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Exam 3 Flashcards

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AP® Biology flashcards Biology 101 flashcards
1
Q

a form of programmed cell death in multicellular organisms

A

Apoptosis

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2
Q

a transcription factor that functions as a tumor suppressor and is important in multicellular organisms. It is critical in conserving stability. “guardian of the genome”, “guardian angel gene”, “master watchman”

A

p53

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3
Q

the percent of p53 mutation in commonly occurring human cancers

A

30 to 50

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4
Q

the most common mutation type in p53 that cause tumors

A

Point mutation

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5
Q

a point mutation resulting in amino acid substitutions

A

Missense mutation

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6
Q

a mutation in which a sense codon that encodes an amino acid is changed to a stop codon.

A

Nonsense mutation

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7
Q

a genetic mutation caused by insertions/deletions of a number of nucleotides in a DNA sequence that is not divisible by three.

A

Frameshift mutation

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8
Q

this is where the great majority of p53 mutations are

A

DNA binding domain

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9
Q

a mutation in one allele of the gene interferes with or obstructs the function of the wild type copy of the gene

A

Dominant interfering or dominant negative mutation

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10
Q

How the p53 usually functions

A

Homotetrameric transcription factor

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11
Q

in these cells, 15/16 of the subunits may lack normal function and 1/16 of the subunits may have normal function

A

Heterozygous at p53 locus

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12
Q

lifetime of p53

A

20 minutes

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13
Q

this is what causes elevated p53 levels

A

Posttranslational stabilization

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14
Q

This can lead to cell cycle arrest, DNA repair, block of angiogenesis, or apoptosis. This can also induce the expression of p21Cip1

A

Rapid Increase in p53

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15
Q

a potent CDK inhibitor of the cyclin CDK complexes and is able to halt cell proliferation in the late G1, S, G2 phases of cell cycle. Expression of this is absent in p53 mutant cells

A

P21Cip1

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16
Q

exposure to cells to this increases p53 levels

A

X rays

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17
Q

this influences the cellular responses

A

p53 genotype

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18
Q

leukocytes derived from the thymus that were used to illustrate the loss of viability in cells with wild type p53 compared to mutant p53

A

Thymocytes

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19
Q

this controls p53 levels in human/mouse cells and is a target gene of p53. Elevated levels of p53 induces expression of this and this will then bind to p53 and export it to the cytoplasm for degradation.(negative feedback)

A

Mdm2/Hdm2

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20
Q

these are what degrade p53 in the cytoplasm after export due to Mdm2/Hdm2

A

Cytoplasmic proteosomes

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21
Q

this of amino acid residues on the N terminal domain will block the Mdm2 binding thus saving p53 from degradation

A

Phosphorylation

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22
Q

the kinases that are responsible for p53 phosphorylation when DNA is damaged.

A

ATM/ATR and Chk1/Chk2

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23
Q

this can cause phosphorylation of p53 which saves it from degradation.

A

DNA damage

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24
Q

also known as p14ARF and this will associate with and inactivate MDm2 in the nucleus. It will function as a tumor suppressor through preventing p53 degradation

A

ARF

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25
Q

these form at the surface of an apoptotic lymphocyte

A

Blebs

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26
Q

this usually happens to the chromatin in apoptotic cells and this will shrink the nucleus

A

Condense

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27
Q

the genomic DNA in apoptotic cells is usually this way

A

Fragmentation

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28
Q

the intrinsic apoptotic pathway which is stress activated

A

Mitochondrion dependent pathway

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29
Q

the extrinsic apoptotic pathway

A

Receptor activated apoptotic pathway

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30
Q

this is a pro survival family and it contains BH4 and BH3, BH1, and BH2 of the receptor domain.

A

Bcl 2 family

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31
Q

this protein of the Bcl 2 family promotes cell survival

A

BH4

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32
Q

these are pro apoptosis families

A

Bax and BH3 only family

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33
Q

this lacks the BH4 domain

A

Bax family

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34
Q

two key proapoptotic proteins. Open channels in mitochondria and cause release of cytochrome c.

A

Bax and Bak

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35
Q

there must be this between pro and anti apoptotic proteins in a cell.

