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BIO230 Section 2 > 2.12: Cancer > Flashcards

2.12: Cancer Flashcards

1
Q

describe the clonal origins of cancer

A
  • cancer develops from one cell that gains a mutation that allows it to survive, grow, and divide to form a tumor
  • progeny of this cell can gain additional mutations along the way to make it more successful
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2
Q

cancers are classified by the cell type from which they arise, so state where the following arise from:
1. carcinoma
2. sarcoma
3: leukemia

A
  1. carcinoma: cancers developing from epithelial cells
  2. sarcoma: cancers developing from connective tissue and muscle
    3: leukemia: cancers developing from blood cells
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3
Q

why are carcinomas the most common cancer

A

frequently dividing tissues are more likely to accumulate mutations, carcinomas are most common because epithelial cells have the highest cell division rates (the highest change to acquire mutations)

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4
Q

distinguish between tumors and cancer

A

tumors: cells that survive, grow and divide inappropriately: acquisition of mutations, increased cell survival/decreased cell death, increased cell division

cancer: malignant tumor with cells that have invaded the surrounding tissue: changes to cell-cell adhesion, can invade the basal lamina (for epithelial ++) and surrounding tissues

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5
Q

metastasis allows tumor cells to colonize additional tissues, explain the steps of metastasis

A
  1. benign tumor forms
  2. tumor invades surrounding tissue (becomes cancerous)
  3. cells enter blood or lymph vessles
  4. cells circulate
  5. cells escape vessel into other tissues
  6. cells grow and divide to form a metastatic (secondary) tumor)
    *survival rate is extremely low but only one cell needs to survive
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6
Q

explain how changes in cell adhesion can promote tumor growth

A

healthy tissues sometimes extrude cells (eg shedding of cells from epithelial lining), when healthy cells leave their protective environment they lose access to survival factors and undergo apoptosis.

tumor cells are able to escape this apoptosis, and may be extruded into the body, rather than the lumen, promoting metastasis

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7
Q

tumor cells can recruit other cells to form a?

A

microenvironement

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8
Q

why can cancers easily accumulate additional mutations

A

because some mutations promote genetic instability: they allow cancer cells to gain additional mutations quickly. for example, mutations in cell cycle checkpoints or dna repair (can’t fix mut)

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9
Q

cancers can accumulate additional mutations due to genetic instability, how might this show up on a karyotype?

A

a healthy karyotype is 22 autosome pairs and 1 pair of sex chromosomes. there might be large scale rearrangements due to abnormal assortments and/or point mutations leading to change in nucleotide (changes shape)

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10
Q

highlight the relevance of aflatoxin B1

A

some chemicals are harmless until they are ingested and metabolized by the liver enzymes. aflatoxin B1 can be found in some fungi or grown on grains/peanuts (natural sources) or cig smoke (unnatural sources). in this liver, there are cytochrome P-450 enzymes to convert aflatxin B1 into aflatoxin-2,3-epixide which then becomes a carcinogen bound to guanine in dna

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11
Q

how many dna repair pathways do cells have to fix any errors in dna replication

A

2

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12
Q

state the enzyme that converts aflatoxin b1 to aflatoxin-2,3-epoxide in the liver

A

cytochrome p-450 enzymes

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13
Q

what can the ames test be used to detect

A

chemical mutagens

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14
Q

describe how the ames test works

A

you mix together a test compound (potential mutagen), a culture of histidine-dependent salmonella, and homogenized liver extract (however you need to test with and without the liver extract bc of the aflatoxin b1 example). you put this mix onto a agar medium lacking histidine. incubate it at 37ºC for 2 days. if it’s a non mutagen then you’ll barely see colonies, if it is then you count colonies of hisitidine independent bacteria

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15
Q

explain how viruses can cause mutations

A

viral proteins mediate the controlled replication of the virus in outer cell layers (such as papillomavirus) and this leads to a benign growth/wart. when there is unregulated production of viral proteins, it drives cell proliferation in the basal cell layer with integrated gene encoding viral proteins which leaves to eovlution of malignant tumor (eg hpv driven tumors)

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16
Q

Why is a homogenized liver extract added to the Ames test?
a) It supplies the cells that might be modified to become cancerous.
b) It provides the chemicals that might cause mutations.
c) It modifies the chemicals that might cause mutations.
d) It provides histidine to the test.

