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Human Bioscience: Impaired Body Function > Cancer > Flashcards

Cancer Flashcards

1
Q

what is cancer?

A

A complex group of >100 diseases affecting a wide range of tissues

Caused by mutations in genes controlling cell growth after exposure to carcinogens

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2
Q

Most cancer mutations are in somatic cells but many cancers cluster…

A

…..in families

  • Shared environment and genes
  • 1% of mutations are inherited – but extra somatic mutations also required
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3
Q

Cancer is characterised by

A
  • Loss of growth control leading to an unregulated increase in cell number
  • Metastasis and invasion of other tissues
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4
Q

Cancers differ in:

A
  • Tissue of origin
  • Causal factor(s)
  • Molecular mechanisms
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5
Q

Incidence & importance

A 
-Cancer affects 1 in 3 people
worldwide
-Leading cause of death in
NZ and second worldwide
-According to the Ministry of
Health in NZ in 2015:
Incidence (number of
cases/year): 23,215
Mortality (number of
deaths/year): 9,615
-About 1/2 the number of
people that get cancer will
die from it
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6
Q

Development of cancer

A

– benign vs malignant

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7
Q
  • neoplasia
A

Tumour that starts when cells that have
lost growth control proliferate to form a
new growth

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8
Q

Cells do not die via

A

apoptosis, which
normally keeps the number of cells
constant

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9
Q

Tumour is benign if

A

the neoplastic cells

are clustered in a single mass

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10
Q

Tumour becomes malignant once

A

cells

have undergone metastasis

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11
Q

Benign tumours

A

-Cells that are well differentiated and look like normal cells
-May perform the normal function of the tissue. e.g. secrete hormones, although may over-secrete - insulinoma
-Cells grow relatively slowly but this is not supressed by apoptosis or
contact inhibition
-Size may be limited to just a few mm by lack of blood supply
-Surrounded by a fibrous capsule & confined to original location
-Do not infiltrate, invade, or metastasize
-Can damage nearby organs by compressing them

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12
Q

Malignant tumours

A

-Cells are less differentiated and do not look like normal cells
-Do not perform the normal function of the tissue
-May secrete new signalling molecules, enzymes or toxins etc.
-Cells grow rapidly since they have lost the ability to control
proliferation and differentiation
-No fibrous capsule
-Cells infiltrate & invade surrounding tissues and metastasize to
form new tumours at distant sites
-Tumour sends “legs” into surrounding tissue
-Gives name to Cancer = Crab, -based on these legs
-Can compress and/or destroy surrounding tissues

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13
Q

Tumour growth can be

A

very rapid

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14
Q

Tumour classification

A

according to tissue of origin

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15
Q

Benign tumours

A

Tissue name + “-oma”

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16
Q

Malignant tumours (cancers)

A

Carcinomas
Adenocarcinomas
Sarcomas
Leukaemias

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17
Q

Carcinomas

A

are derived from epithelial cells. – the most common type of cancers

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18
Q

Adenocarcinomas

A

are derived from glandular epithelial cells

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19
Q

Sarcomas

A

are derived from mesenchymal cells

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20
Q

Leukaemias

A

are derived from haemopoietic cells

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21
Q

Carcinomas: Examples

A

Adenocarcinoma, Squamous cell , and others

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22
Q

Carcinomas:Adenocarcinoma

A

Lung, colon, breast,
pancreas, stomach,
oesophagus, prostate,
ovary

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23
Q

Carcinomas:Squamous cell

A

Skin, oropharynx, larynx,

lung, oesophagus, cervix

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24
Q

Carcinomas:Others

A

Small-cell lung-, large cell lung-, haptic-, renal and bladder- carcinomas

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25
Q

Control of cell number: Most cells in adult tissues are

A

terminally differentiated and

quiescent (non-dividing). exceptions include; hair follicles, blood and gut stem cells

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26
Q

Control of cell number: Within each tissue, cell death, by apoptosis or necrosis, is
balanced by

A

cell division, often of stem cells, leaving the total

number of cells constant

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27
Q

Control of cell number: Cell division is tightly regulated by

A

growth factors which allow

quiescent cells to enter the cell cycle and divide

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28
Q

Control of cell number: If differentiated cells start dividing again or dividing cells lose control of

