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Semester 2 > MoD Session 10 > Flashcards

MoD Session 10 Flashcards

1
Q

What are the extrinsic factors that increase cancer risk?

A

Environment

Lifestyle

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2
Q

What are the 5 leading behavioural and dietary risks in developing cancer?

A 
High BMI
Low fruit and veg intake
Lack of physical activity
Tobacco use
Alcohol use
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3
Q

Which leading behavioural and dietary factors act synergistically to increase cancer risk?

A

Tobacco and alcohol use

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4
Q

When adjusted for age, what does the incidence of cancer compared to that in the 1900s show?

A

It hasn’t changed much, individual risk has increased due to extrinsic factors

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5
Q

Why does increasing dietary intake of fruit and veg reduce the risk of cancer?

A

Decreases GI transit time
Fibre absorbs carcinogens and removes them
Rich in antioxidants

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6
Q

What are the three main categories of extrinsic factors that increase cancer risk?

A

Infections
Radiation
Chemicals

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7
Q

What did 2-napthylamine, an industrial carcinogen, show about neoplasia?

A

Long delay
Depends on dosage
Organ specificity

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8
Q

What does the organ specificity of a carcinogen depend on?

A

Where it comes into contact with

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9
Q

Give three examples of industrial carcinogens.

A

Vinyl chloride
Coal tars
Asbestos

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10
Q

What type of cancer is vinyl chloride associated with?

A

Liver

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11
Q

What explains the lag time between carcinogen exposure and development of neoplasia?

A

Need for high level of promoter exposure over a long period of time in combination with an initiator to form a monoclonal population

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12
Q

Describe the Ames test when it shows a mutagen is an initiator.

A

Rat liver, salmonella which requires histamine and possible mutagen–> media w/minimal histidine –> incubate –> high number of revertants

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13
Q

What is an initiator?

A

A mutagen

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14
Q

What do promoters do on neoplasia?

A

Cause prolonged proliferation

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15
Q

What are pro-carcinogens?

A

Chemicals converted by P450 to become carcinogens

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16
Q

What is a complete carcinogen?

A

A chemical which is both an initiator and a promoter

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17
Q

How does cigarette smoke act as a complete carcinogen?

A 
Initiator = 2-napthylamine
Promoter = hot water
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18
Q

What classes can initiators be sorted into?

A 
Polycyclic aromatic hydrocarbons
Aromatic amines
N-nitroso compounds
Alkylating agent
Diverse natural products
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19
Q

How do alkylating agents cause DNA damage?

A

Disrupts covalent bonds on DNA

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20
Q

Give two examples of natural carcinogens.

A

Aflatoxin

Asbestos

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21
Q

How can N-nitroso compounds be formed?

A

In industry
Smoked food
Produced in stomach

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22
Q

How far does UV radiation penetrate?

A

No deeper than the skin

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23
Q

How does ionising radiation such as X-Ray and nuclear radiation cause DNA damage?

A

Strips electrons from atoms

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24
Q

What are the three types of direct damage caused by ionising radiation?

A

Alter bases

Single/double strand breaks

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25
Q

What is the main exposure for most people to ionising radiation?

A

Radon released from rocks

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26
Q

How does radiation cause indirect DNA damage?

A

Free radical production

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27
Q

How can carcinogenic infections cause cancer?

A

Directly affect genes that control cell growth
Indirectly carcinogenic
Reduced immunity

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28
Q

How does HPV cause cervical cancer?

A

Expresses E6 which inhibits p53
Expresses E7 which inhibits pRB
No apoptosis and no cell-cycle breaks

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29
Q

How does EBV behave as an indirect carcinogen?

A

Chronic liver inflammation –> free radicals

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30
Q

How do Hep B and C act as indirect carcinogens?

A

Cause regeneration

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31
Q

How does Helicobacter pylori cause cancer?

A

Indirectly carcinogenic causing gastric inflammation

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32
Q

How do parasitic flukes cause cancer?

A

Lay eggs in bile ducts and bladder mucosa –> metaplasia and inflammation

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33
Q

What viral infection leads to Kaposi’s sarcoma?

A

Human herpes virus 8

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34
Q

How does reducing immunity cause cancer?

A

Allows other potentially carcinogenic infections to occur

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35
Q

How many hits are needed for germline mutations to occur?

A

2

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36
Q

How does the pathogenesis of inherited familial cancers differ to that of sporadic cancers?

A

Familial - 1st hit in germline, only need one somatic hit

Sporadic - 2 somatic hits needed

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37
Q

How do the graphs of unilateral (sporadic) and bilateral (inherited) cancer v.s. time differ?

