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HLSC 222 - Pathophysiology Across the Lifespan > Chapter 10 - Biology of Cancer > Flashcards

Chapter 10 - Biology of Cancer Flashcards

1
Q

How is cancer a form of Darwinian evolution?

A

tumour development has cells with a heritable change that have a survival advantage, so outcompete their neighbours

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2
Q

What is the leading cause of suffering and death worldwide?

A

cancer

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3
Q

Cancer is a collection of more than ___ diseases

A

100

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4
Q

Is cancer age related?

A

yes, the longer we live, the greater chance DNA replication has a mutation

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5
Q

Is cancer genetic or epigenetic?

A

it can be both

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6
Q

Epigenetic

A

how behaviours and environment cause changes that affect gene function

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7
Q

What 3 factors influence risk and development of cancer?

A

environment, heredity, behaviour

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8
Q

Cancer is derived from the Greek work Karinoma meaning ____. Why?

A

crab; describes the projections of the tumour into near tissues

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9
Q

Original Tumour Definition

A

any swelling caused by inflammation

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10
Q

Current Tumour Definition

A

new growth or neoplasm (abnormal growth)

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11
Q

Are all tumours cancer?

A

no

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12
Q

Benign Tumour

A

non-cancerous

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13
Q

Malignant Tumour

A

cancerous

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14
Q

Well-differentiated Cells

A

normal tissues that grow and spread slowly

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15
Q

Undifferentiated Cells

A

made of abnormal cells that grow and spread quickly

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16
Q

What kind of cells do benign tumours have?

A

well-differentiated cells and connective tissue

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17
Q

Do benign tumour invade beyond its capsule?

A

no, they maintain a normal structure

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18
Q

Are benign tumours dangerous?

A

they can be

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19
Q

Benign Meningioma

A

tumour at the base of the skull that can compress the brain

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20
Q

Malignant tumour progress to ____

A

cancer

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21
Q

Malignant tumours grow ______ and have ______ organization

A

rapidly; abnormal

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22
Q

Anaplasia

A

loss of cellular differentiation

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23
Q

What type of cells do malignant tumours have?

A

undifferentiated

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24
Q

Pleomorphic

A

variability in size and shape

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25
Q

Stroma

A

supporting structure

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26
Q

Metastasis

A

ability to spread far beyond tissue of origin

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27
Q

What is the most deadly characteristic of malignant tumours?

A

metastasis

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28
Q

Carcinomas

A

cancers arising from epithelial tissue

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29
Q

Adenocarcinomas

A

cancers arising from ductal or glandular structures

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30
Q

Do benign tumours metastasize?

A

no

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31
Q

Benign tumours have a ____ mitotic index, malignant tumours have a _____ mitotic index

A

low; high

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32
Q

What is a carcinoma in situ (CIS)?

A

a pre-invasive epithelial tumour of glandular or squamous cell origin

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33
Q

What does “pre-invasive” mean?

A

the cancer develops incrementally as it accumulates specific genetic mutations

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34
Q

Are CIS considered malignant?

A

No, they have not broken the basement membrane or invaded surrounding stroma

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35
Q

Situ

A

in natural or original place

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36
Q

CIS remain _____ for a long time

A

stable

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37
Q

Can CIS progress?

A

yes they can progress into invasive or metastatic cancers

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38
Q

Can CIS disappear?

A

yes they may regress

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39
Q

CIS either…

A

remains, progresses, disappears

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40
Q

How to classify CIS?

A

vary from low-grade to high-grade

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41
Q

Which class of CIS are more likely to become an invasive carcinoma?

A

high-grade

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42
Q

Cancer is predominantly a disease of ______

A

aging

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43
Q

Mutation

A

cancer cells acquire characteristics that provide them an advantage over other cells

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44
Q

What is the advantage of cancer cells mutating?

A

increased growth rate and/or decreased apoptosis

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45
Q

Do cancer cells need growth factors to multiply?

A

no

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46
Q

Cancer cells lack contact inhibition meaning…

A
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47
Q

Anchorage independence

A
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48
Q

Do cancer cells undergo apoptosis?

A

no, they are immortal

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49
Q

How many mutations are required for cancer cells to form?

A

multiple

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50
Q

Tumour Microenvironment

A

mixture of cells (cancerous and not) and their secretions

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51
Q

Stage 1 of Cancer: Tumour Initiation

A

production of initial cancer cells, first stage of development

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52
Q

What does tumour initiation depend on?

