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BIOC212 > FABIAN 1 AND 2 > Flashcards

FABIAN 1 AND 2 Flashcards

1
Q

what are sarcomas?

A

cancers arising in bone or in soft tissue of body (ie muscle)

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2
Q

how did Rous study the sarcoma virus?

A

filtered tumor homogenate from a cancerous chicken
transferred to a new chicken
that chicken got cancer
virus: rous sarcoma virus (RSV)
the homogenate was smaller than a cell=a virus

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3
Q

what makes a cell transformed? (7 things)

A
  1. immortal
  2. altered morphology (round)
  3. loss of contact inhibition (cells can grow on top of each other)
  4. anchorage independent growth (dont need a solid substrate to grow)
  5. reduced requirement for growth factors
  6. increased transport of glucose
  7. tumourgenicity (make tumours)
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4
Q

how can tumors be identified with imaging?

A

with a PET scan
radiolabelled glucose shows up where tumours are present

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5
Q

what is a retrovirus?

A

retroviruses use encoded enzymes (reverse transcriptase) to reverse transcribe their RNA genome into complementary DNA (cDNA) and then insert it into the host genome

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6
Q

what are the proteins coded for by viral RNA genomes?

A

gag gene = core proteins
pol gene = reverse transcriptase and integrase
env gene = envelope protein

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7
Q

what additional gene does RSV contain?

A

src gene
essential for triggering the formation of sarcomas

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8
Q

where was the src sequence found?

A

in both RSV infected cells and in uninfected cells

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9
Q

how does the pro viral DNA integrate?

A

randomly

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10
Q

how does it happen that ALV pro viral DNA causes cancer?

A

randomly integrated next to c-src, and then that gets transcript and packaged into new viral particle (RSV)

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11
Q

what are c src and v src called in this situation?

A

proto oncogene (c-src)
oncogene (v-src)

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12
Q

what type of protein is an Src protein?

A

a tyrosine kinase (phosphorylates specific tyrosines in substrates)
src can also autophosphorylate

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13
Q

what is a kinase?

A

an enzyme that removes high energy phosphate group from ATP and transfers it to suitable protein substate
thereby modifies the functional state of the substrate protein

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14
Q

what are many oncogenes?

A

kinases

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15
Q

what is selective growth advantage?

A

the different between birth and death in a cell population
allows cancer cells to outgrow the surrounding normal cells

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16
Q

what is an oncogene?

A

a gene that increases the selective growth advantage of a cell in which it resides

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17
Q

what is a proto oncogene?

A

a normal gene that can become an oncogene as a result of mutations or increased expression

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18
Q

what is a tumour suppressor?

A

a gene that when inactivated or lost leads to an increase in the selective growth advantage of the cell in which it resides

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19
Q

how is DNA of cancer cells transferred to normal cells?

A

by transfection

20
Q

what were early experiments of transfection to identify non viral oncogenes?

A

chemically transformed mouse fibroblasts: NIH T3 cells, great at taking up DNA
isolate their DNA
treat the DNA with 3-methylchloranthrene (3MC), a potent carcinogen
put that into normal mouse cells
formation of a focus of transformed cells
inject into mice: the mice form tumours

21
Q

how can a proto-oncogene be turned into an oncogene? (4 things)

A
  1. amplification: a genetic alteration producing a large number of copies of small segment in genome (higher levels of expression)
  2. insertion/deletion (indel): insertion or deletion of a few nucleotides
  3. translocation: a specific type of rearrangement where regions of two non homologous chromosomes are joined
  4. point mutations: single nucleotide substitutions
22
Q

what is a driver mutation?

A

a mutation that directly or indirectly confers a selective growth advantage to a cell

23
Q

what is a passenger mutation?

A

a mutation that does not confer a selective growth advantage (along for the ride)

24
Q

what is special about the number of mutations?

A

they vary across cancers (some have a lot of mutations some very little)

25
Q

what is karyotyping?