A

Balance

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36
Q

death signals activate Bax and Bak, these disrupt mitochondrial membrane releasing cytochrome c and Smac/DIABLO, there is assembly of apoptosome and liberation of caspases from IAP inhibition, there is activation of procaspase 9, activation of procaspase 3, 6, 7, cleavage of death substrates, then cell death.

A

Apoptotic caspase cascade

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37
Q

the ‘wheel of death’. Assembly of 7 spoked wheel in which Apaf1 forms the spokes and cytochrome c molecules form the tips of the spokes. This will activate procaspase 9 into caspase 9.

A

Apoptosome

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38
Q

this is on the inner surface of the nuclear membrane and is involved in the observed chromatin condensation and nuclear shrinkage.

A

Lamin

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39
Q

this is inhibitor of DNase which liberates it to cause fragmentation of chromosome DNA.

A

ICAD

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40
Q

these lead to collapse of the cytoskeleton and is responsible for the observed formation of blebs protruding from the plasma membrane and the formation of apoptotic bodies(condensed hulk of cells).

A

Cytoskeletal proteins

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41
Q

these are examples of cytoskeleton proteins.

A

Actin, plectin, vimentin

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42
Q

the estimated amount of death receptors in human genome

A

30

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43
Q

three subunit ligand complexes will bind to these and cause receptor trimerization. There cytoplasmic tails of these receptors will act via the FAS associated death domain(FADD) protein to assemble a death inducing complex signal (DISC)

A

Death receptors

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44
Q

the death inducing signaling complex that activates procaspases 8 and 10

A

DISC

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45
Q

these will activate procaspases 3, 6, and 7.

A

Caspase 8 and 10

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46
Q

induces the expression of Fas receptor and sensitizes the cell to any Fas ligand. This also induces the expression of IGF binding protein 3 and sequesters IGF 1 and IGF 2(the prosurvival and anti apoptotic ligands of IGF receptor). It also induces Bax expression and the expression of foxo3.

A

P53

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47
Q

a common cell death receptor

A

Fas receptor

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48
Q

the ability to proliferate indefinitely

A

Cell immortality

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49
Q

this cell type has the ability to proliferate indefinitely

A

Embryonic stem cell

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50
Q

viable, differentiated cells that lose the ability to divide

A

Senescent cells

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51
Q

the number of times that cells from human embryos or newborns can divide

A

50 to 60

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52
Q

a pedigree of cells related through mitotic division

A

Cell lineage

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53
Q

the number of tumor cells to display a tumor on an x ray

A

10^8

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54
Q

The number of tumor cells in a tumor in which it is first palpable

A

10^9

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55
Q

the number of tumor cells in a tumor that causes death, this requires a doubling of 40 times.

A

10^12

56
Q

a cell will need to double this many times to be 10^6 kilograms.

A

60

57
Q

This can lead to the loss of many cells in each generation through a cells lineage. This is normal in non cancerous cells and it is basically just the loss of some cells

A

Attrition

58
Q

this measures the cumulative physiological stress and the allowed quota for a cell. Once a cell reaches a certain damage threshold they enter senescence. It also has an allowed quota threshold in regards to usage and cells will then enter a state of crisis then apoptosis.

A

Cell generational clock

59
Q

this condition can lead to early onset of senescence compared to low oxygen levels

A

High oxygen

60
Q

these cell clock regulators help in the onset of senescence

A

p53 and p16

61
Q

this from p16INK4A induces a cell phenotype indistinguishable from that of cells that have entered replicative senescence

A

Ectopic expression

62
Q

inactivation of these is needed to circumvent senescence. What cancer cells do?

A

P53 and Rb

63
Q

these are located at the ends of chromosomes. Composed of 5’ TTAGGG sequence in tandem repeats thousands to times. These act to prevent end to end fusion of chromosomal DNA molecules. Its length registers the number of cell generations.

A

Telomeres

64
Q

a key protein in maintaining normal telomere structure. Inactivation of this results in massive end to end fusion of chromosomes. Too short is supposed to lead to crisis

A

TRF2

65
Q

the number of base pairs of telomeres shortened per cell generation.

A

50 to 100

66
Q

the length of telomeric DNA in normal human cells

A

5 to 10 kbp

67
Q

this region of telomeric DNA extends beyond the C rich strand which results in a 3’ overhang that is often several hundred nucleotides long.