A

Bilateral - straight line

Unilateral - curve

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38
Q

What are oncogenes?

A

Abnormally activated proto-oncogenes

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39
Q

How many alleles must be activated for an oncogene to be turned on?

A

1

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40
Q

How does a RAS mutation cause cell cycle entry?

A

G-protein activated –> cyclin D –> CDK

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41
Q

How does mutant RAS cause a constant cell cycle?

A

It is always active so allows cells past the cell cycle restriction point

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42
Q

What proto-oncogene mutation is common in colorectal cancer and melanoma?

A

RAS

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43
Q

What is the function of tumour suppressor genes?

A

Inhibit neoplasticism growth

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44
Q

How many alleles must be inactivated in tumour suppressor gene mutation?

A

2

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45
Q

What allows unrestrained passage of cells through the restriction point?

A

Inactivation of both RB alleles

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46
Q

Give examples of some proto-oncogenes.

A 
BRAF
BCL2
RAS
HER2
Cyclin D1
PDGF
MYC
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47
Q

What is BLC2?

A

An apoptosis regulator

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48
Q

What is BRAF?

A

Intracellular kinase

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49
Q

What is MYC?

A

Transcription factor

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50
Q

What are the three methods of DNA repair which are mutated in carcinoma?

A

Nucleotide excision
Mismatch repair
Double strand DNA breaks

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51
Q

What causes Xeroderma Pigmentosum?

A

Autosomal recessive mutation of 1 of 7 genes affecting nucleotide excision repair

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52
Q

What does Xeroderma Pigmentosum cause?

A

Early onset skin cancer from UV exposure

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53
Q

What inheritance pattern does hereditary non-polyposis colon cancer show?

A

Autosomal dominant

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54
Q

What does mismatch repair mutation cause?

A

Microsatellite instability

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55
Q

What are the intrinsic factors that increase cancer risk?

A

Age
Sex
Heredity

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56
Q

How do BRAC1 and BRAC2 cause familial breast carcinoma?

A

Causes double strand DNA break which causes chromosomal instability

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57
Q

What does nucleotide excision mutation cause?

A

Nucleotide instability

58
Q

What is genetic instability?

A

Alterations accounting for accelerated mutation rate

59
Q

What is genetic instability counteracted by?

A

‘Caretaker’ tumour suppressor genes

60
Q

Do mutations to DNA repair have to be inherited?

A

No, seen in sporadic cases

61
Q

What normal cellular replication process can be abnormal in malignant cells?

A

Chromosome segregation

62
Q

How does the adenoma-carcinoma sequence progress?

A

Normal epithelium –> early adenomal dysplastic crypt –> intermediate adenoma –> late adenoma –> carcinoma –> metastasis

63
Q

What is progression in malignant neoplasm?

A

Alterations of multiple TS genes and proto-oncogenes which involves genetic instability

64
Q

How many mutations are needed for malignant neoplasm to establish?

A
65
Q

What are the 6 hallmark cellular behaviours from cancer mutations?

A 
Self-sufficiency in growth signals
Resistance to growth stop signals 
Cell immortalisation
Sustained angiogenesis ability
Resistance to apoptosis
Ability to invade and metastasise
66
Q

What is the one enabling feature seen with the 6 hallmarks of cellular behaviours in cancer mutations?

A

Genetic instability

67
Q

Which cellular behavioural hallmark is only seen in malignant neoplasm?

A

Ability to invade and metastasise

68
Q

What does HER2 gene amplification in breast cancer cause?

A

Self-sufficiency in growth signals

69
Q

What does CDKN2A gene deletion in melanoma cause?

A

Resistance to growth stop signals

70
Q

What do most cancers do to overcome cell senescence?

A

Activate telomerase genes

71
Q

What does VEGF activation, which occurs in many cancers, allow?

A

Sustained angiogenesis ability

72
Q

What does BLC2 gene transcription in lymphoma do?

A

Cause resistance to apoptosis

73
Q

In gastric cancer, what allows for invasion and metastasis?

A

E-Catherine mutation

74
Q

How does a neoplasm become more genetically heterogenous?

A

More mutations are acquired as proto-oncogenes and TSG interact to affect hallmarks of cancer

75
Q

Give a brief overview of the progression of cancer.

A

Somatic cells exposed to environmental carcinogens –> monoclonal population forms –> progression over many years/decades –> hallmarks of cancer

76
Q

What increase in risk does having a sibling with a given cancer cause?

A

2-3 fold

77
Q

What are cancer family syndromes?

A

Patients are afflicted by several types of cancer and often develop more than one type

78
Q

How can secondary cancers be caused by therapy for primary cancer?

A

X-Rays and antineoplastic drugs are powerful carcinogens

79
Q

What can be considered as a phenotype that predisposes to melanoma?

A

Fair complexion

80
Q

What phenotype predisposes dye-stuff workers to bladder cancer?

A

Poor acetylator

81
Q

What inborn differences can be considered as a cancer phenotype?

A

Enzymes that inactivate or detoxify carcinogens

82
Q

What is usually the first sign of cancer in retinoblastoma?

A

Abnormal reflection in pupil (child does not complain of poor eyesight) - leukokoria = cat’s eye reflex

83
Q

How does retinoblastoma usually progress?

A

Develops from outer layer of retina –> grows backwards into eye

84
Q

When do hereditary and sporadic retinoblastoma usually appear?

A

Hereditary - children, often bilateral

Sporadic - adults, usually unilateral

85
Q

How do two successive mutations cause retinoblastoma?

A

1st mutation affects one locus on one chromosome

2nd affects same locus on the other allele

86
Q

What happens to the RB1 genes in a normal, healthy individual?

A

Occasional cell inactivates one of its two good RB1 genes but won’t cause a tumour

87
Q

Why does the occasional cell inactivation of an RB1 copy in people with hereditary retinoblastoma cause a tumour to develop?

A

They only have one good copy

88
Q

When is the first mutation in hereditary retinoblastoma present?

A

In the sperm or ovum before fertilisation

89
Q

When is a likely time for the only functioning RB1 gene in a patient with hereditary retinoblastoma to be lost?

A

Development of the retina when mitoses are occurring

90
Q

Why does retinoblastoma become dominant by pedigree analysis?

A

It occurs commonly in mutant retinoblastoma carriers

91
Q

What are children with hereditary retinoblastoma at a greater risk of?

A

Other tumours e.g. Osteosarcoma, risk increased by irradiation which may be used therapeutically

92
Q

How does pRB stop the normal cell cycle?

A

Encodes a phosphoprotein that binds to DNA which is phosphorylated through the cycle and loses its suppressor function

93
Q

What is the most common genetic change in human cancer?

A

Mutation in TSG p53

94
Q

What is the pathogenesis of familial polyposis of the colon?

A

Carriers inherit predisposition to develop polyps of colon in adolescence –> turn into carcinoma at 40 in 80% of patients

95
Q

What is the treatment of familial polyposis?

A

Early preventative colectomy

96
Q

How are breast and colon cancers thought to occur in adults?

A

Dominantly inherited syndromes which predispose to these cancers

97
Q

What enzyme is lacking in Xeroderma Pigmentosum?

A

Endonuclease that repairs UV light DNA damage

98
Q

How can an error during meiosis to form ovum or sperm increase the risk of neoplasia?

A

Meiotic instability forms root of later mitotic instability

99
Q

How does Down’s syndrome affect the risk of developing leukaemia?

A

Increases by 20 fold

100
Q

What do men with Klinefelter’s syndrome have a 2-3 fold increased risk of?

A

Breast cancer

101
Q

Congenital defects in which system predispose to cancer?

A

Immune

102
Q

How can karyotyping be used to examine tumour progression?

A

Increasingly severe karyotypic aberrations are seen with tumour progression

103
Q

What chromosome change is seen in 90% of chronic myelogenous leukaemia cases?

A

Balanced translocation of Philadelphia chromosome (chromosome 22)

104
Q

What is the usual chromosomal change seen in balanced translocation of the Philadelphia chromosome?

A

Part of gene on 22 fuses with abI oncogene on chromosome 9

105
Q

What is the result of a balanced Philadelphia translocation?

A

More powerful than normal tyrosine phosphorylase

106
Q

Where is the Philadelphia chromosome found in chronic myelogenous leukaemia patients?

A

All myeloid cells - incl. erythrocyte, granulocyte and megakaryocyte

107
Q

What indicates that a clone deriving from a pleuripotent stem cell has overcome the entire bone marrow in CML?

A

Presence of Philadelphia chromosome in all myeloid cells

108
Q

What is seen with the N-myc gene in neuroblastoma and the neu (Her2) gene in breast cancer?

A

Gene amplification in association with tumour progression

109
Q

What chromosomal abnormality occurs in many tissues where it may have survival value?

A

Polyploidy

110
Q

What chromosomal abnormalities become a visible aspect of progression in tumours?