A

growth then this can lead to cancer

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29
Q

Properties of Normal Cells

A

-Dependent on growth factors for cell division
-Cells have a finite number of cell divisions
-Contact inhibition of growth
-Cells need to be stuck down to the
Extracellular Matrix (ECM) to survive
-DNA damage, cell stresses and detachment for the ECM can cause death by apoptosis
-Cells usually stay in one place
-Have a stable genome
-Depend on normal blood supply

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30
Q

Properties of Tumour cells

A

-Able to divide in the absence of growth factors
-Cells have unlimited number of cell divisions
-No contact inhibition of growth
-Cells have impaired cohesiveness/adhesion
and show anchorage independent growth
-Tumour cells evade apoptosis
-Cells can invade other tissues and migrate to other parts of the body (metastasis)
Have an unstable genome due to defects in
sensing DNA damage and repairing it
-Secrete factors to stimulate new blood vessel growth as the tumour grows

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31
Q

Telomere length helps control

A

cell lifespan

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32
Q

Cells contain telomerase, an enzyme which

A

can elongate telomeres

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33
Q

Telomerase activity is essential for

A

allowing cells to keep proliferating

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34
Q

As cells age, telomerase becomes

A

inactive and hence telomeres shorten & cells lose the ability to divide – limits lifespan

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35
Q

Increased telomerase activity allows cells to

A

proliferate indefinitely and leads to cancer

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36
Q

Cell proliferation is regulated by transit through

the

A

cell cycle

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37
Q

Four phases OF Cell proliferation:

A
  • G1 – gap between M & S phase
  • S phase – DNA synthesis/replication
  • G2 – gap between S & M phase
  • M phase – mitosis, cytokinesis/division
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38
Q

Cell proliferation: In adult most cells are terminally differentiated
and

A

no longer divide - quiescent (G0)

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39
Q

If differentiated cells start dividing again or

cycling cells lose control then this can lead to

A

uncontrolled proliferation & cancer

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40
Q

Transit through cycle regulated by

A

checkpoints

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41
Q

Cell cycle checkpoints control

A

cell growth

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42
Q

Progression through cell cycle checkpoints controlled by

A

Cyclin Dependent

Kinases (CDKs) and CDK inhibitors

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43
Q

Cyclin Dependent

Kinases (CDKs) and CDK inhibitors ensure:

A
  • Correct sequence of phases (G1, S, G2, M)
  • Cellular and environmental conditions are favourable
  • DNA is properly replicated and undamaged
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44
Q

G1/S transition checkpoint

A

Are growth factors present?
Are nutrients available?
Is DNA damaged?
Is the cell big enough?

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45
Q

G2/M transition checkpoint

A

Has DNA replicated?

Is DNA damaged?

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46
Q

Checkpoint failure causes

A

cell-cycle arrest and can lead to cell death by apoptosis

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47
Q

G1/S Checkpoint is regulated by

A

Growth Factors and DNA damage

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48
Q

Transit through the G1/S

checkpoint requires an

A

an active Cdk4/6-cyclinD complex

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49
Q

Cdk4/6 is activated by

A

growth factors

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50
Q

p21 & p27 are

A

Cdk inhibitors that

inhibit Cdk4/6

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51
Q

p53 is a transcription factor

induced by

A

DNA damage that

controls expression of p21 and p27

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52
Q

p53, p21 & p27 are examples of

A

Tumour Suppressors as they inhibit

cell division

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53
Q

Cells need growth factors and

A

intact DNAto progress through G1/S

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54
Q

Cancer is caused by mutations in genes controlling

A

cell number

  • Mutations that enhance cell proliferation
  • Mutations that supress cell death (apoptosis)
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55
Q

Mutation of DNA repair genes causes

A

genome instability

-makes further mutations more likely

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56
Q

Most mutations are somatic and acquired by

A

environmental interactions

-e.g. exposure to carcinogens and lifestyle factors

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57
Q

Some germline mutations may be inherited and predispose someone to
cancer e.g.