A

C

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17
Q

state the classes of cancer-critical genes

A

oncogenes (gain of function dominant mutation), tumor suppressor genes (loss of function recessve mutation)

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18
Q

what is the normal version of oncogenes called

A

protooncogenes

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19
Q

what are the characteristics of oncogenes

A
  • mutated versions have increased activity in tumor cells
  • mutations are dominant - only one copy of the gene needs to be mutated
  • genes that normally promote cell-survival, growth, and division
20
Q

state the describe the different mutations that can lead to oncogene over-activity + the type of modification

A
  • deletion of point mutation in coding sequence: hyperactive protein made in normal amounts
  • regulatory mutation: normal protein greatly over produced by loss of cis reg elements
  • gene amplification: normal protein greatly overproduced
  • chromosome rearrangement (cells use chromosomes tgt): 1/2 of both genes = hyper production and putting gene near a promoter/enhancer (reg sequence) leads to overproduction
  • epigenetic modifications that increase oncogene expression
21
Q

how can epigenetic modifications cause cancer

A

they increase oncogene expression

22
Q

a _________ can cause an overactive receptor

A

deletion

23
Q

explain how a deletion can cause an overactive receptor

A
  • deleting key amino acids in ec ligand-binding domain can produce a version that is always active (think of rtks)
24
Q

list 3 examples of how a deletion can cause an overactive receptor

A

survival factor receptors, growth factor receptors, mitogen receptors

25
Q

_________ can create an overactive version of Ras

A

point mutations

26
Q

explain how an overactive version of Ras is produced

A
  • point mutations can create an overactive version of ras
  • a point mutation can disrupt the gtpase activity of ras oncogene
  • it cannot hhydrolyze gtp, so the signaling pathway is always on == ras always activates Raf (MAPKKK) and that pathway leading to always getting mitosis
27
Q

overexpression or gene amplification can increase _____ activity which is a __________ mutation

A

myc activity, regulatory mutation

28
Q

state the example of regulatory mutations given in the slides

A

overexpression or gene amplification can increase myc activity

29
Q

describe the result of myc activity

A

myc oncogene TF promotes cell cycle progression:
- increased g1-cdk activity
- increased g1-cdk expression
- increased e2f expression
- decreased Rb activity (increased phosphorylation)

30
Q

chromosomal rearrangements can create __________

A

overactive proteins

31
Q

explain how Abl is an example of chromosomal rearrangements

A

chromosomal rearrangements can create a
overactive proteins. Abl is a tyrosine kinase involved in cell signaling - it activates survival and proliferation. a chromosomal rearrangement creates a fusion between bcr-abl called the philadelphia chromosome. this removes the regulatory component of Abl making it hyperactive

32
Q

what is the philadelphia chromosome

A

it is the fusion between bcr and abl which is a chromosomal rearrangement

33
Q

what are the characteristics of tumor suppressor genes

A
  • usually underactive/inactive in tumor cells
  • mutations are recessive - both copies of the gene must be mutated to have a cancer-promoting effect
  • genes that normally act to repress cell survival, growth and division
34
Q

the loss of Rb function is an example of which class of cancer causing mutations

A

tumor suppression genes

35
Q

the loss of rb function can lead to tumor progression; distinguish between mechanisms of normal (healthy) individuals, hereditary retinoblastoma, nonhereditary retinoblastoma

A

normal: ocasional cell inactivates one of its two good rb genes = no tumor

hereditary = inherited mutant rub gene and occasional cell inactivates its only good rb gene copy = excessive cell proliferation leading to retinoblastoma = most people with inherited mutation develop multiple tumors in both eyes

nonhereditoary: the occasional cell inactivates its copy of the good rb gene has to happen twice to get excessive cell proliferation = only about 1 in 30000 normal people develops one tumor in one eye

36
Q

in retinoblastomas, why do some people develop multiple tumors in both eyes and why do some only develop one tumor in one eye

A

to get multiple tumors the mechanism is hereditary retinoblastomas so there is an increased likelihood of developing a tumor. the one tumor in one eye is non hereditary mechanisms

37
Q

state the result of loss of p53 function

A

it allows tumors to grow despite genetic changes

38
Q

describe the loss of p53 function

A
  • p53 tumor suppressor is activated under many different stress conditions when the cell might be in danger
  • p53 normally leads to cell-cycle arrest, senescence or apoptosis – they give cells a chance to fix the damage before killing it
  • loss of p53 function allows cells to survive when they should not
39
Q

under what conditions will the p53 tumor suppressor be activated

A

stress conditions, cells sense danger

40
Q

state the normal function of p53

A

cell-cycle arrest, senescence or apoptosis

41
Q

cancer critical genes _________ on several key pathways

A

converge

42
Q

list the key cancer critical gene examples for the following key pathways:
1. cell cycle
2. cell proliferation
3. cell survival

A
  1. cell cycle: rb: cell cycle entry
  2. cell proliferation: ras: signaling cascade that drives cell growth
  3. cell survival: p53: tolerance to stress and dna damage
43
Q

t/f multiple mutations are required for cancer progression

A

true

44
Q

what type of tumor cells frequently accumulate similar mutations in a characteristic order

A

colorectal tumor cells

45
Q

what does gleevec target (knowledge of cancer critical genes can lead to new treatments)

A

a drug that specifically targets the bcr abl kinase created by the philadephia chromosome rearrangement

46
Q

The human papillomavirus (HPV) gene E7 produces a protein that inhibits
Rb. Which of the following might help treat cancers caused by HPV?
a) A drug that inhibits p27.
b) A drug that activates E2F.
c) A drug that activates G1-Cdk.
d) A drug that inhibits S-Cdk.

A

D

BIO230 Section 2 (12 decks)

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