A

Aneupoidy and polyploidy

111
Q

What precipitates a cascade of increasing chromosomal instability in tumour development?

A

Destabilising mutation early in tumour development

112
Q

What are chromosomal fragility syndromes?

A

Rare inborn abnormality of DNA repair

113
Q

Give three examples of chromosomal fragility syndromes.

A

Fanconi’s anaemia
Ataxia telangiectasia
Xeroderma Pigmentosum

114
Q

What are chromosomal fragility syndromes associated with?

A

An increased risk of tumour development

115
Q

What do many, if not most, cancers develop from?

A

Precursor lesions

116
Q

Give examples of some known precancerous lesions.

A

Forms of metaplasia, dysplasia, carcinoma in situ, some benign lesions and sundry lesions

117
Q

How do epithelial and connective tissue metaplasias vary?

A

Epithelial virtually all precancerous

CT generally safe

118
Q

What does metaplasia imply?

A

Expression of a different but normal set of genes

119
Q

Give two examples of precancerous metaplasia.

A

Gastric epithelium in oesophagus - Barrett’s epithelium

Abnormal hyperplastic epithelium (leukoplakia) on tongue or exocervix

120
Q

What does dysplasia refer to?

A

Cellular changes that are too irregular for hyperplasia and not irregular enough for neoplasia

121
Q

What does dysplasia in surface epithelia blend into which is definitely neoplastic?

A

Carcinoma in situ

122
Q

Describe what is meant by ‘carcinoma in situ’.

A

Covering epithelium replaced by layer of cancer cells
All boundaries respected
Thickness about the same as normal epithelium
Basement membrane intact

123
Q

What changes the diagnosis of in situ carcinoma to invasive?

A

Epithelial boundary breakdown

124
Q

In carcinoma in situ of the cervix, what does Pap smear show?

A

Epithelial cells sloughed off failed to mature
Not normal flat, eosinophilia cell with shrivelled pyknotic nucleus
Cells retain structure and basophilia of basal cells

125
Q

What is Bowen’s disease?

A

Carcinoma in situ of epidermis which appears reddened, scaly and crusty

126
Q

Why is carcinoma in situ of the exocervix better visualised after swabbing with iodine?

A

Normal squamous cells have glycogen and stain brown

Carcinoma cells don’t produce glycogen so remain unstained

127
Q

How does the peak age for cervix carcinoma in situ and carcinoma compare?

A

In situ - 30 y.o.

Carcinoma - 45 y.o.

128
Q

How does the time taken for progression in cervix carcinoma compare to that in bladder, stomach and lung.

A

Cervix - 15 years
Bladder - 5 years
Stomach and lung -

129
Q

What can happen to both dysplasia and carcinoma in situ of the cervix?

A

Unpredictably persist, regress or progress to invasive cancer

130
Q

Is it possible to tell what the course of either dysplasia or carcinoma in situ of the cervix will be?

A

Nope

131
Q

Why can a sarcoma in situ not exist?

A

Lack the boundary of a basement membrane to serve as a definition of invasiveness

132
Q

Give examples of benign growths which given enough time can progress to carcinoma.

A 
GI polyps
Paipllomas of the larynx
Large congenital naevi
Pigmented moles
V. occasionally: leiomyomas of the uterus and fibroadenomas of breast
133
Q

Why can ongoing chronic inflammation be a precursor to cancer?

A

Likely to be secondary due to sustained cell proliferation from constant epithelial damage and regeneration

134
Q

How long does chronic inflammation have to persist in liver cirrhosis to cause carcinoma?

A

Decades

135
Q

Why does decades of chronic inflammation in cirrhosis lead to hepatocellular carcinoma?

A

Has a strong inflammatory response

136
Q

Which two types of chronic gastritis can prelude gastric carcinoma?

A

Autoimmune or bacterial

137
Q

Which chronic inflammatory disease carries a heavy risk of colon cancer?

A

Ulcerative colitis

138
Q

How does asbestos lead to carcinoma?

A

Causes chronic inflammation

Absorbs carcinogens onto fibre surface

139
Q

Which type of asbestos is more dangerous?

A

Blue - sharp spikes get stuck in peripheral lungs where they cannot be wafted out by mucociliary escalator

140
Q

What is asbestos?

A

Naturally occurring silicate fibre of which there is a whispy white type and sharper blue type

141
Q

What is the most common condition associated with asbestos exposure which is benign and doesn’t usually cause a problem?

A

Pleural plaques

Semester 2 (45 decks)

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