A

Rb – retinoblastoma, BRCA1/2 – breast cancer

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58
Q

A single mutation is not enough. Each cancer arises from an

A

accumulation of several mutations over a lifetime – “multi-hit hypothesis”

  • From 2 to 20 depending on the type of cancer
  • Colon (4-5), Lung (10-15)
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59
Q

Identifying inherited mutations allows

A

screening for individuals

who are at particular risk (e.g. BRCA1/2 for breast cancer)

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60
Q

Sequencing genes mutated in cancers can give a

A

molecular
fingerprint for each cancer (a list of genes which are mutated)
-Diagnosis and targeted treatments
-Understanding mechanism and development of new therapies

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61
Q

Many genes mutated in cancer identified since the

A

early 1970s

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62
Q

Fall into two main types, which positively & negatively regulate cell proliferation

A
  • Oncogenes

- Tumour suppressor genes

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63
Q

First genes identified were termed

A

oncogenes – genes that cause cancer

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64
Q

Oncogenes are mutated forms of the normal genes that

A

positively regulate cell division - proto-oncogenes

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65
Q

Proto-oncogenes encode components of

A

growth factor signalling pathways that stimulate cell proliferation by allowing progression from G0/G1 into S-phase when growth factors are present

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66
Q

Examples of proto-oncogenes

A 
Growth factors (EGF) & receptors (HER2)
Signalling proteins (Ras) & protein kinases (Src, Abl)
Transcription factors (Myc, Jun, Fos)
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67
Q

Mutations can be point mutations, insertions, deletions, translocations
etc, but cause a

A

gain of function in which the protein is increased in expression or activated in the absence of growth factors

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68
Q

This stimulates cell proliferation in the

A

absence of growth factors

e.g. Ras-MAPK pathway > > > G1/S transition

69
Q

Tumour suppressor genes

A

were identified later (1980/90s)

70
Q

Tumour suppressor genes negatively regulate

A

Tumour suppressor genes negatively regulate

71
Q

Usually encode proteins at

A

cell cycle checkpoints that block progressionthrough G1/S and G2/M if there is a problem

  • p53, p21/27 – prevent cell division if DNA is damaged (G1/S & G2/M)
  • p21/27, Rb, E2F – prevent G1/S transition if no growth factors
72
Q

Mutations cause a

A

loss of function (decreased expression or no activity)

73
Q

Mutations Usually requires

A

both alleles to be inactivated since some normal protein may allow the checkpoint to function
-Knudson’s two-hit hypothesis for retinoblastoma (Rb inactivation)
-This allows cells to progress through the cell cycle in the absence of
growth factors, with DNA that is damaged or not fully replicated

74
Q

Given that the Ras-ERK and PI3K-Akt signaling pathways are activated by growth factors such as

A

EGF, IGF, and fibroblast growth factor (FGF), which play major roles in control of cell fate, they can thus be considered developmental signaling pathways that are hijacked in cancer.

75
Q

Growth factors activate the

A

Ras-MAPK pathway
-This activates Cdk4/6 and allows
progression through the G1/S
checkpoint and cell division

76
Q

In 30% of all cancers, activating

mutations are found in the

A

Ras protein

77
Q

In cells with activated Ras the pathway

is always

A

active and cell division is independent of growth factors

78
Q

The normal Ras gene is therefore a

A

proto-oncogene and the activated form

an oncogene

79
Q

p53 is a sensor for

A

DNA damage

80
Q

p53

A

“the guardian of the genome”

81
Q

Transcription factor activated by

A

DNA damage
-Causes cell-cycle arrest if DNA is damaged by
upregulating expression of p21 and p27 that inhibit Cdk4/6 and the G1/S transition

82
Q

p53 Allows time to repair

A

DNA damage

-If damage is extensive cell dies by apoptosis

83
Q

50% of all human cancers have inactivating mutations in p53, mainly in

A

DNA binding domain

84
Q

p53 Allows cell division when

A

DNA is damaged

85
Q

p53 is a

A

tumour suppressor gene (TSG)

86
Q

Types of mutations

A

-Some may be inherited e.g.
mutations in Rb give rise to
retinoblastoma

-Most are sporadic, due to
environmental factors

-Multiple mutations are required
for full cancer phenotype

-Mutation of genes involved in
DNA repair is common and gives
rise to genome instability which
make further mutations likely

87
Q

Stages of cancer development

A
  • Initiation
  • Promotion
  • Progression
88
Q

Stages of cancer development-Initiation

A

Exposure to a chemical or physical carcinogen
-Activation or inactivation by metabolism
or excretion

Damage to DNA
-May be repaired or cause cell death
Proto-oncogene activation or tumour
suppressor inactivation

89
Q

Stages of cancer development-Promotion

A

Altered cells stimulated to divide by a tumour promoter
-Altered cell may remain dormant or be
removed by immune system