A

G rich

68
Q

an enzyme that adds specific DNA sequence repeats to the 3’ end of DNA strands in the telomere regions. Adds the telomeres onto chromosomes. This enzyme is largely lost during differentiation. It is not detectable in normal cells but clearly detectable in 85 to 90% of tumor cells.

A

Telomerase

69
Q

the core of this has two subunits which are a reverse transcriptase and a 451 nucleotide long RNA

A

Telomerase holoenzyme

70
Q

The two subunits of the telomerase holoenzyme in human cells.

A

hTERT and hTR

71
Q

hTERT and hTR

A

Human telomerase reverse transcriptase and telomerase associated RNA

72
Q

there may be at least this many more subunits of the telomerase holoenzyme existing

A

8

73
Q

these escape from a cell population at low frequency in crisis and begin to grow robustly. These are said to be immortalized.

A

B lymphocytes

74
Q

expression levels of this are suggested to determine the levels of enzyme activity in a cell. Ectopic expression of this enables cell to gain the ability to proliferate indefinitely

A

hTERT

75
Q

disengagement from the second chromosome and unequal crossing over can cause this

A

Alternative lengthening of telomeres (ALT)

76
Q

production of a new tumor or tumors. Driven by a sequence of randomly occurring mutations and epigenetic alterations of DNA that affect the genes controlling cell proliferation, survival and other traits associated with the malignant cell phenotype

A

Tumorigenesis

77
Q

cancer incidence increases to a much greater magnitude in these individuals

A

Males

78
Q

these have proven to cause lung cancer which likely results in death.

A

Cigarettes

79
Q

the cumulative exposure to this determines the likelihood of developing a tumor rather than the age at which exposure began.

A

Carcinogen

80
Q

hyperplastic metaplastic and dysplastic tumors

A

Benign

81
Q

neoplastic and metastatic tumors

A

Malignant

82
Q

loss of APC on chromosome 5q and loss of p53 on chromosome 17p are associated with this percent of colon carcinomas

A

90%

83
Q

mutant and activated alleles of the K ras gene are found in close to this percent of colon carcinomas

A

50%

84
Q

the loss of TSG on chromosome 18q occurs in close to this amound to colon carcinomas but the identity of the inactivated TSG remains unclear.

A

60%

85
Q

this may create chromosomal instability

A

DNA hypomethylation

86
Q

loss of APC causes a hyperplastic epithelium. The DNA hypomethylation will cause an early adenoma. Activation of K ras leads to an intermediate adenoma and loss of 18q TSG causes late adenomas. Then, loss of p53 will cause a carcinoma.

A

Colon carcinoma progression

87
Q

a mutant cell spawns a large flock of descendants and then a new mutation somewhere in the descendants will trigger another wave of clonal expansion.

A

Clonal succession

88
Q

these are resistant to transformation by single mutated gene

A

Normal cells

89
Q

this usually requires collaborations of two or more mutant genes.

A

Cell transformation

90
Q

this is seen in rat embryo fibroblast experiments in which simultaneous induction of ras and myc or ras and E1A generate foci of transformed cells.

A

Oncogene collaboration

91
Q

Ras, pRb, p53, telomers, and PP2A

A

Intracellular pathways in cell transformation

92
Q

this is deregulated by the ras gene.

A

ras

93
Q

this is deregulated by CDK4 and D1 or SV40 LT or HPV E7

A

pRb

94
Q

this is deregulated by DN p53 or SV40 LT or HPV E6

A

p53

95
Q

this is deregulated by hTERT or myc and SV40 LT

A

Telomeres

96
Q

this is deregulated by SV40 sT and sometimes myc or Akt/PKB and Rac1 or PI3K or B56 shRNA.

A

PP2A

97
Q

this many distinct cellular regulatory circuits need to be altered before human cells can grow as tumor cells in nude mice

A

5

98
Q

cell transformation usually requires this many or more mutant genes collaborating

A

2

99
Q

the agents that cause genetic alterations (mutagens)

A

Initiating agent

100
Q

the agents that collaborate with the genetic alterations created by the initiating agent to drive the proliferation of cells

A

promoting agents

101
Q

common initiating carcinogen

A

DMBA

102
Q

common promoting agent

A

TPA

103
Q

this is done by painting once with an initiator then multiple painting over that with a promoter. Then painting the papilloma that forms with the initiator.

