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Molecular cell bio > F lec 21 > Flashcards

F lec 21 Flashcards

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Biology 101 flashcards
1
Q

a group of over-proliferating cells

A

tumour

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2
Q

tumours that are not able to invade neighbouring tissues and therefore are not cancerous

A

benign tumours

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3
Q

a tumour that can invade nearby tissues

A

malignant tumour (cancer)

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4
Q

cancer that has spread to secondary sites - via the travel of cancer cells through lymph or blood systems

A

metastatic tumour

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5
Q

cancer that arise from epithelial cells - most common and most dangerous cancer in humans

A

carcinomas

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6
Q

cancers that arise from connective tissue or muscle

A

sarcomas

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7
Q

cancers that arise from white blood cells

A

leukemias and lymphomas

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8
Q

2 competing theories on the origins/ causes of cancer:

A

chemical mutagens, viruses

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9
Q

____________________ are mutagens that cause cancer by mutating our genes

A

carcinogens

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10
Q

process by which we can change normal cells to cancer cells in vitro using mutagens - proved these mutagens could cause cancer

A

in vitro transformation

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11
Q

normal cells grown in culture will form a ________________

A

monolayer

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12
Q

normal cells grown in culture that lose contact with the place surface will undergo apoptosis - this is known as ________________ _______________

A

anchorage dependence

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13
Q

normal cells grown in culture that lose contact with the place surface will undergo ______________ - this is known as anchorage dependence

A

apoptosis

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14
Q

normal cells grown in culture will divide about _____(#) times before replication induced senescence occurs

A

30

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15
Q

normal cells grown in culture can enter senescence before their “30” time limit of cell division if they reach a _________________ _______________ due to contact inhibition

A

uniform monolayer

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16
Q

normal cells grown in culture can enter senescence before their “30” time limit of cell division if they reach a uniform monolayer due to ______________ ________________

A

contact inhibition

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17
Q

normal cells grown in culture require added ____________________ containing growth and survival factors to grow

A

serum

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18
Q

4 characteristics of cancer cells in culture compared to normal cells in culture:

A

loss of contact inhibition, loss of anchorage dependence, reduced requirement for added serum, ability to divide indefinitely (immortality)

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19
Q

the first characterized virus that causes tumours - led to a model that cancer is caused by infectious agents

A

RSV (rous sarcoma virus)

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20
Q

RSV is a _________________ that has an RNA genome and a reverse transcriptase enzyme to make a DNA copy of its RNA - the DNA copy is then integrated into the host cell genome

A

retrovirus

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21
Q

first animal virus to have its genome sequenced

A

SV40 (integrated DNA into host genome even though it wasnt a retrovirus)

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22
Q

the specific gene within RSV found to be responsible for its cancer causing abilities

A

src

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23
Q

retrovirus that causes cancer with slow onset

A

MLV

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24
Q

retrovirus that causes cancer quickly

A

RSV

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25
Q

what does RSV have that MLV doesnt?

A

src gene

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26
Q

what caused doubts about viral origins of cancer in humans: (2 things)

A

could not find viruses in most human tumours, most human cancers cannot be transmitted from person to person

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27
Q

Varmus and Bishop found that all chickens contain a ________ ___________ whether they have been infected with RSV or not

A

src gene

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28
Q

difference between endogenous src gene in chickens and the src gene carried by the virus

A

viral src gene lost most of its introns

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29
Q

even animals that dont get infected by RSV have this ________ __________ that was discovered to be the gene causing cancer in viruses

A

src gene

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30
Q

based on the observation that even chickens and other animals that have not or cannot be infected by RSV to cause cancer, researchers came up with the theory that it is not the presence of the gene that causes cancer, but rather cancer is caused by the __________________ of specific genes

A

overexpression (or in some cases the underexpression)

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31
Q

cancer is caused by the ____________________ of specific genes that originated from our own genome (proto-oncogenes), that are carried in viruses (viral oncogenes)

A

overexpression

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32
Q

cancer is caused by the overexpression of specific genes that originated from our own genome (________________), that are carried in viruses (viral oncogenes)

A

proto-oncogenes

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33
Q

advantage of incorporating the src gene into the viral genome for the virus and expressing that gene at high levels

A

causes the infected cell to divide more (which is good for the virus cuz then it can infect more cells)

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34
Q

MLV has slower onset of cancer because it does not contain one of those __________________ in the viral genome