90
Q

Stages of cancer development-Progression

A

-Develop more mutations
-Uncontrolled cell replication and loss of
specialisation
-Cells are more aggressive and invasive

91
Q

intravasation

A 
Cells in a primary tumour develop the
ability to escape into the circulation -
-Loss of adhesion
-Secretion of proteases to degrade
basement membrane
-They survive and travel in the blood or
lymphatic system
92
Q

Extravasation

A

Exit into surrounding tissues via proteases –
-Develop into a secondary tumour or
metastasis

93
Q

Growth of new blood vessels

(angiogenesis) enables the tumour to

A

grow rapidly

Metastasis to multiple distant sites and
rapid growth are life threatening

94
Q

Host risk factors

A
  • Hereditary predisposition
  • Reproductive hormones – can act as tumour promoters
  • Obesity
  • Immune surveillance of tumour antigens
95
Q

Environmental risk factors

A
  • Chemical carcinogens (mutagens)
  • Viruses & bacteria
  • Radiation
96
Q

A diet rich in fruit and vegetables
seems to protect against many
cancers due to

A

plant secondary
metabolites responsible for the
flavour and colour of plants called
phytochemicals

May protect by blocking effects of
carcinogens or suppressing
growth of tumour cells

97
Q

food Blockers

A

Flavanols – Green Tea

Glucosinolates - cruciferous plants: cabbage family, radishes, mustard, water cress

98
Q

food Suppressors

A

Genistein (soy), gingerol (ginger), limonene (citrus), resveratrol (red wine),
glycyrrhizin (liquorice ), curcumin (cumin), aspirin (willow bark)

99
Q

Clinical manifestations – local effects

A

Mainly physical effects due to compression or blockage of structures close by:
Neurological problems due to compression of structures by brain tumours
Intestinal obstruction due to a colon carcinoma

100
Q

Clinical manifestations – local effects: Blood vessels

A

Blockage or bleeding

101
Q

Clinical manifestations – local effects: Effusions – build up of fluid

A

-Pleural effusion due to metastatic cancer cells growing in between lung
plural membranes, -also pericardial effusion
-Ascites – build up of fluid in peritoneal cavity – peritoneal carcinoma

102
Q

Clinical manifestations – systemic effects: Various types of malnutrition

A

Malabsorption
Anaemia
Anorexia & Cachexia

103
Q

Clinical manifestations – systemic effects:

A

Fluid and electrolyte imbalances

Fatigue and sleep disturbances

104
Q

Clinical manifestations – systemic effects: Paraneoplastic syndromes

A

Symptoms unrelated to the initial tumour site

Ectopic hormones or factors secreted by tumour cells

105
Q

Clinical manifestations – systemic effects: Pain

A

mainly in the later stages

106
Q

Cancer anorexia-cachexia syndrome

A

-Protein/energy malnutrition due to:
-Increased energy demand of rapidly
growing cancer cells (glucose)
-Reduced energy intake & malnutrition
Loss of appetite
Altered taste
Reduced absorption
-Not completely explained by energy demands of tumour
-Pro-inflammatory cytokines (TNFα, IL-1, IL-6) also supress appetite

107
Q

Cancer anorexia-cachexia syndrome: Death may occur due to

A

cachexia linked starvation rather than the actual cancer

Early active nutritional intervention is important

  • Increased energy & protein
  • Small, frequent, easily digestible meals, not bulky low energy high fibre foods!

Unexplained weight loss may mean an undiagnosed cancer

108
Q

Paraneoplastic syndromes

A

rare disorders that are triggered by an altered immune system response to a neoplasm. They are defined as clinical syndromes involving nonmetastatic systemic effects that accompany malignant disease.

see lecture notes

109
Q

Seven warning signs of cancer

A

C.A.U.T.I.O.N.

110
Q

C.A.U.T.I.O.N.