A

specific mutations

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53
Q

Stage 2 of Cancer: Tumour Promotion

A

population of cancer cells expands with diverse phenotypes, the cells undergo additional mutations

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54
Q

Stage 3 of Cancer: Tumour Progression

A

tumour spreads to near (invasion) and far (metastasis), more mutations occur

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55
Q

Point Mutations

A

small-scale genetic changes, alteration of one or a few base pairs

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56
Q

Translocations

A

large-scale genetic changes

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57
Q

Driver Mutations (small-scale)

A

drive the progression of cancer forward

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58
Q

Passenger Mutations (small-scale)

A

don’t contribute to malignant phenotypes, just random events

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59
Q

Chromosome Translocations (large-scale)

A

large changes in chromosome structure

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60
Q

During chromosome translocation…

A

a section of one chromosome is translocated to another

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61
Q

Gene Amplification (large-scale)

A

rather than 2 normal gene copies, tens or hundreds are made

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62
Q

HER2 Proteins

A

too many receptors signalling cells to grow and divide too quickly

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63
Q

Clonal Proliferation Model

A

advantage of cancer cells that causes them to replicate faster than neighbours

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64
Q

What drives the accumulation of mutations?

A

rapid cell division and impaired DNA repair mechanisms

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65
Q

What does inactivation of the antigen presenting cell cause?

A

the cell seems normal but proliferates excessively

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66
Q

What does the mutation that activates K-ras cause?

A

normal cell that proliferates too much

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67
Q

What does a loss of DCC and an over-expression of COX-2 cause?

A

rapidly proliferating cell undergoing structural changes

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68
Q

What does a loss of TP53 and the activation of telomerase cause?

A

uncontrollable abnormal cell growth

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69
Q

Transformation

A

process by which a normal cell becomes a cancer cell

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70
Q

What directs transformation?

A

accumulation of genetic changes that drive it to malignancy

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71
Q

Do all cancer cells have the same mutations?

A

not necessarily, some have their own set of mutations

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72
Q

What is the result of transformation?

A

heterogenous mixture of cells that accumulate more and more mutations

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73
Q

Heterogenous

A

diverse in character

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74
Q

Which cancer cell triggers the initial pro-inflammatory response?

A

the initial cancer cells

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75
Q

Who is affected by the initial pro-inflammatory response?

A

the cancer cells that triggered it and the neighbouring nonmalignant cells

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76
Q

What is recruited during the pro-inflammatory response?

A

-Inflammatory and immune cells (macrophages, T and B cells)
-tissue repair cells (fibroblasts, adipocytes, mesenchymal stem cells, endothelial cells)

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77
Q

What do these recruited cells form?

A

a stroma/ tumour microenvironment

78
Q

What does the stroma do?

A

surround and infiltrates the tumour

79
Q

What % of the tumour mass may the stroma contribute to?

A

90%

80
Q

What directs stroma growth?

A

-cancer cell proliferation
-cell additions

81
Q

How does abnormal wound healing affect cancer cells?

A

increase proliferation and increases the diversity of said cells

82
Q

Many cancer cells die but the surviving cells are more _______

A

aggressive and take on a metastatic phenotype

83
Q

How do cancer cells gain the ability of uncontrolled growth?

A

sustained proliferation signals

84
Q

What is pro-oncogene?

A

mutations that control sustained proliferation signals

85
Q

What does pro-oncogene do?

A

blocks the body’s mechanism of stopping uncontrolled growth

86
Q

What is the 1st hallmark of cancer?

A

uncontrolled cellular proliferation

87
Q

When do normal cells enter proliferative phases?

A

in response to growth factos

88
Q

What do growth factors do?

A

bind to receptors on the cell surface and activate signalling pathways to stimulate DNA synthesis and growth

89
Q

Proto-oncogenes

A

normal genes that direct protein synthesis and growth

90
Q

Oncogenes

A

mutated proto-oncogenes cells

91
Q

Oncogenes are _______ of normal regulatory mechanisms

A

independent

92
Q

How do stroma contribute to uncontrolled growth?

A

by producing their own growth factors

93
Q

Which growth receptors are activated by cancerous oncogenes?

A

RAS, P13K, D-cyclins

94
Q

What do translocations cause?

A

excessive and inappropriate oncogene production

95
Q

What does Burkitt Lymphoma produce? How?

A

abnormal B-lymphocytes by translocation changing normal chromosomes

96
Q

How do cancer cells stop tumour suppressor genes?

A

evading growth suppression by 2 mutations to inactivate tumour suppressor genes

97
Q

What do normal tumour-suppressor genes do?

A

inhibit proliferation, stop cell division of damaged cells, prevent mutations

98
Q

Anti-oncogenes

A

tumour suppressor genes

99
Q

What must be inactivated for cancer to continue?

