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Genetics E3 > Cancer > Flashcards

Cancer Flashcards

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Biology 101 flashcards
1
Q

What is transformation?

A

the failure of cells to remain constrained in their growth properties and give rise to tumors, uptake of naked DNA

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2
Q

What is the process of transformation?

A

naked DNA – transformation –> cancer

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3
Q

What is contact-inhibition?

A

normal cells that stop growing/multiplying when touching

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4
Q

What is multilayer of uninhibition?

A

cancer cells that pile on top of each other they essentially ignore the contact inhibition

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5
Q

What is a benign tumor?

A

a tumor that grows to a certain size and then stops, usually with a fibrous capsule surrounding the mass of cells

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6
Q

what is a malignant tumor?

A

a tumor whose cells can invade surrounding tissues and spread to other organs

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7
Q

what is metastasis?

A

the spreading of malignant tumor cells throughout the body so that tumors develop at new sites

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8
Q

chemotherapy

A

cancerous cells interfere with DNA synthesis by either slowing down DNA synthesis, interrupting chain elongation, or lack of specific nucleotides, when you kill S phase cells you kill a lot of normal cells

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9
Q

oncogenes

A

cancer-causing, dominant cancer genes, a gene whose action promotes cell proliferation

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10
Q

recessive cancer genes

A

a tumor suppressor genes/inhibit cancer progression

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11
Q

rous sarcoma virus (oncogene)

A

cell free (virus) filtrates could also induce tumor development

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12
Q

gag

A

precursor protein that is cleaved to produce virus particle proteins

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13
Q

pol

A

encodes a precursor that is cleaved to produce reverse transcriptase and an enzyme needed for the integration of the proviral DNA into the host cell chromosome

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14
Q

env

A

precursor to the envelope glycoprotein

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15
Q

src protein

A

has three domains but one contains a kinase (adds phosphate groups, reversible)

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16
Q

activation of src

A

V-src is missing C terminus and the inhibitory phosphorylation site, so its always active

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17
Q

inputs that turn on activation

A

phosphate removed
binding interrupted
phosphate added (to a different spot)

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18
Q

src pathway

A
  1. growth factors: if there’s too much will go to receptor pushing pathway forward), oncogene
  2. growth factor receptors: acting via tyrosine-specific protein-kinase activity
  3. GTP binding protein (intracellular transducer): turn on and off certain genes
  4. src protein kinase (intracellular transducer): turn on and off certain genes
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19
Q

proto-oncogene

A

normal gene, usually concerned with the regulation of cell proliferation, that can be converted into a cancer-promoting oncogene by mutation, mRNA is reversed transcribed and gets inserted into retroviral genome

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20
Q

“activation”

A

proto-oncogene is being “converted” to an oncogene

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21
Q

classes of proto-oncogene

A
  1. GF
  2. GFR
  3. IT
  4. NTF
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22
Q

direct isolation of human oncogenes

A
  1. tumor cells (where the oncogenes are, easy to grow in labs)
  2. isolate total cellular DNA
  3. partial restriction digest
  4. ligate marker gene
  5. marked genes
  6. transform into mouse host cells
  7. isolate total DNA
  8. re-transform mouse host cells
  9. re-isolate DNA
  10. package into virus
  11. isolate viral plaques with marker
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23
Q

tumor suppressor gene

A

like breaks on a car, takes away both “breaks in cell cycle”, genes which cause cancer when both copies of the gene are mutated in a diploid and lead to loss of function

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24
Q

RB1

A

makes protein pRB that helps stop cells from growing too quickly, causes retinoblastoma if mutated

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25
Q

p53

A

stops cell cycle & encourages cell death, is stabilized (by phosphorylation) upon DNA damage, is a transcription factor (turns on and off genes which DNA damage allows for), turns on p21

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26
Q

FAS1

A

targeted by p53 b/c its involved in apoptosis

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27
Q

p21

A

“clamp”, clamps onto cyclin complex to stop from phosphorylation hence stops cell cycle

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28
Q

retinoblastoma

A

gene product reversibly inhibits progression through cell-cycle (p53)

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29
Q

hereditary

A

have to knock out both genes for cancer

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30
Q

sporadic

A

non-inherited mutation

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31
Q

cancer process

A

normal epithelium – (loss of APC) –> hyper-proliferative epithelium – (increased genetic instability, loss of p53?) –> early adenoma – (activation of K-Ras) –> intermediate adenoma – (loss of Smad4 and other tumor suppressors) –> late adenoma – (loss of p53?) –> carcinoma – (other unknown alterations) –> metastasis

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32
Q

pancreatic cancer

A

fast and deadly

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33
Q

prostate

A

slow

34
Q

c. elegans

A

doesn’t develop the way we do (disadvantage), “bag of worms” phenotype as offsprings have to eat their way out of mom due to no vulva mutation

35
Q

concept of drosophila development genetics

A

many mutants have been isolated that identify the proteins and their functions that are responsible for specific transitions

36
Q

no transition

A

avoids this by temp changes by temp sensitive mutations, death (phenotype)