A

process of pairing and ordering a cell’s chromosomes

26
Q

what is cytogenetics?

A

the study of inheritance in relation to the structure and function of chromosomes

27
Q

what is the Philadelphia chromosome?

A

a translocation between chromosomes 9 and 22
makes a fusion gene

28
Q

what is BCR-Abl in simple terms?

A

translocation leads to a new gene in CML (chronic myeloid leukaemia)

29
Q

what is abl?

A

tyrosine kinase
proto oncogene

30
Q

what does BCR stand for?

A

break point cluster region

31
Q

what does the fusion of those two chromosomes lead to?

A

Abl kinase constitutive activity
emits strong growth promoting signals in a dis regulated matter
becomes hyper activated
cannot be turned off

32
Q

how is BCR-abl counteracted?

A

by using imatinib (Gleevec)
binds to the ATP binding site of BCR-Abl fusion protein
cannot phosphorylate
the substrate cannot enter the kinase site
acts as a competitive inhibitor
doesn’t kill normal cells

33
Q

how does the erbB2 signalling work?

A

erbB2 is a receptor tyrosine kinase
responds to epidermal growth factors (inserts into plasma membrane)
neuro/gluoblastoma derived oncogene homolog
human epidermal growth factor receptor 2 (HER2)
dimerisation activates proliferation and survival gene expression signalling pathways

34
Q

how are receptor tyrosine kinases organised?

A

ectodomain protrudes in extracellular space to recognise and bind the ligan
the hydrophobic transmembrane domain threads through the plasma membrane
the kinase domain sits inside the cell and transmits information

35
Q

what can mutations lead to in RTKs?

A

can result in ligand independent kinase activation
RTK over expression may cause the cell to become hyper responsive to low levels of growth factors and or cause ligand independent RTK dimerisation due to mass effect (many RTKs, they come in contact and dimerise)

36
Q

how can gene copy number be assessed?

A

by fluorescence in situ hybridisation (FISH)

37
Q

how is IHC analysis used for ERBB2/HER2 breast cancer cells?

A

look at protein level
measure the amount of protein by staining
may not be due to gene amplification but just high expression
take a tissue section
use an antigen, primary antibody, and secondary antibody with an enzyme that shows the stain

38
Q

what does traztuzumab (Herceptin) do?

A

binds to extracellular domain of the receptor and inhibits HER2 homodimerisation
prevents HER2 mediated signalling

39
Q

what are the 3 Ras genes?

A

K ras
H ras
N ras

40
Q

how do missense (point) mutations lead to mutant Ras proteins?

A

one of the most highly mutated genes in cancer
mutations in G(glycine) 12 and 61 turn Ras from proto oncogene to an oncogene
lead to GTPase negative feedback mechanism to be inactivated
found in many cancers
Ras is then constitutively active

41
Q

how does retinoblastoma vary in children with no familial history vs those with familial history?

A

no family history (sporadic form): single tumour in one eye, radiation and surgery effective
family history (familial form): multiple foci of tumours in both eyes, appear earlier, surgery and radiation can treat but then there is a greater risk of getting bone cancers and other tumours later in life

42
Q

what is the Knudson 2-hit hypothesis?

A

rate of appearance in familial was consistent with one random event (the other event is already present tin the family) and sporadic was consistent with two random events

43
Q

what are mitogenic pathways?

A

pathways that regulate/stimulate mitosis

44
Q

what is Rb?

A

a nucleur protein (has an NLS) that can be phosphorylated by a number of mitogenic signalling pathways
Rb acts as a transcriptional repressor that determines if the cell will enter S phase
if there is DNA damage: not phosphorylated, binds to E2F

45
Q

how do early cancer cells find ways to eliminate wild type copies of TSGs? (tumour suppressor genes)

A

mitotic recombination which leads to loss of heterozygosity (LOH)
can occur during G2 phase
subsequent segregation of chromatids leads to pair of daughter cells that have undergone LOH

46
Q
A

BIOC212 (32 decks)

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