Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Biology Of Cancer > 4: genetics of cancer > Flashcards

4: genetics of cancer Flashcards

You may prefer our related Brainscape-certified flashcards:
AP® Biology flashcards Biology 101 flashcards
1
Q

causes of damage to cell genomes?

A

-Errors during replication
- constant attack from endogenous biochemical processes
- Occasional attack from exogenons mutagens and their Metabolites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what kind of Errors during replication can happen?

A
  • DNA pol has proofreading that digest faulty DNA → mutation in this domains can lead to earlier death
  • mismatch repair (MMR)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what does the Mismatch repair?

A

copying repeated Sequences ?
- MMR enzymes monitor recently synthesized DNA to detect miscopied DNA Sequences
→ defects in MMR are responsible for accumulation of a variety of mutations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

examples constant attack from endogenous biochemical processes?

A
  • Depurination (most common)
  • Base deamination
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what happens with depurination?

A

the Beta-N- glycosidic bond between adenine or guanine and the deoxysibose is hydroyzed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

when does Depurination occur?

A

when a purine base A or G is removed from the DNA deoxyribese backbone Via hydrolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what is Base deamination?

A

the removal of an amino group from a base.
Examp. → cytosine become s Uracil because of removal amino group
if uracil is not replaced it will become adenine in the new DNA strand during replication

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

examples of Exogenous mutagens?

A
  • UV radiation → produces pyramidine dimers
  • Reactive oxygen Species (ROS)
  • chemical carcinogens
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what causes the UV radiation?

A

pyramidine dimers → bond between adjecent pyrimidines in a strand / mostly thymine
-DisruptS normal pairing
- replication can not pas this lesion → cell will die When many are not repaired

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is Reactive oxygen species?

A

The striking of water by radiation causes it to lose an electron and become highly reactive
Result = Ros → reacts with DNA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are chemical carcinogens?

A

-Base- modifying agents → alkylating agents
- DNA aducts
- Base an alogues → molecules that can substitute for normal bases in nucleic acids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what can Exogencus alkylating agents do?

A

covalently alter DNA bases by attaching alkyl groups → methyl groups

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

with what can DNA aducts interfere?

A

DNA transcription and replication and induce mutations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what can P53 do?

A

recieves info about genetic damage, May arrest the advance of the cell through its growth - and _ division cycle and orchestrate localiad responses in that cell to facilitate the repair of damage
damage to severe → may decide te signal apoptosis mechanism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What signals can induce P53 induction?

A
  • U V radiation
  • X-rays
  • genotoxic agents
  • inhibitors of DNA synthesis
  • Agents that disrupt the microtubule of the ctoskelet
  • hypoxia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

how does p53 transcription factor work with MdM2?

A

key target of P53 is Mdm2 gene, When active as Tf it encourages the synthesis of Mdm2, the agent of it’s own destruction
- creates Negative feed back loop to ensure that P53 molecules are degraded → very low_steadu_state lends P53 proteins in normal, unperturbed cells

17
Q

What happened with DNA damage → P53 accumulation to functional levels

A
  • phosphorlation of amino acid in N-terminal domain
    alters domain that is recognized and bound by Mdm2 → p53 protected from Mdm2 → no ubiquitlaten of P53
  • DNA damage _activated ATM kinase phosphorylates Mdm2 that causes in acti vation and destabilization
18
Q

Mobilization of repair Machinery (P53)

A

_ DNA damage in G1 leads to activation of P53
- P53 induces P21 cip 1
- p21 halts cell proliferation
- same time ‘ components of cellular DNA repair machinery are mobilized
- cells lacking functional P53 are unable to repair the DNA

19
Q

function Base excisien repair (BER)?

A
  • repair of lesions in DNA, derived from endogenous sources → Ros, depurination, deamination
  • Repair enzymes DNA glycosylases
20
Q

function Nucleotide EXcision repair (NER)?

A
  • repair lesions creedted by Exogenous agents as photons and chemical carcinogens
  • Repair enzymes that recognize bulky helix distorting lesions → PCNA and RPA
21
Q

What is PCNA?

A

proliferating -cell nucleus antigen

22
Q

What is RPA?

A

replication protein A, binds single-strand DNA

23
Q

What are the 2 damage detection sub pathways?

A
  • Global genomic NER → itmoves DNA damage anywheren in the genome
  • Coupled NER (TC-NER) → specifically repairs transcription- blocking Lesions in actively transcribed DNA
24
Q

features of homology directed repair (HR or HDR)?

A
  • During late S phase and G2 phase of the cell cycle it uses sequences in the undamaged sister chromatic : homology
  • RAD51,BRCA1 and BRCA2 are involved in these steps
25
Q

features of Non homologous end joining (NHEJ) ?

A
  • liken no Sequence of sister Chromatid is available
  • Reconstruction of double helix that lacks some of the base pairs that were present in original DNA
26
Q

features familiar retina blastoma?

A
  • childhood eye tumor
  • sporadic, single eye,unilateral
  • familial, multiple foci of tumors, bilateral, autosomaal dominant
  • In activation of 2 functional Copies off the Rb gene?
  • knudsen model
27
Q

feature of familiar diseases?

A

you need 1 mutation in 1 alleIe where you need 2 alleles to mutate if you don’t carry the gene

28
Q

features Li-fraumeni syndrome?

A
  • mutant P53 allele inherited,autosomal dominant
  • high probability of develop ing Some term of malignancy early in life
  • More than 500 germline p53 identified
  • many at CpG site
29
Q

what kind of malignancy can Iiefraumen syndrome cause?

A
  • breast cancer
  • gli oblastoma
  • leukemia
  • lang cancer
  • pancreatic Carcinoma
  • Sarcoma
    -Wilms tumor
30
Q

features Xeroderma pigmentosum?

A

inherite d defect in NER
- GG-NER
- mutatien in the xp gene, high risk of Squamous cell Carcinoma and melanoma development from UV exposed skin lesions

31
Q

features Cockayne Syndrome?

A
  • TC NER
  • CS patients have a mutation in one of the two Cs genes
32
Q

features hereditary non-polyposis colon cancer (HN PCC )?

A
  • responsible for 2-3% of colon cancer cases
  • 80 ‘% life time risk of developing Colon Carcinomas
  • increased susceptibility te brain tumors, Ovarian carcinoma’s
  • Germ_line mutations in MSH2 and MLH1 Mismatch repair genes
    -inherit 1 defective allele of MMR gene and loose the wild type copy.
  • The resulting inability te properly detect and repair sequence mismatches leads te high rates of mutations in genes that have Microssatelite repeats nested in their sequence
33
Q

features BRCA1 familial breast and Ovarian cancer?

A
  • a lot involve gem-line transmission of a mutant BRCA 1 or BRCA 2 allele
  • Carriers have 50-70 risk of dendoping Breast cancer before 70 and 10-20 % of Ovarian cancer
  • defect in homology-directed repair of dsDNA breaks

Biology Of Cancer (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions