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MCB II Block 1 > Cancer 2 > Flashcards

Cancer 2 Flashcards

1
Q

name some common causes of cancer

A 
inherited cancers
chromosome aberrations
chemical carcinogens
diet
ionizing radiation
oncogenic viruses
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2
Q

describe how viruses can cause cancer

A

when virus affects host cell ,some viruses express viral oncogenes. they inhiit the host cells tumor suppressor genes
some viruses can undergo insertional event, it inserts into host cell genome which could disrupt tumor supresser gene or oncogene

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3
Q

inherited cancer

A

pt inherits mutation that directly causes a type of cancer

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4
Q

direct inherited cancer

A

if pt inherits mutation in gene, that gene mutation is responsible for onset of that type of cancer
includes hereditary cancer

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5
Q

indirect inherited cancer

A

chromsoome instability syndrome

pts inherit mutations → chromosomal instability, that causes mutations which causes cancer

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6
Q

what is an example of an indirect inherited cancer

A

xeroderma pigmentosum

they can’t repair UV light, susceptible to skin cancer

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7
Q

aquired chromosome rearrangements, what is most common example

A

philadelphia chromosome

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8
Q

philadephia chromosome is caused by what

A

translocated chromosome b/w chromosm 9 & 22

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9
Q

what is the philadelphia chromosome

A

22q- caused by translocation of chrom. 9 & 22

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10
Q

abelson (ABL)

A

intracellular tyrosine kinase

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11
Q

what is abelson normally involved in

A

normally involved in transducing signaling

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12
Q

what happens as result of t(9:22)

A

transcribe fusion gene encoding for brand new fusion protein

contains exons for BCR & ABL which has constitutevely active tyrosine kinase activity

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13
Q

translocations are mostly involved in what kind of cancer

A

leukemias & lymphomas

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14
Q

deletion in 1p is commonly found in what ancer

A

colorectal

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15
Q

if there are deletions that cause cancer, what kind of gene was most likely located in it

A

tumor supressor

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16
Q

chemical carcinogenesis

A

multistep process involving many genes

target: oncogene & tumor suppressor gene

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17
Q

what is first step in chemical carcinogenesis

A

initiation: change in DNA 9mutation

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18
Q

what is 2nd step in chemical carcinogenesis

A

promotion- clonal expansion

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19
Q

what is 3rd step chemical carcinogenesis

A

progression - cells aquiring more and more mutations

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20
Q

how is DNA damage a form of cancer treatment

A

cancer cells very susceptible for DNA damage, so most cancer cells killed

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21
Q

UV radiation causes formation of what

A

thymine dimers - if not exised, abnormal cross linking b/w bases and breakage of DNA

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22
Q

alkylating agens

A

attach alkyl group to base

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23
Q

chemical crosslinking

A

aka aduct formation

chemical group prevent attachment to base

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24
Q

in alkylation and chemical crosslinking, as a result of covlalent attachemnt, what happens

A

the are no longer guanines, so abnormal cross inking, strand breakage

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25
Q

direct acting carcinogen

A

chemical is directly alkylating or forming aduct in DNA

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26
Q

indirect carcinogen

A

metabolized before reacting with DNA

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27
Q

ex of indirect carcinogen

A

benzo-a-prene (in tobacco smoke)

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28
Q

what is an example of what is involved in most lung cancer

A

smoking

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29
Q

smoking causes what percent of cancer death

A

1/3

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30
Q

onset of sporadic cancer is over age of

A

45

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31
Q

if sporadic cancer is under age of 45 assume its

A

hereditary

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32
Q

describe why people in eastern china have such a high rate of dying of liver cancer by age 45

A

aspergillus flavus mold makes toxin aflatoxin B1

people eat the mold and toxin and the toxin is converted into reactive hepoxide and induces changes in genome

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33
Q

in cigarette smoke benzo-apyrene is converted to what

A

BPDE

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34
Q

how much of cancer could be prevented by healthy diet and healthy weight

A

30-40%

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35
Q

obesity is strongly linked to what kind of cancer

A

GIT, breast, prostate, cervix, uterus

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36
Q

low fiber, high glycemic index is associated with what cancer

A

GIT cancer

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37
Q

radiation results in what

A

breakage of genome, which could cause cancer

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38
Q

viruses associated with how many tumors

A

10-20%

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39
Q

when cell is transofmred, what does it mean

A

initiated to start proliferating

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40
Q

EBV

A

(Epstein–Barr virus)virus can cause burkitts lymphoma - usually found in mandble

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41
Q

HTLV stands for what

A

human t cell lymphema virus

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42
Q

HTLV results in what

A

t cell leukemia

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43
Q

HIV infection and cancer

A

aids - immuno supression which could result in infection of opportunistic virus

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44
Q

HPV linked to what cacner

A

cervical

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45
Q

HPV is what kind of virus

A

DNA virus

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46
Q

when HPV infects what does it do

A

contains oncogenes E6 & E7 which inactive p53 and Rb (tumor suppressors)