A

C-hange in bowel or bladder habits
A- sore that does not heal
U-nusual bleeding or discharge from any body orifice
T-hickening or a lump in the breast or elsewhere
I-ndigestion or difficulty swallowing
O-bvious change in a wart or mole
N-agging cough or hoarseness

111
Q

Screening & diagnosis

A 
Indirect, non-specific tests
Cytology
Diagnostic imaging
Tumor markers
Microarray technology
112
Q

Screening & diagnosis:Indirect, non-specific tests

A

Liver function, abnormal hormones, blood count, blood in stools, sudden
unexplained weight loss, etc

113
Q

Screening & diagnosis: Cytology

A

Pap smear, tissue biopsy, bone marrow

Immunohistochemistry – e.g. estrogen or EGF receptor

114
Q

Screening & diagnosis: Diagnostic imaging

A

X-rays e.g. chest or mammogram, computed tomography - CT scan

Magnetic Resonance Imaging - MRI

Ultrasound

115
Q

Screening & diagnosis: Tumor markers

A

e.g. prostate-specific antigen (PSA)

Need confirmation & to be done regularly to monitor progression of disease

116
Q

Screening & diagnosis: Microarray technology

A

Gene chips to measure mRNAs

Check expression of specific cancer-associated genes (oncogenes & TSGs)

117
Q

Specific tumour markers

A

molecules produced by tumor cells or other cells of the body in response to cancer or certain benign conditions. Most tumor markers are secreted into blood and may be estimated in blood, but they may also be measured in urine, tissues etc.

see lecture notes

118
Q

Tumour grading

A

Microscopic/histologic examination of cells appearance and state of
differentiation and number of mitotic cells (Grade I – 4)

119
Q

Tumour grading:

A

Grade l - Cells differ slightly from normal cells and are well differentiated
Grade ll - Cells are more abnormal and moderately differentiated
Grade lll - Cells are very abnormal and poorly differentiated
Grade lV - Cells are immature and undifferentiated

120
Q

Tumour staging

A

Clinical, radiographic, surgical examination of extent and spread of
tumour to help with treatment and prognosis

Specific for each type of cancer

121
Q

Tumour staging: TNM staging

A

T 1 – 4 = tumour size
N 0 – 3 = lymph node involvement
M 0 – 1 = metastasis

122
Q

Tumour staging: Overall Stage Grouping - American Joint Committee on Cancer (AJCC)

A

Stage 0 - Cancer in situ
Stage l - Tumour limited to the tissue of origin
Stage ll - Limited local spread
Stage lll - Extensive local and regional spread
Stage lV – Metastasis to distant sites

123
Q

Prevention

A

Avoidance of environmental exposure
Diet, smoking, alcohol, obesity etc
Products e.g. sunscreen, sunhats, clothing
Vaccination - HPV
Routine screening - smear, mammography, fecal occult
blood test, gene screen, protein profile etc
Education & Health promotion programmes
Ministry of Health
Cancer Society
NZ Cancer Strategy

124
Q

Treatment I: Surgery

A

Determined by extent of disease
Excellent if no metastasis and detected early enough
May trigger metastasis?

125
Q

Treatment I: Radiation therapy

A

Repeated low doses from a beam, implantation of a radioactive
source (brachytherapy) or systemic administration of radioisotopes
Generates DNA strand breaks through free radical formation
Cell dies by the apoptopic pathway
Not so effective if the tumour has mutations in the p53 tumour
suppressor gene

126
Q

Treatment II: Chemotherapy

A

Major treatment that targets rapidly dividing cells
Multiple rounds
Combinations of drugs help with resistance
Often combined with radiation therapy
Side effects – anaemia, hair loss, nausea/vomiting

127
Q

Treatment II: Hormone and anti-hormone therapy

A

Cancers responsive to / dependent on hormones

128
Q

Treatment II:Immunotherapy

A

Stimulate the immune system to kill cancer cells
Cytokines, cancer vaccines etc
Administer sensitized NK cells or T-cells (CAR-T cells)

129
Q

Treatment II: Immunotherapy

A

Stimulate the immune system to kill cancer cells
Cytokines, cancer vaccines etc
Administer sensitized NK cells or T-cells (CAR-T cells)

130
Q

Treatment II: Targeted therapies

A

Mainly monoclonal antibodies that target specific proteins/processes
Bevacizumab binds VEGF receptor - blocking angiogenesis
Trastuzumab (Herceptin) binds HER2 - overexpressed in 20-30% breast cancers

131
Q

Cancers in New Zealand

A 
NZ has a growing & ageing population
More people are developing cancer
In New Zealand, about 1 in 3 people who get cancer are cured
Most prevalent cancers in NZ
1. Lung – biggest cause of cancer in NZ
2. Bowel – NZ has one of highest rates in world
3030 people were diagnosed and 1191 died in 2011
3. Breast
Around 600 deaths per year
Skin
Prostate
Cervical
132
Q

