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KCSU17 Genetics > cancer > Flashcards

cancer Flashcards

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1
Q

collection of disorders that share a common feature of uncontrolled cell growth

A

cancer

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2
Q

mass of cells

A

tumor AKA neoplasm

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3
Q

programmed cell death

A

apoptosis

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4
Q

malignant

A

infectious or virulent

invades neighboring cells/tissues, enter blood vessels and go to different sites

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5
Q

benign

A

not harmful in effect

grow only locally and can’t spread by invasion or metasiss

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6
Q

tumors of epithelial tissue

A

carcinoma

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7
Q

tumors of connective tissue

A

sarcoma

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8
Q

tumors of lymphatic tissue

A

lymphoma

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9
Q

tumors of glial cells of CNS

A

glioma

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10
Q

tumors of hematopoietic organs

A

leukemia

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11
Q

cancer

A

when cells fail to differentiate and begin to divide without constraint

typically is not the result of 1 mutation, result of multiple gene mutations over a period of time

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12
Q

why is age such a large factor in cancer

A

multiple gene mutations over time in dividing cells result in cancer

more time=more divisions

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13
Q

primary basis of carcinogenesis

A

genetic alteration of cell regulatory systems

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14
Q

what determines carcinogenesis

A

interaction of genes with environment

genes may predispose you to cancer development, but environment also plays a role

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15
Q

how is the cell cycle regulated

A

checkpoints

proteins participate in regulation thru complex series of interactions among activators and repressors of the cycle

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16
Q

if a regulator identifies a defect…

A

fix or induce apoptosis

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17
Q

pRb

A

inhibitor

bind to E2f and causes cell cycle to stop before S phase begins

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18
Q

cyclin D

A

activator, CDK

binds to pRb –> inactivates it via phosphorylation

releases E2f complex and allowing cell cycle to progress thru S

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19
Q

CDK inhibitors

A

inactivate CDKs

cause cell cycle to stop

cause pRB activation

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20
Q

examples of CDK inhibitors

A

p16 and p21

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21
Q

p53

A

acts thru p21

halts cell cycle or induces apoptosis in response to DNA damage

activates p21 to halt the cycle

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22
Q

tumor supressor genes

A

inhibit cellular proliferation and block uncontrolled cell division

prevents tumor participation

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23
Q

mutation of TSG means

A

regulatory product not present

cell divides uncontrollably

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24
Q

TSGs have ___ properties

A

recessive

both copies must be inactivated

requires 2nd hit

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25
Q

TSG not present then…

A

loss of function mutation occurs in inhibitory factors of cell regulation

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26
Q

TSG =

A

break pedal

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27
Q

protooncogenes

A

non cancerous genes involved in basic regulation of normal cell function

when mutation occurs here it becomes oncogene

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28
Q

oncogene

A

gene whose constantly active regulator product can lead to unregulated cell grown and differentiation

oncogene = GAS pedal

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29
Q

oncogene activation via

A
  1. retroviral transduction
  2. point mutations
  3. insertion mutations
  4. chromosomal translocations
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30
Q

oncogenes have ___ properties

A

dominant

only 1 req. mutated copy causes disease

involves retrovirus

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31
Q

oncogenes are seen in which cell cancers

A

SOMATIC cell cancers

not germline

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32
Q

types of viruses that give rise to tumor cells (non genetic)

A
  1. virus w/DNA genome

2. retroviruses

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33
Q

retroviruses

A

viruses with RNA genomes

uses reverse transcriptase to transcribe RNA into DNA and insert oncogenes into DNA of host cell

transforming host into tumor producing cell

i.e. HIV or HTLV

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34
Q

TSG v. oncogene

function of normal version

A

TSG - regulates cell growth and proliferation, induce apoptosis

oncogene - promotes cell growth and proliferation

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35
Q

TSG v. oncogene

mutation (at cell level)

A

TSG - recessive (both copies inactivated)

oncogene - dominant (only one copy)

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36
Q

TSG v. oncogene

effect of mutation

A

TSG - LOSS of function

oncogene– GAIN of function

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37
Q

DNA repair genes

A

repair structural abnormalities in DNA

tumors can occur if these are defective

some breast cancers are caused by defects here

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38
Q

retinoblastoma

gene and cause (TSG or OG)

A

RB1 gene

tumor supressor

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39
Q

retinoblastoma pathphys

A

RB1 gene encodes for pRb which down regulates cell cycle

pRB inactivates E2F, applies a BREAK to the cell

defective pRB leads to unregulated cell differentiation, causing a tumor*

40
Q

TP53 gene

A

causes multiple cancer

tumor supressor

most commonly altered gene

41
Q

types of TP53 mutations

A
  1. TP53 germline mutations
  2. TP53 somatic mutations
  3. TP53 polymorphisms
42
Q

Li-fraumeni syndrome

A

only inherited cancer syndrome with TP53

autosomal dominant

43
Q

Li-fraumeni syndrome

prevalence and age of onset

A

children/young adults

44
Q

most common type of TP53 mutation?