A

Inducing skin carcinomas in mice

104
Q

the painting with the initiator causes a mutation in ras. Then the repeated painting with the promotor cause a proliferation of cells with this mutation. The second painting with initiator causes a p53 mutation then promotor independent expansion can occur to proliferate the tumor cells with both a ras mutation and a p53 mutation.

A

Mouse skin carcinogenesis

105
Q

error by DNA polymerases, endogenous biochemical processes, and exogenous mutagens with their metabolites.

A

Major sources of mutation

106
Q

many DNA polymerases have this ability that allows them to minimize the number of bases that are mis incorporated and retained in the recently synthesized strand. A mutation in the coding for this protein can result in tumor formation

A

Proofreading

107
Q

MMR. These proteins function to recognize and repair the mistakes made by DNA polymerases.

A

Mismatch repair enzymes

108
Q

Short repeated DNA sequences

A

Microsatellite sequences

109
Q

These sometimes happen at replication forks

A

Double strand breaks

110
Q

this is when the amine groups on bases are lose

A

Base deamination

111
Q

this will turn to uracil when deaminated

A

Cytosine

112
Q

this will turn to hypoxanthine when deaminated

A

Adenine

113
Q

This will turn into Xanthine when deaminated

A

Guanine

114
Q

This will turn into Thymine when deaminated

A

5 Methylcytosine

115
Q

when the chemical bond linking a purine base(A and G) to deoxyribose breaks spontaneously. Breaks the deoxyribose from the base.

A

Depurination

116
Q

ROS. These are endogenous compounds that are highly reactive and can damage DNA. Examples include the superoxide ion, hydrogen peroxide, and hydroxyl radical. These oxidate the bases in DNA.

A

Reactive oxygen species

117
Q

these produce covalent cross links between adjacent pyrimidine bases in DNA.

A

Ultra violet radiation

118
Q

this can react with cytochrome P450 to cause a DNA adduct

A

Aflatoxin B1

119
Q

a form of DNA damage caused by covalent attachment of a chemical moiety to DNA.

A

DNA adduct

120
Q

These can cause DNA adduct formation when they become oxidized and attach to a base.

A

Heterocyclic amines

121
Q

a way for cells to prevent DNA molecules from attack and an example is skin cells using melanin to shield UV radiation

A

Physical shielding

122
Q

a way for cells to prevent DNA molecules from attack and an example is a cellular detoxification system against ROS.

A

Chemical defense

123
Q

GST. These enzymes use the sulfhydryl group of the cysteine residue of glutathione to detoxify reactive compounds.

A

Glutathione S transferase

124
Q

loss of expression of this protein leads to prostate carcinomas

A

GST pi

125
Q

the function to detect nucleotides of abnormal chemical structure. These include dealkylating repair, base excision repair, and nucleotide excision repair. These look for abnormal structure will mismatch repair look for wrong positions.

A

DNA repair enzymes

126
Q

these are repaired by homology directed repair or nonhomologous end joining.

A

Double strand DNA breaks

127
Q

the transfer of an alkyl group from one molecule to another. Dealkylating repair enzymes can restore normal base structure.

A

Alkylation

128
Q

a univalent radical consisting of only carbon and hydrogen bonds. Known as free radicals and are highly reactive.

A

Alkyl

129
Q

ENU. Alkylating agent.

A

Ethylnitosourea

130
Q

MGMT. This is a dealkylating repair enzyme.

A

O6 methylguanine DNA methyltransferase

131
Q

this tends to repair lesions in the DNA that derive from endogenous sources

A

Base excision repair

132
Q

this largely repairs lesions created by exogenous agents. Typically dimers

A

Nucleotide excision repair

133
Q

this uses homologous DNA sequences in a sister chromatid to instruct repair. Occurs in the S and G phases and is typically error free.

A

Homology directed repair

134
Q

this is not instructed by homologous DNA sequences in a sister chromatid. This occurs in the G1 phase and is largely error prone.

A

Non homologous end joining

135
Q

this is caused by defects in 1 of 8 distinct genes encoding components of the nucleotide excision repair complex. These patients are extremely sensitive to UV light.

A

Xeroderma pigmentosum

Cancer Biology (2 decks)

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