A

oncogenes

35
Q

MLV is slower acting because it does not posses its own oncogene, BUT VIRUSES HAVE ENHANCERS AND INCREASE GENE EXPRESSION WHERE THE DNA INTEGRATES - so the DNA could integrate nowhere near an oncogene and so it wouldnt cause cancer that first time it infects, but as it spreads to other cells it has higher chance of landing near an oncogene in the host genome and overexpressing that oncogene to cause cancer eventually (WHERE it integrates matters)

A

JUST READ IT

36
Q

RSV is fast acting to cause cancer because it does not matter where it integrates in the host genome - since it possesses its own copy of the oncogene in the host it will already cause overexpression of that oncogene no matter where it integrates into the genome and so therefore less is up to chance compared to the MLV slower acting cancer causing virus

A

JUST READ IT

37
Q

method used to identify genes that are altered by a mutagen to cause cancer is called _______________

A

transfection (changing the DNA of the host)

38
Q

transfection experiments to identify genes altered by a mutagen to cause cancer:

A

DNA, calcium phosphate

39
Q

transfection experiments to identify genes altered by a mutagen to cause cancer:

A

transient

40
Q

transfection experiments to identify genes altered by a mutagen to cause cancer:

A

stable

41
Q

after creating transformed cancer cells in vitro, you can inject them into ____________________ mice and the mice will grow that tumor

A

immunocompromised

42
Q

after injecting an immunocompromised mouse with transformed cancer cells, researchers can identify the growth of the human tumor in these mouse cells using a repeat sequence called _________ that is unique to human cells –> the goal is to identify DNA causing cancer with the Alu sequence in the tumor in the mice (slide 28)

A

Alu

43
Q

the gene that researchers identified in the tumors grown in mice using Alu was the ________ gene (slide 28)

A

Ras

44
Q

the mutation in the ras gene identified from the carcinoma human cancer that made the protein constitutively active

A

V12

45
Q

in the human carcinoma analyzed, the ras gene had a V12 mutations that caused it to be _______________ ______________

A

constitutively active (always turned on- anakin skywalker and princess padme amidala have entered the chat)

46
Q

in the human carcinoma analyzed, the ras gene had a V12 mutations that caused it to be constitutively active - the reason for this constant activity is probably because this mutation caused the Ras gene to lose its ___________ activity

A

GTPase (since the Ras functions as a GTPase when functioning normally so without GTPase activity it will always be bound to GTP and therefore turned on)

47
Q

in cancer cells, oncogenes can be ___________________

A

amplified (= 100s copies of the oncogene in some cancer cells)

48
Q

5 things that can affect the activity of a protein of an oncogene causing cancer:

A

hyperactive protein made in normal amounts due to mutation in the gene, normal protein greatly overproduced due to regulatory mutation, normal protein greatly overproduced due to gene amplification, normal protein overproduced because of chromosome rearrangement because of new nearby regulatory sequence, fusion to actively transcribed gene produces new hyperactive fusion protein (type of chromosome rearrangement)

49
Q

seen in a stained karyotype, a massive amount of ___________________ _____________________ can lead to the overexpression of proto-oncogenes

A

chromosomal rearrangements

50
Q

using a FISH probe against myc, we can see multiple copies of a gene that dont even look like theyre on chromosomes - these are called ________________ ________________ __________________ - tiny bits that circulate away from the chromosome and replicate like crazy in the host cells and sometimes fuse together and join to a chromosome to form a homogeneous staining region

A

double minute chromosomes

51
Q

using a FISH probe against myc, we can see multiple copies of a gene that dont even look like theyre on chromosomes - these are called double minute chromosomes - tiny bits that circulate away from the chromosome and replicate like crazy in the host cells and sometimes fuse together and join to a chromosome to form a _________________ _______________ _________________

A

homogeneous staining region (basically a bunch of copies of the same gene so huge amplification of this myc gene)

52
Q

the viral copies of oncogenes are expressed at high levels by ______________ _______________

A

viral enhancers

53
Q

type of experiment used to determine what caused the cancer (oncogenes, chemicals, or virus)

A

cell fusion experiments

54
Q

in cell fusion experiments, a _____________ cell is fused with a _______________ cell

A

cancer, normal

55
Q

in cell fusion experiments, if the cancer was caused by a virus, the fusion cell will usually appear __________________

A

cancerous (bc the virus gets fused in too its still present)

56
Q

in cell fusion experiments, if the cancer was caused by oncogenes, the fusion cell should appear ________________

A

cancerous (this is what we would expect)