A

somatic mutations

50% of all human tumors

45
Q

TP53 somatic mutations are found in which % of tumors

A

70% of colorectal
40% of breast
60% of lungs

50% of all tumors

46
Q

TP53 ,mutations

genetic links

A

gene location on 17p13.1

47
Q

TP53 protein product

A

tumor protein p53

48
Q

TP53 pathophys

A

p53 regulates division and prevents amor formation

interacts with genes to control cell cycle if damage is present

can arrest cell cycle thru p21 or apoptosis

49
Q

if TP53 is mutated

A

cells with damaged DNA may evade repair and destruction and continue replicating

50
Q

Environmental influcens of TP53

A

DA can become damaged by toxic chemicals, radiation, or UV rays

normally increases P53

carcinogenic substances induce specific TP53 mutations

51
Q

benzopyrene

A

found in cig smoke, increases p53

52
Q

Li-fraumeni syndrome

clinicat presentations

A

associated with breast, osteosarcoma, brain tumors, and other cancers

53
Q

colon cancer is from which genes

A

APC (tumor supressor)

HNPCC (DNA repair)

54
Q

APC gene

A

found in everyone
tumor supressor on 5q21-q22

both copies myst be mutated for tumor progression

55
Q

prevalence APC gene

A

85% of all sporadic colon tumors

56
Q

APC gene

genetic predisposing factors

A

colon cancer is multi gene dz

includes KRAS gene SMAD4 gene and TP53 gene

57
Q

APC proteins control

A

how often cell divides
how it attaches to other cells
ensures correct chromosome # of cells during division

58
Q

APT mutations (are/are not) sufficient enough to complete progression to metastatic dz

A

ARE NOT sufficient

59
Q

FAP

A

FAMILIAL adenomatous polyposis

characterized by early appearance of multiple adenomas or polyps of colon starting during ten years

100-1000s polyps formed, causing increased risk of cancer

60
Q

colonic adenomas

A

precursors of colon cancer

61
Q

FAP inheritance

A

autosomal dominant

62
Q

FAP age of onset

A

39 years of age

63
Q

milder type of FAP

A

autosomal recessive

caused by MUTYH mutation

fewer polyps (less than 100)

64
Q

HNPCC

A

hereditary nonpolyposis colorectal cancer

aka Lynch Syndrome

65
Q

inheritance pattern of HNPCC

A

autosomal dominant

66
Q

prevalence and age of onset HNPCC

A

2-5% of population

those w/gene have 70-82% risk increase of colon cancer

67
Q

genes linked to HNPCC

A

MLH1
MLH2

MSH2
MSH6

PMS6

68
Q

genetic links to development HNPCC

A

DNA repair genes

mutations in these genes are mismatch repair genes that confess increased lifetime riskto develop colorectal cancer

69
Q

HNPCC pathophys

A

not as many polyps ad FAP but ea. polo is more likely to be cancer

increased risk for uterine, ovarian, stomach, brain and other cancers too

70
Q

clinical presentations of HNPCC

A

don’t see multiple polyps but ea. polyp has high likelihood of become cancer

71
Q

HNPCC v. FAP

A

FAP = lgr # of polyps, ea. low probability of developing cancer (still lg # = higher likelihood of developing cancer)

HNPCC= presents at an earlier age, smaller number of polyps, ea. has hit probability for cancer

72
Q

typical age of colonscopy

A

50

if familiar history, screen earlier

73
Q

risk of colon cancer

avg. risk

A

no family hx or 2nd/3rd degree relative had it

begin screening at 50

74
Q

risk of colon cancer

moderate

A

two 1st degree relatives with CRC at any age, or 1 with CRC before age 60

begin colonoscopy at 40, screen every 5 yrs

75
Q

risk of CRC

w/HNPCC or suspected HNPCC

A

being colonoscopies at 20-25

continue every 1-2 years

76
Q

risk of CRC

FAP or suspect FAP

A

colonoscopies at 10-12

continue every 2 years

77
Q

genes associated with breast cancer

A

BRCA 1
BRCA 2

DNA repair mechanisms defect

78
Q

breast cancer inheritance factors

A

caused by both genetics and environment

5-10% of breast cancer is hereditary (1-3% from BRCA genes)

79
Q

breast cancer prevalence

A

1 in 8 women

80
Q

genetic predisposing factors of breast cancer

A

risk doubles if first degree relative is affected

BRCA 1 and BRCA 2 are major contributors of INHERITED breast cancer

81
Q

inheritance of BRCA genes

A

autosomal dominant

82
Q

BRCA 1 on which choromosome

A

17q21

83
Q

BRCA 2 on which chromosome

A

13q12.3

84
Q

BRCA pathophys

A

mutations result in loss of function

follow a two hit model for TSG

participated in DNA repair process – repair double stranded breaks

inactivation of BRCA genes result in incorrect repair and instability

85
Q

which population of women are at a higher risk

A

Ashkenazi Jew

86
Q

BRCA 1 clinical presentations

A

50-80% increased risk for breast cancer

20-50% risk for ovarian cancer

87
Q

BRCA 2 clinical presentation

A

50% lifetime risk for breast cancer

10-20% risk of ovarian

88
Q

treatment protocols BRCA

A

mammogram at 25 for those w/family history

pelvic exam 6-12 months

CA=125 levels at age 25

prophylactic oophorectomy reduces BC risk by 50% and ovarian cancer risk by 90%

89
Q

CML is which chromosome (and disorder)

A

philadelphia chromosome

translocation of chromosomes 9 and 22

90
Q

chromosome 9 (CML)

A

proto-oncogene designated c-ABL

91
Q

break in chromosome 22 occurs

A

in middle of gene detonated BCR

92
Q

CML is which type (TSG or OG)

A

oncogene activation

93
Q

CML pathophys

A

BCR fusion with c-ABL caucuses oncogene on FISH or karyotypic

produces abnormal fusion protein that activates all the time and only affects myeloid cells (increase in number of PH-1 cells)

94
Q

CML clinical presentation

A

another motion in protooncogene causes increased mitosis and blast iris (cells fail to differentiate)

95
Q

treatment of CML

A

Gleevec

prevent progression of disease by binding to active site of ABL Protein and inactivate it

KCSU17 Genetics (14 decks)

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