37
Q

cellular blastoderm

A

single layer of embryonic epithelial tissue that makes up a blastula

38
Q

gastrulation

A

makes many layers of embryonic epithelial tissue

39
Q

segmentation

A

division of a cell

40
Q

balanced lethal system

A

SM1 chromosome is multiply inverted to suppress crossing over, has dominant curly mutation that is homozygous ltheal

41
Q

maternal effect mutations

A

isolated as female sterile mutations, earliest developmental mutants, code for mRNAs provided by mother

42
Q

bicoid, bcd

A

“grow a head gene”, lacks head and thoracic structures, causing an interesting death, anterior
1. transcription factor = initiates transcription of hunchback (defines posterior)
2. translational inhibitor = inhibits translation of caudal (defines posterior)
3. primary anterior morphogen

43
Q

nanos

A

“grow a tail” gene, lacks a tail, posterior end, is tethered, nos protein is translational repressor (of hunchback), major target is the maternally supplied transcript of the hunchback gene

44
Q

morphogens

A

substances that define different cell fates in a concentration-dependent manner, bicoid was the first morphogen described at the molecular level

45
Q

spaetzle

A

follicle cells secrete into ventral side of oocyte binds to toll (more famous in humans, grows the ventral side or ventral midline)

46
Q

zygotic/segmentation

A

genes turned on by embryo (first genes to be turned on), genes that are first transcribed in the zygote, refine the anterior/posterior patterning into segments, subdivided into gap, pair-rule, and segment polarity

47
Q

gap

A

proteins expressed in very low #’s (turned on after maternal affect), shows a gap in segmentation, re the first zygotic segmentation genes transcribed

48
Q

pair-rule

A

cause deletions in pattern elements from every alternate segment, after gap genes have divided the body axis into rough generalized regions, pair-rule gene generate more sharply defined sections

49
Q

segment polarity

A

deletion of part of each segment and its replacement by a mirror image of a different part of the next segment

50
Q

homeotic genes

A

help assign a unique identity to each segment (turned on and off by zygotic segments), are regulated by the gap, pair-rule, and segment polarity genes

51
Q

bithorax complex

A

extra set of ribs @ L1, T3 (w/halteres) turned into T2 hence another pair of wings)

52
Q

homeobox

A

controls genes by binding 8 bp region upstream highly conserved in evolution, DNA binding motif

53
Q

imaginal discs

A

bloom in metamorphosis, differentiate into most of the structures of the adult insect such as legs, wings, and head

54
Q

antennapedia complex

A

antenna turned into legs

55
Q

eyeless

A

critical for eye development (compound eye)

56
Q

pax 6

A

human homolog for eyeless

57
Q

eyes absent

A

required at an early stage in development for the compound eye

58
Q

sin oculis

A

transcription factor that directs eye formation

59
Q

sevenless

A

required for the specification of the drosophila R7 photoreceptor

60
Q

boss

A

bride of sevenless, requires sevenless, triggers differentiation of the R7 photoreceptor cell in the compound eye

61
Q

drop dead

A

late onset mutant (adult lethal), post eclosion, emerged as adult

62
Q

behavior

A

the actions of reactions of persons or things under specified circumstances (ex: E. coli with chemoattraction, seeking and avoidance)

63
Q

do genes influence behavior

A

yes

64
Q

concordance

A

both twins have a trait

65
Q

discordant

A

only one twin has the trait

66
Q

fruitless

A

males court males, balanced lethal, transcription factor, no obvious homolog in humans but conserved

67
Q

male version

A

male behavior regardless of actual sex

68
Q

female version

A

female behavior regardless of actual sex

69
Q

females expressing the male version of fruitless

A

court females

70
Q

males expressing the female version of fruitless

A

do not court females

71
Q

vomeronasal (VNO) organ

A

not aware of stimuli

72
Q

main olfactory epithelium (MOE)

A

aware of stimuli

73
Q

TRP2

A

allows distinguish males and females, unable to distinguish between males and females if this is mutated

74
Q

circadian rhythm

A

many organs have their own circadian rhythm but all are in sync, a physiological cycle of about 24 hours that is present in all eukaryotic organisms and that persists even in the absence of external cues

75
Q

period (per)

A

conserved, duplication and divergence, forms heterodimer with timeless

76
Q

timeless (tim)

A

forms heterodimer with period

77
Q

dClock

A

forms heterodimer with cycle

78
Q

cycle (cyc)

A

forms heterodimer with dClock

79
Q

oscillating feedback loop

A
  1. period and timeless genes turn on mid-day
  2. in the evening, the two proteins join together, and can enter the nucleus
  3. period and timeless proteins shut down transcription of their corresponding genes
  4. period and timeless proteins also inhibit the transcription of the genes clock and cycle
  5. light can break down the timeless protein
  6. clock and cycle proteins activate the transcription of period and timeless
  7. period and timeless genes turn on in mid-day
80
Q

suprachiasmatic nucleus

A

involved in circadian rhythm, regulated by daylight

81
Q

non-rode/cone photoreceptors (ipRGCs)

A

help synchronize circadian rhythms

Genetics E3 (1 decks)

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