57
Q

in cell fusion experiments, in most causes of chemical induced cancers, the fusion cell appeared ________________

A

normal (this is what actually happened to chemically induced oncogenes- chemical induced and oncogenes are synonomous)

58
Q

in cell fusion experiments, in most cases of _____________ ________________ cancers, the fusion cell appeared normal

A

chemical induced

59
Q

since in most cases of chemical induced cancers, the fusion cell appeared normal, this argued that something present in normal cells can ________________ the fusion cell

A

rescue (change it from cancerous back to normal “save it”) (perhaps normal cells have genes that protect them from getting tumours)

60
Q

the familial form of retinoblastoma mutation tended to behave like a _________________ genetic mutation

A

dominant (if one parent has it 50% chance a kid will get it)

61
Q

form of retinoblastoma that is hereditary in nature, occurs very early in childhood, and usually occurs in both eyes

A

familial form (Retinoblastoma)

62
Q

form of retinoblastoma that usually appears later in life and almost never occurs in both eyes

A

sporadic form (no hereditary component)

63
Q

hypothesis about retinoblastoma where one normal allele of a gene is sufficient for normal function but then when the second mutation happens cancer is triggered (or abnormal function)

A

knudson’s 2 hit hypothesis

64
Q

normally, Rb inhibits the cell cycle promoter ________

A

E2F (so Rb is a tumor suppressor gene)

65
Q

in homozygous mutants for Rb, that cell will then ___________________ because of the higher expression of E2F and S phase cyclins, forming the Rb tumor

A

hyperproliferate

66
Q

loss of heterozygocity of a gene can occur by: (4 things we talked about)

A

nondisjunction causing chromosome loss, chromosome loss then chromosome duplication, deletion, point mutation removing function

67
Q

other than changes to the DNA itself, loss of heterozygocity can also occur by ________________ ___________ _________________ - somatically inherited chromatin modifications

A

epigenetic gene silencing (gene no longer transcribed even tho its still present)

68
Q

E2F should be an oncogene, but when it is overexpressed it does other things to the cell such that the cell ___________

A

dies (so in theory it would be an oncogene but in reality it just kills the cell if overexpressed)

69
Q

type of mutation where the patient will develop cancer almost certainly in life and will probably develop multiple cancers - guaranteed to get cancer and probably multiple cancers if you happen to live long enough to get the second one by not dying from the second one

A

p53 mutation

70
Q

the name of the disease of p53 mutation where the patient is guaranteed to get cancer and probably more than one cancer

A

Li-Fraumeni syndrome

71
Q

mutations in _______________ are not passed on

A

oncogenes

72
Q

it would be expected based on life span and number of cells that elephants would have a higher rate of cancer, but they actually get cancer rarely - elephant cells difficult to grow in culture cuz they undergo apoptosis alot - the reason for both of these things is they have like 20 fckn copies of _______

A

p53 (pretty much no chance they will lose all 20 copies of p53)

73
Q

well over 50% of human cancers include homozygous ______ mutants

A

p53

74
Q

2 things that cancer actually requires to happen:

A

overexpression of oncogenes, loss of tumor suppressor genes (cancer requires both to happen- only having one then the person is on their way to cancer but if both of these are there then they have cancer fosho)

75
Q

cancer progression requires ______________ genetic events

A

multiple

76
Q

•Most cancers derive from a single cell that acquires a somatic mutation that helps promote tumour formation.

A

clone

77
Q

Loss of a single tumour suppressor or gain of a single oncogenic mutation is ______________ (sufficient/ not sufficient) to cause cancer. Multiple somatic mutations must accumulate to produce cancer

A

not sufficient

78
Q

________________ _______________ facilitates rapid acquisition of new mutations - increasing the likeliness of cancer developing - can occur in many different ways but in all cases the checkpoint pathways need to be inactivated to allow these cells to survive and keep dividing

A

genomic instability

79
Q

genomic instability resulting from the failure to arrest the cell cycle in response to double stranded DNA breaks is called the ______________________________________________

A

breakage-fusion-bridge cycle

80
Q

•chromosome rearrangements, gene amplification, anneuploidy

A

genomic instability

81
Q

formation of new blood vessels - something cancer cells do to help survive they get their own supply of blood greedy bois

A

angiogenesis

82
Q

metastasis of tumours results from changes of genes involved in __________ __________________

A

cell adhesion

83
Q

once _________________ __________________ is acquired in cancer cells, other mutations arise faster

A

genome instability

Molecular cell bio (8 decks)

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