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MCM Test 2 > B2.078 Cancer Biology > Flashcards

B2.078 Cancer Biology Flashcards

1
Q

how does chromic inflammation affect cancer risk?

A

increases risk due to increasing cell proliferation and increased possibility for damage (ROS)

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2
Q

what are proliferative precursor lesions?

A

metaplasia- sustained injury

hyperplasia- hormonal stimulation

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3
Q

how does immunodeficiency affect cancer risk?

A

increases risk due to inability to fight off cancer cells without immuno-surveillance mechanisms

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4
Q

what type of inheritance is exhibited in familial cancer?

A

polygenic or multifactorial

can’t pinpoint specific genes but appears to run in families

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5
Q

what are some clinical features of hereditary cancer?

A 
multiple affected relatives
early age of cancer onset
bilaterally affected organs
multiple primary cancers in same individual
autosomal dominant pattern
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6
Q

what are the differences in risk associated with hereditary cancer associated w tumor suppressor genes vs, DNA repair genes?

A

both risks elevated
tumor suppressor mutation = virtually 100% likelihood of getting cancer
DNA repair mutation = highly likely, but may develop later or possibly not at all if DNA damage never occurs in a cancer specific gene

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7
Q

how many retinoblastoma patients have unilateral vs bilateral tumors?

A

70% uni

30 % bi

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8
Q

what percentage of retinoblastomas are hereditary?

A

40%

all bilateral are hereditary, but not all hereditary forms result in bilateral tumors

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9
Q

how does heritable retinoblastoma affect risk of developing other cancers?

A

400 fold increase

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10
Q

what tumor suppressor gene is associated with Li-Fraumeni Syndrome?

A

TP53

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11
Q

what are some tumors that often result from Li-Fraumeni Syndrome?

A 
breast carcinoma
soft tissue sarcoma
brain tumors
osteosarcoma
leukemia
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12
Q

what gene is associated with familial adenomatous polyposis (FAP)?

A

APC

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13
Q

how is FAP recognizable?

A

100s-1000s of colonic polyps in teenage years

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14
Q

what is the best treatment for FAP?

A

removal of the colon early in life

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15
Q

what is HNPCC?

A

hereditary non-polyposis colorectal cancer

Lynch Syndrome

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16
Q

differentiate between HNPCC and FAP

A 
HNPCC: early onset, but later than FAP
germline mutation in mismatch repair genes
5% of colon cancer
recognized by DNA slips in microsatellites alerting to poor repair mechanisms (MSH)
FAP: very early onset
germline mutation in APC gene
1% of all colon cancer
recognized by polyps
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17
Q

what percentage of breast cancers are inherited?

A

5-10%

18
Q

how does inheriting a BRCA gene mutation affect lifetime risk of cancer?

A

40-85% increase in breast cancer risk

BRCA1 55% and BRCA2 25% ovarian cancer risk

19
Q

what are the steps of chemical carcinogenesis?

A

initiation (permanent DNA damage)

promotion (proliferation stimulation)

20
Q

what are direct acting carcinogens?

A

alkylating/acylating agents
usually weak
used in chemotherapy

21
Q

what are indirect acting carcinogens?

A

aromatic hydrocarbons, dyes, toxins
metabolic conversion required (cp450)
strong carcinogens

22
Q

what are the 2 types of radiation carcinogenesis?

A

UVB exposure and ionizing radiation

23
Q

what is the mechanism by which UVB exposure causes cancer?

A

formation of pyrimidine dimers

normally repaired by nucleotide excision repair (XP pathway), but can be overwhelmed or dysfunctional

24
Q

what is the mechanism by which ionizing radiation causes cancer?

A

chromosomal breakage, translocations, point mutations

25
Q

what are some examples of microbial carcinogens?

A

retrovirus- HTLV-1
DNA virus- HPV, EBV, HBV, HHV8
bacteria- helicobacter pylori

26
Q

how do microbial carcinogens cause cancer?

A

viral integration into genome
direct activation/proliferation by interaction w tumor suppressor genes
increased genomic instability
immunological damage with resultant proliferation of lymphocytes/epithelial cells

27
Q

how do HPV E6 and E7 inactivate Rb protein?

A 
inhibits RB-E2F complex
increases CDK4/cyclin D1
inhibits p21
inhibits p53
increases telomerase
28
Q

what disease is associated with EBV?

A

Burkett lymphoma
set up uncontrolled B-cell proliferation resulting in mutations
(increased C-MYC expression)

29
Q

which oncogenes are affected by translocations?

A 
c-MYC (burkitt lymphoma)
-t(8:14)
BCL2 (follicular lymphoma)
BCR/ABL (chromic myeloid leukemia)
-t(9:22)
30
Q

which tumor suppressor gene is affected by deletions?

A

Rb

31
Q

which oncogenes are affected by gene amplification?

A

N-MYC (neuroblastoma)

HER-2/neu (breast cancer)

32
Q

which oncogenes are affected by point mutations?

A

RAS (many cancers)

33
Q

what are some epigenetic changes that can affect dysregulation of cancer genes?

A

local hypermethylation, global changes in methylation, changes in histones

34
Q

what is a growth fraction?

A

proportion of cells in a cell cycle that are actively dividing

35
Q

what are the 3 routes of cancer spreading?

A

hematogenous
lymphatic
body cavity seeding

36
Q

what are some local effects of cancer related to direct tumor growth?

A 
mass
bleeding
compression/obstruction
rupture/torsion
vascular compromise
necrosis
functional manifestations
37
Q

what are the two major systemic effects of cancers?

A

cachexia - profound weakness, anorexia, anemia
paraneoplastic syndrome- clinical findings not directly explained by anatomic location or functional output of the cancer

38
Q

what are some features of cachexia?

A

equal loss of fat and lean muscle
elevated basal metabolic rate
evidence of systemic inflammation

39
Q

what are characteristics of a good screening test?

A 
high sensitivity
variable specificity
high NPV
variable PPV
variables dependent on prevalence
40
Q

what are some types of cancer screening tests?

A 
clinical exam and procedures
radiological imaging
biochemical measurement
cytologic exam
histologic exam
nucleic acid testing for markers

MCM Test 2 (26 decks)

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