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47
Q

helicobacter pylori is konwn to be associated with what

A

gastric cancer

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48
Q

why does helicobacter pylori cause gastric cancer

A

chronic inflammation

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49
Q

describe how tumor progression is a multistep process

A

Summary: selection of cells with progressive capability for proliferation, invasion & metastasis
after each step, a cell could aquire another mutation that has a selective advantage, and it proliferates even more rapidly

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50
Q

CIN stands for what

A

cervical intraepithelial neuroplasia

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51
Q

APC stands for what

A

adenomatic polyposis coli

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52
Q

what are the intermediate stages of cancer induction

A

polyps, benign adenomas, carcinomas can be isolated

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53
Q

beinign tumor becomes more and more aggressive until

A

it eventually metastisized

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54
Q

how can physical examination diagnose cancer

A

location & size, regional lymphadenopathy

brain tumor - neurological symptoms

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55
Q

regional enlarge lymph nodes

A

if they are hard and non tender, suggest spread of cancer

if they are not hard, suggestive of infection

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56
Q

general symptoms of cancer

A

unexplained weight loss, cachexia, lethargy, anorexia, nausea, confusion
fever, night sweats, infection, bruising
fatigue, anaemia, urogenital bleeed

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57
Q

what is cachexia

A

tissue wasting, occurs in late stage of cacner

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58
Q

hypercalcaemia suggests tumor has spread where

A

suggests cancer has spread to bone

59
Q

hypercalcamia?

A

high calcium level in blood

60
Q

why do pts with leukemia & lymphoma have high amounts of infection?

A

bone marrow taken over by cancerous cells, so can’t produce enough normal cells
pt is anemic (not enough RBC)
recent infections (not enough WBC)

61
Q

PSA test can test for what cancer

A

prostate

62
Q

CA125 test can test for what

A

ovary

63
Q

CEA can test for what cancer

A

colon & lung (blood tests)

64
Q

what radiology tests can be used to detect cancer

A

xray, ct ,mri pet

65
Q

cancer is a ____ process

A

multistep

66
Q

cancer is a ____ ____ nomatter what the cause

A

genetic disease

67
Q

most cancers are ____, some are inherited

A

sporadic

68
Q

within sporadic cancers, some pts have inherited predisposition. so if first degree relatives are affected, could have

A

inherited predisposition

69
Q

mendelian cancer

A

inherited with mendialan, the cancer causing mutation is in every call of body

70
Q

sporadic cancer is ____

A

multifactoral

71
Q

go through multistep process

A

slide 54

72
Q

cancer is clonal & heterogeneous

A

but not all daughter cells surivive, some won’t have mutations combatible with life

73
Q

eventually mutations will result in disruption of

A

chromosome

74
Q

disruption of chromosomes leads to what in cacner

A

more mutations and more cancer

75
Q

what are two examples of caretaker genes

A

MSH2 & MLH1

76
Q

what are two major genetic changes that happen in cacner

A

activation of proto-oncogene

loss of function of tumor supressor genes

77
Q

are apoptosis genes always included in tumor suppressor and oncogene categories

A

sometimes genes that cause apoptosis are put in with tumor supressor and oncogene ,sometimes they aren’t

78
Q

activation of what kind of gene in cancer regarding cell death

A

activation of anti-apoptotic gene

79
Q

anti-apoptotic gene is type o fwhat

A

proto-oncogene

80
Q

proapoptotic gene is a type of what

A

tumor supressor gene

81
Q

cancer has loss of what gene regarding apoptosis

A

loss of proapoptotic gene expression

82
Q

caretakers do what

A

monitor genome & repair it

they make sure mutations are fixed

83
Q

what kind of mutation happens to tumor suppressor gene to cause cancer

A

loss of function mutation

84
Q

how many mutations need to to occur to have loss of function of tumor suppressor gene

A

2 mutations

85
Q

what specifically has to happen for true loss of functio of tumor suppressor gene

A

both alleles of same tumor suppressor have to be lost

86
Q

what kind of mutation results in proto-oncogene

A

gain of function mutation

87
Q

how many mutations have to occur to have proto-oncogene

A

1 mutation

88
Q

1 loss of function in 53 and 1 loss of function of RB - affect on cell?

A

no affect

89
Q

single mutation of proto-oncogene results in what

A

oncogene - promotes proliferation

90
Q

proto-oncogene is what

A

any gene that normally simtulates cell proliferation

91
Q

a point mutation in proto-oncogene can potentially do what

A

activate it

92
Q

mutation in promoter region of proto-oncogene

A

drives increased expression of w.t. gene.

