Cancer Genetics Flashcards

1
Q

what two mutations do 100% and 90% of cancers have respectively?

A

p16Rb is 100

p53 is 90

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2
Q

viral oncogenes…how?

A

genes similar to human genes controlling cancer can insert themselves into human genome and cause cancer

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3
Q

what did we discover first, viral or cellular oncogenes?

A

viral actually led to cellular discovery because when we realized viral were similar to genes they inserted around we realized the cellular genes could cause cancer too if mutated

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4
Q

protooncogene definition

A

gene important for cell growth and development that can become an oncogene by mutation or over or under expression

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5
Q

two common tumor suppressor genes

A

p53 and p16ink4a

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6
Q

La Fraumeni Syndrome cause

A

one mutant allele of p53 which is in charge of killing bad cells…so only need one more muation on other allele to maybe have cancer

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7
Q

pathway affecting the G1 cycle and regulation of it

A

Rb blocks G1…inhibit growth
cyclins and cdk4 block Rb…promote growth
p16 blocks cyclins and cdk4…inhibit growth
p53 activated Rb so inhibits growth

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8
Q

how does Rb problems lead to cancer?

A

if Rb is low, then cell can proliferate since it is an inhibitor of growth

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9
Q

how does cdk4/cyclins lead to cancer?

A

if these are upregulated and have a lot of them then they turn more Rb off and not as much inhibition of growth

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10
Q

how does p16 lead to cancer?

A

since it blocks cdk4/cyclin from inhibiting the Rb…if no p16 can have free running cdk4/cyclins that inhibit Rb and lead to more growth

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11
Q

how does p53 lead to cancer?

A

p53 enhances Rb activity so without p53 may have less active Rb and more cell growth

it also leads to apoptosis so without will have less cell death

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12
Q

how do PTEN and Bcl2 lead to cancer?

A

both of these are blockers of apoptosis

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13
Q

examples of genomic instability in cancer

A

mismatch repair, nucleotide excision repair, chromsome segregation, telomere structure

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14
Q

how do we usually get to cancer?

A

normally a multistep process with many genetic events

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15
Q

is hyperplasia physiologic or pathologic?

A

can be both…increase in normal cells number

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16
Q

is hypertrophy physiologic or pathologic?

A

can be both, growth in cell size

17
Q

is metaplasia physiologic or pathologic?

A

can be both…change in cell type

18
Q

is metaplasia reversible?

A

usually yes

19
Q

two examples of metaplasia

A

smoking and change epithelia in lungs…

acid reflux and change to get more goblet cells in esophagus epithelium

20
Q

dysplasia characteristics

A

atypical proliferation of cells with variation in size/shape, nuclear enlargement and irregularity
also has disorderly arrangement…lack of polarity and odd mitotic location

21
Q

type of neoplasia

A

can be well differentiated or poorly differentiated

22
Q

anaplastic neoplasia

A

no cellular differentiation

23
Q

what defines neoplasia

A

excessive growth of tissue that is uncoordinated and autonomous

24
Q

characterstics of benign neoplasm

A

slow growing localized growth… that resembles surrounding tissue and is well differentiated

25
Q

common name ending for a benign neoplasm

A

-oma

26
Q

paraneoplastic syndrome mechanism and what it is associated with?

A

symptoms not due to neoplastic cell localization…rather due to tumor cells secreting humoral factors

associated with malignant neoplasms

27
Q

differences in dysplasia, carcinoma in situ and carcinoma

A

dysplasia is abnormal appearing cells in epithelium
carcinoma in situ is dysplastic changes involving all layers of epithelium down to basement membrane
carcinoma is when dysplastic changes have now become malignant and are growing through the basement membrane

28
Q

mesenchymal neoplasm name

A

sarcoma

29
Q

epithelium neoplasm name

A

carcinoma

30
Q

what is the histologic grade of neoplasms based on?

A

how well differentiated the cells are…well to moderate to poor differentiation

31
Q

anatomic stage grading with TNM

A

tumor-0-4
nodes involved- 0-4
metastasis-0/+