Lung Cancer: Incidence

A

Occurs most often in adults 40 - 70 yrs old
Most common cause of death for men and second most common for women in NZ
Usually diagnosed late & after metastasis, but people can survive if caught early

133
Q

Lung Cancer: Risk factors

A

80-90% due to long term exposure to carcinogens in tobacco smoke (Polycyclic
Aromatic Hydrocarbons – PAHs)
Passive smoking may also cause lung cancer but still not clear
Occupational exposure
Asbestos; processing of steel nickel chrome and coal gas; radiation; radon gas

134
Q

Lung Cancer: Signs & symptoms

A

Persistent, worsening cough
Coughing up excessive phlegm with blood
Chest pain with coughing or breathing
Recurring chest infections

135
Q

Lung Cancer: Diagnosis

A

Symptoms; health and work history - smoking and other
exposure; physical exam; then decide on tests
Chest x-ray, CT scan
Sputum cytology
Bronchoscopy
Fine needle aspiration of tumour
Thoracentesis – check pleural fluid for cancer cells
Mediastinoscopy – biopsy of lymph nodes in mediastinum

136
Q

Lung Cancer:Prevention & treatment

A

Cessation of smoking
Surgery
Radiation
Chemotherapy

137
Q

Bowel Cancer:Incidence

A

New Zealand has very high rate (3030 cases in 2011)
Occurs most often in adults 50+ yrs old, slightly more prevalent in men
Early detection and treatment gives 90% chance of long term survival

138
Q

Bowel Cancer:Risk factors

A

Increasing age & low fibre, high fat diet
Inflammatory bowel > 10yrs (e.g. ulcerative colitis)
Familial Adenomatous Polyposis (FAP) ~ 1% of cases
-Mutations in the Adenomatous
-Polyposis Coli (APC) gene
Rapid tumour initiation, slow progression
Hereditary nonpolyposis colorectal cancer (HNPCC) ~ 2-4% of cases
-Slow initiation, rapid progression

139
Q

Bowel Cancer:Signs & symptoms

A

Blood in bowel motions or change in bowel habits for several weeks
Abdominal discomfort e.g. bloating, cramps etc
Unexplained weight loss, tiredness, anaemia

140
Q

Bowel Cancer:Diagnosis

A

Rectal and abdominal exam
Blood tests
Colonoscopy; CT colonography etc

141
Q

Bowel Cancer:Prevention

A

Maintain a healthy diet & weight
Regular exercise
Quit smoking & cut back on alcohol
Bowel screening helps earlier detection
-Fecal blood test
-NZ pilot in 2011, rolled out in 2017
-Available for all 60-74 yr olds by 2020

142
Q

Bowel Cancer:Treatment

A

Surgery
Radiation
Chemotherapy

143
Q

Breast cancer:Incidence

A

Most common cancer in women (1 in 9 will be affected)
Most will have no family history
~ 3000 new diagnoses each year (20 in men) with ~ 600 deaths

144
Q

Breast cancer:Signs & symptoms

A 
Change in breast shape or lumps in breast
Thickening of tissue
Nipple changes e.g. skin dimpling
Blood stained discharge from nipple
Rash
Painful area
145
Q

Breast cancer – risk factors: Host risk factors

A

Being female
Age – 70% of cases will be 50+ yrs
Having previously had breast cancer
Increased number of abnormal cells in milk ducts
Affected first degree relative (risk doubles)
Mutation of BRCA1 (Chr 17) and BRCA2 (Chr 13) genes
Both are TSGs involved in DNA repair
-10% of all breast cancers – the rest are sporadic
-Found in 33% of women with breast cancer under 29, only 2% in 70+ yrs
-BRCA1 – predisposes to breast and ovarian cancer
-BRCA2 – predisposes to breast cancer only

146
Q

Breast cancer – risk factors:Environmental risk factors

A

Nulliparity – not having given birth
First child after 30
High fat diet, alcohol use
Oestrogen replacement therapy

147
Q

Breast cancer – hormone and growth factor receptors: Circulating oestrogen and progesterone

A

Can act a tumour promoters if receptor is present
Oestrogen receptors (ER) expressed in ~80% of
breast cancers
Progesterone receptors (PR) expressed in ~60%
of breast cancers