93
Q

if there is overexpression, even if it is w.t, it is:

A

oncogenic change

94
Q

both gene amplification and regulatory sequence mutation resutls in what

A

overexpression of wild type

95
Q

what two things can happen with chromosome translocation regarding oncogene activation

A

over-expression: promoter region from different gene that joins to the chromosome, that promoter region is now controlling the proto-oncogene of the other genes promoter. the new promoter is a lot stronger, so increased protein expression

chimeric gene product: like philadelphia chromosome - it’s always switched on, brand new protein produced that is hyperactive

96
Q

mutation in promoter region, gene amplification, or translocation, in all of it there is what

A

overexpression

97
Q

draw out oncogene mechanism chart

A

pg 64

98
Q

anythng that normally simtulates proliferation is a

A

proto-oncogene

b/c if they are activated - excessive proliferation

99
Q

what are two examples of hereditary cancer via oncogene activation

A

Multiple endocrine neoplasia type 2 (MEN2)

Hereditary papillary renal carcinoma

100
Q

why are oncogene activation hereditary cancer rare

A

not usually compatible with survival

101
Q

MEN2 stands for what

A

Multiple endocrine neoplasia type 2

102
Q

pts with hereditory oncogene cancer usually present with cancer when

A

early in life

103
Q

pts with MEN2 are at risk for developing what

A

pheochromocytoma

104
Q

what are two types of MEN2

A

MEN2 A

MEN2B

105
Q

MEN2 have gain of function utation where

A

RET (can echo, i think she talked abou tmroe)

106
Q

what change is frequently found in MEN2 who develop tumors

A

1p loss

107
Q

What is summary of MEN2

A

they have gain of function but it is not sufficient to form tumors, add’l mutations are needed

108
Q

MET is what

A

hepatocyte growth factor receptor

109
Q

in hereditary papillary renal carcinoma, where is mutation

A

MET (HGFR) mutation

110
Q

inherited mutation in MET results in risk of developing what cacner

A

renal carcinomas

111
Q

growth factors normally involved in stimulating proliferation/survival are all what

A

proto-oncogens

112
Q 
PDGF/PDGFR
FGF/FGFR 
HGFR (MET)
RET (RTK)
VEGF
EGFR
HER2
are all examples of what
A

growth factor - proto-oncogene. they are all commonly found activated in cancer

113
Q

RAS is what kind of protein

A

signal transducing protein (GTPase)

114
Q

Signal transducing proteins
RAS (GTPase)

Non-receptor TKs
ABL

Transcription factors
MYC
JUN, FOS

are all what

A

proto-oncogenes, can be activated in different ways

115
Q

RAS activation

A

found activated in a ton of cancers
found in 90% of pancreatic cancers
50% colon

116
Q

RAS is bound to what

A

GDP

117
Q

when RAS bound to GDP it is

A

inactive

118
Q

When RAS bound to GTP it is

A

active

119
Q

when RAS is active what does it do

A

activates GEF

120
Q

if RAS is active, what will it do

A

just keep activating GEF and other kinases

121
Q

MYC is

A

TF that is activated at end of RAS pathway

122
Q

MYC - targetgene?

A

cyclin D

123
Q

if MYC is switched on it results in

A

tumor formation

124
Q

What cancers do you often find MYC activation in

A

burkitt lymphoma

breast, colon, lung

125
Q

burkitt lymphoma and follicular lymphoma are examples of what

A

overexpression of w.t. proto-oncogene

126
Q

Burkitt lymphoma is translocation b/w which chromosome

A

8 & 14

127
Q

as a result of 8 & 14 translocation

A

overexpression

128
Q

resulting chromosome that contains original centromere from chrom 8 is what

A

der 8

129
Q

der 14 has which centromere

A

original centromere from chromosome 14

130
Q

chrom. 8 has what gene sequence

A

MYC

131
Q

chrom. 14 has what gene

A

IGH

132
Q

how is translocation of chrom 8& 14 aquired

A

they are all acquired translocation. as soon as cell aquires it, it overexpresses MYC, so cell proliferates rapidly.

133
Q

What are the four stages of progression of cancer development in uterine cervical epithelium

A
  1. normal stratified squamous epithelium
  2. low grade CIN
  3. high grade CIN
  4. malignancy
134
Q

t(8;14) is what cancer?

A

burkitt lymphoma

135
Q

t(14;18) is what cancer?

A

follicular lymphoma

136
Q

t(9;22) is what cancer?

A

chronic myeloid leukemia

137
Q

t(15;17) is what cancer?

A

acute promyelocytic leukemia

138
Q

t(11;22) is what cancer?

A

ewing sarcoma

139
Q

which two types of cancer from translocations lead to over-expression of proto-oncogene?

A

burkitt lymphoma

follicular lymphoma

140
Q

which three types of cancer from translcoations create fusion/chimeric gene?

A

Chronic myeloid leukaemia
Acute promyelocytic leukaemia
Ewing Sarcoma

141
Q

which gene is affected that leads to over-expression of proto-oncogene in burkitt lymphoma?

A

MYC

142
Q

which gene is affected that leads to over-expression of proto-oncogene in follicular ymphoma?

A

BCL2

143
Q

fever, night sweats, infection & bruising are symptoms of what

A

leukemia & lymphoma

MCB II Block 1 (12 decks)

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