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Genetics E3 > Cancer > Flashcards

Cancer Flashcards

(81 cards)

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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
p53
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
26
FAS1
targeted by p53 b/c its involved in apoptosis
27
p21
"clamp", clamps onto cyclin complex to stop from phosphorylation hence stops cell cycle
28
retinoblastoma
gene product reversibly inhibits progression through cell-cycle (p53)
29
hereditary
have to knock out both genes for cancer
30
sporadic
non-inherited mutation
31
cancer process
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
32
pancreatic cancer
fast and deadly
33
prostate
slow
34
c. elegans
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
concept of drosophila development genetics
many mutants have been isolated that identify the proteins and their functions that are responsible for specific transitions
36
no transition
avoids this by temp changes by temp sensitive mutations, death (phenotype)
37
cellular blastoderm
single layer of embryonic epithelial tissue that makes up a blastula
38
gastrulation
makes many layers of embryonic epithelial tissue
39
segmentation
division of a cell
40
balanced lethal system
SM1 chromosome is multiply inverted to suppress crossing over, has dominant curly mutation that is homozygous ltheal
41
maternal effect mutations
isolated as female sterile mutations, earliest developmental mutants, code for mRNAs provided by mother
42
bicoid, bcd
"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
nanos
"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
morphogens
substances that define different cell fates in a concentration-dependent manner, bicoid was the first morphogen described at the molecular level
45
spaetzle
follicle cells secrete into ventral side of oocyte binds to toll (more famous in humans, grows the ventral side or ventral midline)
46
zygotic/segmentation
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
gap
proteins expressed in very low #'s (turned on after maternal affect), shows a gap in segmentation, re the first zygotic segmentation genes transcribed
48
pair-rule
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
segment polarity
deletion of part of each segment and its replacement by a mirror image of a different part of the next segment
50
homeotic genes
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
bithorax complex
extra set of ribs @ L1, T3 (w/halteres) turned into T2 hence another pair of wings)
52
homeobox
controls genes by binding 8 bp region upstream highly conserved in evolution, DNA binding motif
53
imaginal discs
bloom in metamorphosis, differentiate into most of the structures of the adult insect such as legs, wings, and head
54
antennapedia complex
antenna turned into legs
55
eyeless
critical for eye development (compound eye)
56
pax 6
human homolog for eyeless
57
eyes absent
required at an early stage in development for the compound eye
58
sin oculis
transcription factor that directs eye formation
59
sevenless
required for the specification of the drosophila R7 photoreceptor
60
boss
bride of sevenless, requires sevenless, triggers differentiation of the R7 photoreceptor cell in the compound eye
61
drop dead
late onset mutant (adult lethal), post eclosion, emerged as adult
62
behavior
the actions of reactions of persons or things under specified circumstances (ex: E. coli with chemoattraction, seeking and avoidance)
63
do genes influence behavior
yes
64
concordance
both twins have a trait
65
discordant
only one twin has the trait
66
fruitless
males court males, balanced lethal, transcription factor, no obvious homolog in humans but conserved
67
male version
male behavior regardless of actual sex
68
female version
female behavior regardless of actual sex
69
females expressing the male version of fruitless
court females
70
males expressing the female version of fruitless
do not court females
71
vomeronasal (VNO) organ
not aware of stimuli
72
main olfactory epithelium (MOE)
aware of stimuli
73
TRP2
allows distinguish males and females, unable to distinguish between males and females if this is mutated
74
circadian rhythm
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
period (per)
conserved, duplication and divergence, forms heterodimer with timeless
76
timeless (tim)
forms heterodimer with period
77
dClock
forms heterodimer with cycle
78
cycle (cyc)
forms heterodimer with dClock
79
oscillating feedback loop
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
suprachiasmatic nucleus
involved in circadian rhythm, regulated by daylight
81
non-rode/cone photoreceptors (ipRGCs)
help synchronize circadian rhythms

Genetics E3 (1 decks)

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