix the damage prior to commencing

83
Q

what would happen if there was a mutation in p53

A

the cell would continue through the cell cycle even in the presence of DNA damage. This can lead to the replication of a cell with mutations = cancer phenotype

84
Q

describe how p53 also promotes apoptosis in response to damaged DNA

A

it’s a transcription factor for Puma, which is a pro-apoptotic protein. Puma interacts with Bcl2 = release of Bak/Bax = apoptosis is activated

85
Q

what would happen if there was a mutation in p53 in terms of apoptosis

A

even if there was DNA damage, no Puma would be produced = cell survives. Cells would proliferate = increases the chance of a cancerous phenotype

86
Q

T or F: most human tumors have mutations in p53 or in proteins that regulate the activity of p53

A

true

BIOL 3321 - cell and molecular bio (19 decks)

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