Lecture 24 Flashcards

1
Q

Intestinal epithelial cells: replaced every –

A

few days

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2
Q

Skin cells: replaced every –

A

2-4 weeks

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3
Q

Hepatocytes, heart muscle cells, neurons: replaced only during –

A

healing processes

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4
Q

Cancer occurs when the mechanisms that maintain these normal growth rates malfunction to cause –

A

excess cell division

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5
Q

A cell with impaired abilities to control its proliferation and tissue characteristics.

A

transformed cell

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6
Q

CANCER IS A – DISEASE

A

GENETIC

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7
Q

Cancer results from multiple genetic changes in a –

A

single cell

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8
Q

Cancer = Accumulation of mutations over lifetime:

A

late life disease

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9
Q

proto-oncogenes → oncogenes (gain-of-function)

A

promote cell growth

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10
Q

tumor suppressor→loss of function

A

restrain cell growth

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11
Q

care-taker genes→loss of function

A

protect genome integrity (repair)

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12
Q

Encode proteins that stabilize the genome

Tumors arise from both increase in point mutations and chromosome instability

A

care taker genes

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13
Q

Tumor cells frequently show – (i.e. highly aberrant chromosome compliments).

A

aneuploidy

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14
Q

Something in M phase cytoplasm causing G1 nuclei to enter mitosis. (induces mitosis)

A

Maturation Promoting Factor (MPF)

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15
Q

MPF is a –

A

Cdk and a cyclin.

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16
Q

Cells divide when cycling band decays. Cycling band called a –

A

cyclin.

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17
Q

T/F: The Cdk is only active when it is bound to cyclin.

A

true

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18
Q

The – of cyclin goes up and down with the cell cycle, therefore the kinase activity of Cdk also goes up and down with the cell cycle.

A

concentration

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19
Q

Cdc2 kinase is a –. In yeast there are two cyclins, a G1 cyclin and a mitotic cyclin.

A

Cdk

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20
Q

In yeast, a – in mitotic cyclin required to enter G1.

A

Decrease

21
Q

Retinoblastoma encodes a protein that inhibits –, required for activation of DNA synthesis machinery

A

transcription factor E2F

22
Q

Rb is a – of Cdk

A

target

23
Q

Cyclins and CDKs are –

A

proto-oncogenes

24
Q

Mutation of cyclins can lead to – expression of cyclins, resulting in kinases that are always active

A

constant

25
Q

Other mutations can lead to CDKs that are active –

A

without cyclin

26
Q

Mutations of – can stimulate constant DNA synthesis and mitosis

A

proto-oncogenes

27
Q

Growth factors are – that stimulate cells to divide

A

mitogens

28
Q

RAS is a G-protein that kinase cascade so RAS is a –

A

proto-oncogene

29
Q

All cancer cells acquire same six characteristics

Ability to proliferate without –

A

external signal

30
Q

All cancer cells acquire same six characteristics

Fail to sense signals that – cell division

A

restrict

31
Q

All cancer cells acquire same six characteristics

– replicative potential

A

limitless

32
Q

All cancer cells acquire same six characteristics

change their - to other cells

A

attachment

33
Q

All cancer cells acquire same six characteristics

obtain a – as they grow larger

A

blood supply

34
Q

All cancer cells acquire same six characteristics

tissue invasion and –

A

metastasis

35
Q

T/F: there are various pathways to cancer

A

true

36
Q

Some cancers are inherited
Heterozygous for mutant allele
Good allele is –, leading down the road to cancer

A

lost

37
Q

familial retinoblastoma – eye tumors

A

many

38
Q

sporadic retinoblastoma – eye tumors

A

one

39
Q

loss of heterozygosity through – and –

A

nondisjunction and mitotic recombination

40
Q

Effectors that can Inhibit Cell Cycle Machinery

– (induces DNA damage in a cell)

A

Ionizing irradiation

41
Q

Inhibits the kinase activity of the G1 cdk and prevents cells from entering into S.

A

p21

42
Q

mutations can be found in 50% of human cancers.

A

p53

43
Q

X-ray damages DNA → P53 is stabilized when DNA is damaged by phosphorylation = active p53 –>

A

production of p21

44
Q

Retinoblastoma is a – gene

A

tumor-suppressor

45
Q

pass if cell size is adequate and chromosome replication is successfully completed

A

G2 checkpoint

46
Q

pass if all chromosomes are attached to mitotic spindle

A

metaphase checkpoint

47
Q

pass if cell size is adequate, nutrient availability is sufficient, and growth factors (signals from other cells) are present

A

G1 checkpoint

48
Q

pass if DNA replication is complete and has been screened to remove base-pair mismatch or error

A

S-phase checkpoint