A

tumour suppressor genes

100
Q

Tumour-Protein P53 is a…

A

classic tumour-suppressor gene

101
Q

P53 aka ‘_______ of the genome’

A

guardian

102
Q

What does P53 do?

A

monitor cellular stress and activates ‘caretaker genes’

103
Q

What do caretaker genes do?

A

repair genetic damage and control apoptosis

104
Q

How many mutations are required to inactivate P53?

A

2

105
Q

What does only a single mutation of P53 result in?

A

increased cancer risk in offspring

106
Q

How do cancer cells stop limits on their division?

A

telomere activation to provide unlimited “tickets” to divide

107
Q

Hayflick Limit

A

limited number of divisions imposed on most body cells

108
Q

What are telomeres?

A

protective caps on each chromosome

109
Q

What happens to telomere caps as cells divide?

A

they shorten with each division

110
Q

What happens when telomeres run out?

A

the cell can no longer divide so the cell dies (apoptosis)

111
Q

What is telomerase?

A

an enzyme that maintains telomeres with cell division

112
Q

Under normal conditions, where is telomerase active?

A

ovaries, testes, stem cells

113
Q

What is the result of cancer cells activating telomerase?

A

unlimited telomeres (= unlimited division)

114
Q

How do cancer cells gain their own blood supply to move around the body?

A

by angiogenesis – the irregular development of vessels

115
Q

What does angiogenesis by cancer cells increase the risk of?

A

hemorrhage

116
Q

Angiogenesis means cancer has access to…

A

the systemic blood system

117
Q

What do advanced cancers secrete?

A

angiogenic factors to promote growth

118
Q

What are the angiogenic growth factors produced?

A

vascular endothelial GF, platelet-derived GF, basic fibroblast GF

119
Q

Are tumour vessels the same as healthy blood vessels?

A

no

120
Q

Do tumour vessels branch the same as healthy blood vessels?

A

no, they branch irregularly from existing capillaries

121
Q

Why are tumour vessels more prone to hemorrhage?

A

the cells are less tight together and are hence more porous so can leak

122
Q

How do tumour vessels promote metastasize?

A

they allow the passage of tumour cells in the vascular system so it can spread

123
Q

How do cancer cells gain the building blocks to gain more cells?

A

they program energy metabolism to increase cellular growth

124
Q

Normal cells use ______ metabolism

A

aerobic (mitochondria ETC)

125
Q

When normal cells have limited oxygen they undergo glycolysis and produce ____ _______.

A

lactic acid

126
Q

Warburg Effect

A

Aerobic glycolysis: cancer cells, even in adequate oxygen presence, use only glycolysis

127
Q

What does the Warburg effect allow cancer cells to do?

A

continually produce lactate

128
Q

What is lactate used for?

A

lipid, nucleoside, amino acid, molecular building block production needed for growth

129
Q

How do cancer cells resist apoptosis?

A

utilizing the intrinsic/extrinsic pathway to activate BAK and block apoptosis

130
Q

Apoptosis: What does the intrinsic pathway do?

A

monitors cellular stress

131
Q

What does the intrinsic pathway activate if a cell can recover?

A

BAX

132
Q

What does the intrinsic pathway activate if a cell must be destroyed?

A

BAK

133
Q

What do BAX and BAK regulate?

A

mitochondrial release of pro-apoptotic molecules (cytochrome C)

134
Q

When is the extrinsic pathway activated from dormancy?

A

when BAK, the death receptor is activated

135
Q

What does activation of both the intrinsic and extrinsic pathways result in?

A

Apoptosis induced by cytotoxic T-cells and natural killer T-cells

136
Q

The dysregulation of apoptotic pathways in cancer cells means they do not…

A

undergo apoptosis

137
Q

What is the major cause of death from cancer?

A

metastasis

138
Q

Can cancer that has not metastasized be cured?

A

Often yes by surgery, chemotherapy, radiation

139
Q

Are surgery, chemotherapy, and radiation effective against metastasized cancer?

A

not usually

140
Q

How do cancer cells develop the ability to metastasize?

A

EMT - epithelial-mesenchymal transition

141
Q

Where do carcinomas originate?

A

highly differentiated epithelial cells in sheets stabilized be adhesions to neighbouring cells

142
Q

What prevents carcinomas from dissociating from the extra cellular matrix (ECM)?

A

their epithelial like characteristics

143
Q

What must happen for cancer cells to metastasize?

A

dissociation from the extra-cellular matrix

144
Q

Metastasis is achieved by a programmed transition from a partially epithelial-like carcinoma to a more ____________ mesenchymal-like carcinoma?

A

undifferentiated

145
Q

When does epithelial-mesenchymal transition occur normally?

