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ISR > Cancer- Regulation of a cancer cell > Flashcards

Cancer- Regulation of a cancer cell Flashcards

0
Q

What is the most common type of DNA damage?

A

single-strand break
Problmes caused by single strand replication:
stalled replication
problems with transcription which leads to altered translation and protein expression.

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1
Q

What causes DNA damage?

A

UV rays
X-rays
radial-rays
although various things both-man made and natural, can damage DNA

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2
Q

What is the other type of DNA damage?

A

Double strand:

x-rays or radial-rays usually cause this mutation, double strand breaks cause the most damage to DNA.

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3
Q

What could some potential problems be from double strand breaks?

A

stalled replication/problems with transcription and can lead to altered translation and protein expression/Loss or gain of chromatids/ chromosomal translocation/ all mutations can promote cancer

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4
Q

What is the one physical protection our cells give us?

A

the epithilial cells create a mechanism used by a cell to shiels agaisnt things that are harmful to the DNA. These cells make a pigment called melanin that actually absorb some of the UV to protect our cells.

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5
Q

What is another way that cells can protect the body from DNA damage?

A

All cells have a molecular repair mechanism within the cell at the level of the DNA.

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6
Q

what are the proteins included in step one of DNA repair?

A

Signal proteins/ sensor proteins/ trnasducers and effector proteins

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7
Q

what does the signal protein do in DNA repair?

A

This protein signals to the sensors that that there is damage in the DNA.

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8
Q

what do the effectors do in DNA repair?

A

these are the proteins that confirm that there is damage in the cell.

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9
Q

what are the transducers job in DNA repair?

A

the transducer then sends a signal to the effectors saying there is a break in the DNA

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10
Q

What is the job of the effectors?

A

This protein tells the whole cell there is DNA damage and also begins checkpoint acivition.

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11
Q

What is step two of DNA repair?

A

effectors activate checkpoints and the cell goes through to find the damaged DNA.

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12
Q

what is the final step of the repair of damaged DNA?

A

after completing all the checkpoints, DNA repair will go through a very long and complex process involving many proteins.

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13
Q

What is Xeroderma pigmentosa?

A

mutation that prevents repair of damaged DNA because o UV radiation.

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14
Q

what are ways that cell scan suppress p53?

A

mutate it to where it can’t function any more.
delete p53 altogether
overpress some proteins that suppress p53 function (mdm2/ mdmx)

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15
Q

what is so special about the relationship of mdm2 and mdmx?

A

they can both do almost all the same things.

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16
Q

What does a radial mutation look like?

A

looks like a Y shape

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17
Q

what is a chromatid break?

A

when one of the chromatid has a break in it becaause of a mutation.

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18
Q

what is a fusion?

A

when to chromosomes join together.

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19
Q

What a re the two bas pairs for DNA

A

adenine-thymine

guanocine- cytosine

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20
Q

what are the three ways a mutations to your DNA can affect your cells?

A

this mutation can either be:
silent
harmful
beneficial

21
Q

what are the three Rs of DNA repair?

A

recognize
remove
replace

22
Q

What is the central Dogma?

A

this is a process cells gothrought to make proteins.when DNA is replicated then transcribed into RNA and then is translated into proteins.

23
Q

what are the three types of RNA in included in translation? and what are their functions?

A

mRNA- keeps the base pairs in order to create the correct amino acids for the the new protein
rRNA-links the mRNA with the tRNA
tRNA- using the anticodon on the rna it matches up with the mRNA codon to place the correct amino acid to form a new protein.

24
Q

What is the stop and start codons for translation?

A

the start codon is AUG

the stop codons are UAG, UGA, and UAA

25
Q

What are the three types of mutations for DNA?

A

Substitution-base pair is replaced with another
insertion-base pair is added into the DNA sequence
deletion- base pairs are deleted from the sequence

26
Q

What are the results of these three mutations?

A

Subsitution- changes one amino acid

insertion or deletion- causes frameshift

27
Q

what are the two genes called that usually have something to do with cancer?

A

tumor-suppressor genes- will stop cell growth and cancer cells require both genes in the cell to be mutated for cancer to work.
proto-oncogene: will stimulate cell growth these are called oncogenes when the cell grows continuously.

28
Q

What steps does cancer take to take over a cell?

A

early-polyp: loos of tumor suppressors
polyp:mutation of proto-oncogene
late polyp: loss of two additional tumor suppressor genes.
malignant tumor: inactivation of p53 tumor suppressor

29
Q

how are oncogenes activated

A 
they are activated by mutations like:
insertional mutagenesis
point mutagenesis
amplfication 
translocation
30
Q

where is N-myc usually amplified?99999

A

in the nueroblastoma

31
Q

what are examples of oncogenes?

A

N-myc, C-myc, Src, H-Ras

32
Q

what are oncogenes?

A

proteins that have the potential to cause cancer by making the cell continue to groow.

33
Q

what\how can tumor suppressor genes cause cancer

A

they have the potential to cause cancer by not stopping a cells growth.

34
Q

What do tumor suppressor do for the cell?

A

they can stop the cell cycle
they can fix DNA damage
they can cause apoptosis

35
Q

what are the most well known tumor suppresors?

A

p53 and RB

36
Q

What does p53 do

A

allows DNA repair or causes cell death:
if moderate damage- it stops the cell from dividing and activates DNA repair enzymes.
If severe DNA damage- causes cell death

37
Q

What does RB do?

A

A normal cell has two RB genes

what it does is hold on to proto-oncogenes until a protein comes along to tell the RB it can let it go and begin cell division

38
Q

what are the three types of cell death

A

apoptosis: suicide or programmed death
autophagy- in response to cell stress
necrosis:pathological cell killing- decay and destruction

39
Q

compare and contrast necrosis and apoptosis?

A

Necrosis: cellular swelling/ membranes are broken down/ATP is deleted/cell lyses causing an inflammatory response/ DNA fragmentation.
Apoptosis: cellular condensation/membranes remain intact/ Requires ATP/cell is phagocytosed/ ladder-like DNA fragments

40
Q

what are characteristics of Apoptosis?

A

shrinks
blebbing
phagocyte signals
nucleus breaks down

41
Q

What is the importance of Apoptosis?

A 
embryo development
maturing organisms
Virus infected cells
immune systems
DNA damage
42
Q

What are caspases?

A

proteins the degrade other proteins

43
Q

What is the extrinsic pathway

A

death ligand, death recoptor, caspase 8 and 3, call death

44
Q

what is the intrinsic pathway?

A

Mitochondria, Cytochrome C, Apoptosome complex, then caspases, cell death

45
Q

What is Bcl-2?

A

Is a small protein withinna family of Bcl proteins that play a crucial role in apoptosis

46
Q

what are the two groups for the Bcl family?

A

pro-survival: anti-apoptosis

pro-apoptosis: anti-survival

47
Q

What are the pro-survival Bcl proteins?

A

Bcl-2 and Bcl-xl

48
Q

What are the pro-apoptotic proteins

A

Bax and Bak

49
Q

What is Bcl-2 function?as well as Bak and Bax

A

Bcl-2 blocks both from the mitochondrion

while Bak and Bax activate cytochrome C which activates the rest of the pathway.

50
Q

What is BH3’s job?

A

BH3 blocks Bcl-2 from blocking bak and bax which in turn means that it is a pro-apoptotic cell.

ISR (3 decks)

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