148
Q

Breast cancer – hormone and growth factor receptors:Amplification of HER2

A

Human Epidermal growth factor Receptor
(HER2/neu) overexpressed in ~15-30% of breast
cancers
Associated with shorter disease-free survival and
overall survival
Acts as an oncogene
-Activates growth factor signalling pathways
associated with cellular proliferation,
survival, angiogenesis and invasion

149
Q

Breast cancer:Diagnosis

A

Medical history; physical exam; mammogram/ultrasound; biopsy and lab testing on
tissue; presence/absence of receptors ER, PR, HER2

150
Q

Breast cancer: Prevention

A

Have regular mammogram (free from 45 - 69 yrs)
Self examination of breast
Lifestyle - healthy weight, physical activity, quit smoking etc

151
Q

Breast cancer:Treatment

A

Surgery, radiation, chemotherapy
Presence or absence of ER, PR and HER2 receptors determine best treatment
Trastuzumab (Herceptin) – monoclonal antibody that blocks HER2
Hormone treatment – block hormone receptors or lower hormone levels
-Tamoxifen – blocks ER in ER+ tumours
-Letrozole inhibits oestrogen production in peripheral tissues (post - menopause)

152
Q

Skin Cancer:Incidence

A

NZ has highest rate in the world
Melanoma ~ 2,000 per year with ~ 350 deaths
Non-melanoma ~ 67,000 per year with ~ 130 deaths

153
Q

Skin Cancer: Risk factors

A 
Family history
Skin that burns easily
Cumulative sun exposure (age) or episodes
of severe sunburn, esp. as a child
Sunbeds
Less common
    -X-ray exposure, scars from burns or disease,
exposure to some chemicals
154
Q

Skin Cancer:Signs & symptoms

A

Red, scaly, rough skin lesions on sun-exposed

areas; hands, head, neck, lips and ears

155
Q

Skin Cancer:Diagnosis

A

Skin checks, mole maps

Biopsy

156
Q

Skin Cancer:Prevention

A

Cover skin, sunscreen, hats, sunglasses etc

Check skin regularly including skin not normally exposed to sun

157
Q

Skin Cancer:Treatment

A 
Surgery
Cryotherapy – liq N2
5-fluoruracil cream
B-Raf inhibitors
Immunomodifiers (IFNα, IL-2, Ipilimumab)
Photodynamic therapy - photosensitiser drug and light or laser
treatment kills tumour cells with reactive oxygen species (ROS)
Radiation
158
Q

Prostate cancer: Incidence

A

Second most frequently diagnosed cancer (15% of all male cancers)
>80% of men will develop prostate cancer by 80 yrs – mostly slow growing

159
Q

Prostate cancer:Risk factors

A

Male > 50 yrs
Poor diet – obesity, link with red meat?
Family history, BRCA1/2
Elevated testosterone

160
Q

Prostate cancer:Signs & symptoms

A

Initially asymptomatic

Frequent urination, pain or difficulty with urination, blood in urine

161
Q

Prostate cancer:Diagnosis

A

Digital rectal examination (DRE), ultrasound, MRI, biopsy

Screening for prostate-specific antigen (PSA) – not clear if this is really useful

162
Q

Prostate cancer:Prevention

A

Diet / exercise?

163
Q

Prostate cancer:Treatment

A

Most are slow growing - managed with drugs to ↓ testosterone (Finasteride)
For aggressive tumours - surgery, radiation / brachytherapy, chemotherapy

164
Q

Prostate cancer:Incidence

A

4th most common cancer in women worldwide

160 new cases in NZ each year and ~50 deaths

165
Q

Prostate cancer:Risk factors

A

HPV greatest risk factor (mostly subtypes 16 & 18)
Number of sexual partners
Family history, smoking, poor diet

166
Q

Prostate cancer:Signs & symptoms

A

Abnormal vaginal bleeding or discharge

Tiredness, pain in pelvic area, legs or lower back

167
Q

Prostate cancer:Prevention

A

Cervical screening using Papanicolaou (Pap) or smear test – every 3 years
HPV vaccination
Barrier protection during intercourse

168
Q

Prostate cancer:Diagnosis

A 
Pap test, visual inspection (colposcopy), and biopsy
Also imaging (ultrasound, CT, MRI, PET, bone scan)
169
Q

Prostate cancer:Treatment

A

Surgery, radiation / brachytherapy, chemotherapy

Human Bioscience: Impaired Body Function (2 decks)

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