A

embryonic development and wound healing

146
Q

Anoikis

A

apoptosis that occurs when normal cells are separated from their ECM

147
Q

Intravasation: How do tumour cells enter circulation?

A

via leaky angiogenesis vessels created by the cancer

148
Q

Where do tumour cells spread?

A

through vascular and lymphatic pathways

149
Q

Extravasation: Where do tumour cells go after they exit circulation?

A

host tissue

150
Q

What allows tumour cells to survive in circulation?

A

cancer clot: platelets that coat the tumour to provide protection

151
Q

Tumour-Initiating Cells aka cancer stem cells

A

the few cancer cells required to form a tumour in a new location

152
Q

Does metastasis guarantee proliferation?

A

No

153
Q

Dormancy

A

stable, non-proliferating state

154
Q

Is dormancy reversible?

A

Yes

155
Q

2/3 of breast cancer deaths occur after a __ year disease-free interval

A

5

156
Q

What are some viruses associated with cancer?

A

Human Papillomavirus (HPV), Epstein-Barr Virus (EBV), Hepatitis B and C

157
Q

Oncolytic Viruses

A

a new cancer therapy that uses these virus to attack cancer cells

158
Q

3 Ways Cancer cells avoid the immune response:

A
  1. don’t produce tumour antigen
  2. MHC gene mutation needed for antigen presentation
  3. immunosuppressive protein production or expressing inhibitory cell surface proteins
159
Q

______ immune system protects against cancer

A

normal

160
Q

__________ fosters cancer

A

immunosuppression (ie. non-hodgkin’s lymphoma, Kaposi sarcoma)

161
Q

What does the release of immunosuppressive factors into the tumour microenvironment increase?

A

resistance to chemotherapy and radiation

162
Q

They phenotype of a macrophage depends on the tumour m____e_______

A

microenvironment

163
Q

What stage do ‘Classic Macrophages’ (M1) respond to?

A

inflammatory stage

164
Q

What do classic (M1) macrophages do?

A

phagocytosis

165
Q

What stage do M2 macrophages respond to?

A

healing

166
Q

What do M2 macrophages do?

A

produce anti-inflammatory mediators to suppress inflammation

167
Q

Do tumour-associated macrophages (TAM) perform like M1 or M2?

A

M2

168
Q

What do TAMs do?

A

block T-cells and NK cells, produce cytokines that are advantageous to tumour growth and spread

169
Q

What is analyzed microscopically to determine cancer staging?

A

present of metastasis

170
Q

Stage I

A

no metastasis

171
Q

Stage II

A

local invasion

172
Q

Stage III

A

spread to regional structures

173
Q

Stage IV

A

distant metastasis

174
Q

Cancer Treatment: Surgery

A

-prevention
-biopsy for diagnosis and staging
-lymph node sampling
-palliative surgery

175
Q

Palliative Surgery

A

used for pain relief rather than dealing with the cause of the condition

176
Q

What does ionizing radiation do?

A

damage cancer cell’s DNA

177
Q

Cancer Treatment: What is the goal of radiation?

A

eradicate cancer without excessive toxicity and damage to normal structures

178
Q

What does chemotherapy target in cancer cells?

A

specific vulnerabilities

179
Q

Cancer Treatment: Why is chemotherapy given in combinations?

A

it can be designed to attack many different weaknesses of the cancer at the same time

180
Q

Paraneoplastic Syndromes

A

a group of rare disorders triggered by an abnormal immune response to a cancerous tumour

181
Q

What causes paraneoplastic syndromes?

A

biological substances released by the tumour

182
Q

What is usually the earliest symptom of unknown cancer?

A

paraneoplastic syndromes

183
Q

Is pain a symptom of early malignancy stages?

A

usually no, if so it is influenced by fear, anxiety, sleep loss, physical deterioration

184
Q

Cachexia Syndrome

A

weakness and wasting of body due to severe chronic illness

185
Q

What is the most severe form of malnutrition?

A

cachexia syndrome

186
Q

Cachexia Syndrome Symptoms

A

anorexia, early satiety, weight loss, anemia, asthenia, taste alterations, altered lipid, protein, carbohydrate metabolism

187
Q

Asthenia

A

weakness, lack of energy and strength

188
Q

What does direct tumour invasion of bone marrow cause?

A

leukopenia and thrombocytopenia

189
Q

Leukopenia

A

reduced WBC count in blood

190
Q

Thrombocytopenia

A

low platelet count in blood

191
Q

What increases the risk of infection?

A

when neutrophil and lymphocyte counts fall

HLSC 222 - Pathophysiology Across the Lifespan (17 decks)

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