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HLSC 222 > Ch. 10 > Flashcards

Ch. 10 Flashcards

1
Q

Cancer

A

Leading cause of suffering and death in the developed world

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2
Q

How is cancer a form of Darwinian evolution

A

Tumor development has cells with heritable change that have a survival advantage, so they outcompete their neighbors

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3
Q

Cancer is a collection of more then _ diseases

A

100

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4
Q

Is cancer age related

A

yes

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5
Q

what modifies the risk of developing cancer and the response to treatment

A

-Environment
-Heredity
-Behavior

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6
Q

Epigenetic

A

Study of how behavior and environment cause changes that affect gene mutation

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7
Q

Cancer is derived from the greek word

A

Karkinoma (Crab)

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8
Q

Karkinoma/hippocrates use crab to describe

A

projections extending from tumors into adjacent tissues

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9
Q

Tumor used to

A

refer to any swelling caused by inflammation

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10
Q

Tumor now

A

reserved for describing new growth or neoplasm

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11
Q

Are all tumors cancer?

A

No

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12
Q

what is a non cancerous tumor

A

Benign

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13
Q

what tumors contain cancer

A

malignant

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14
Q

What kind of cells do benign tumors have

A

-well-differentiated cells
-well-organized stroma

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15
Q

Benign tumors retain

A

-normal tissue structure
-don’t invade beyond capsule

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16
Q

Can benign tumors be dangerous

A

yes
-eg. benign meningioma at eh base of the skull can compress brain tissue

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17
Q

what tumors have cancer

A

malignant tumor

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17
Q

Malignant tumors grow

A

-rapidly
-abnormal organization

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17
Q

Hall mark of cancer

A

Anaplasia

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18
Q

Anaplasia

A

loss of cellular differentation

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19
Q

Pleomorphic

A

vary in size and shape

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20
Q

Malignant tumor structure

A

large, disorganized stroma, with an abnormal structure

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21
Q

Metastasis

A

ability to spread far beyond the tissue of origin/most deadly characteristic of malignant tumors

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22
Q

Characteristics or malignant tumors

A

-Rapid growth
-Anaplasia
-Pleomorphic
-Large stroma
-Metastasis

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23
Q

Cellular differentiation

A

process in which a stem cell alters from one type to a differentiated one
-usually more specialized

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24
Q

Malignant tumor types

A

-Carcinomas
-Adenocarcinomas

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25
Q

Carcinomas

A

Cancers arising from epithelial tissue

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26
Q

Ademocarcinomas

A

cancers arising from ductal or glandular structures

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27
Q

Benign

A

-Grow slow
-well-defined capsule
-not incisive
-well differentiated
-low miotic index
-don’t metastasize

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28
Q

Malignant

A

-grow rapidly
-not encapsulated
-invasive
-high mitotic index
-can metastasis

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29
Q

Situ

A

in natural or original place

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30
Q

Carcinoma in situ

A

preinvasive epithelial tumors of glandular or squamous cells origin

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31
Q

cancers develop- and accumulate

A

incrementally
genic lesions (mutations)

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32
Q

CIS: 3 fates

A
  1. Remain stable for a long time
  2. Progress to invasive/metastatic cancers
  3. regress and dissapear
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33
Q

high grade lesions are more likely

A

to become invasive

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33
Q

CIS cancer cells

A

have not broken through basement membrane or invade surrounding stroma
-not considered malignant

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33
Q

CIS vary from

A

low grade to high grade dysplasia

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34
Q

What is a disease of aging

A

Cancer

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35
Q

what is required for cancer to develop

A

multiple mutations

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36
Q

Mutation

A

cell acquires characteristics that provide an advantage overing neighboring cells

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37
Q

advantage of mutations

A

increased growth rate and/or decreases apoptosis

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38
Q

Result of mutation

A

-decreased need for growth factor to multiply
-anchorage independence to spread through body (metastasis)
-immortality

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39
Q

immortality in cells means

A

no apoptisis

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40
Q

Fundamental cancer concepts

A
  1. cancer is a genetic disease arising from multiple mutations
  2. tumor microenvironment is a mix of cells (cancer and benign) and their secretions
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41
Q

3 cancer stages

A
  1. tumor initiation
  2. tumor premotion
  3. tumor progression
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42
Q

Tumor initiation

A

-producing initial cancer cell
-first stage of development
-depends on specific mutations

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43
Q

Tumor premotion

A

-population of cancer cells expands with diversity of phenotypes
- additional mutatuions

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44
Q

Tumor progression

A

-spread of tumor to adjacent and distal sites
- governed by more mutations and changing microenvironments

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45
Q

2 types of mutations

A

-small scale changes
-large scale changes

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46
Q

Small scale changes are also

A

point mutations

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47
Q

large scare changes are also

A

translocations

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48
Q

Point mutations

A

Alteration of one or a few nucleotide base pairs

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49
Q

result of point mutations

A

profound effects on activity of resulted proteins

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50
Q

Driver mutations

A

mutations that drive the progression of cancer

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51
Q

passenger mutations

A

mutations that don’t contribute to malignant phenotype
-random events

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52
Q

small scale includes

A

driver mutations and passenger mutations

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53
Q

large scale: chromosome translocations

A

-large changes in chromosome structure
-section of one chromosome is translocate

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54
Q

gene amplification

A

-instead of two normal copies of a gene 10s-100s of copies are present

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55
Q

Why does gene amplification make some many copies

A

One section of chromosome is translocated reshuffling the order of nucleotides making new sections

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56
Q

Gene amplification example

A

gene expression of HER2 proteins

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57
Q

Clonal proliferation model

A

selective advantage cancer cell has over neighboring cells

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58
Q

what’s an advantage of clonal proliferation model

A

it can replicate faster than nonmutant neighbors

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59
Q

What is the action of clonal proliferation model

A

increasingly rapid cell division and impaired DNA repair mechanisms of cancer cells

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60
Q

what does the rapid dividing and repairing mechanisms of clonal proliferation create

A

continuing accumulation of mutations throughout progression to mist aggressive metastatic lesion

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61
Q

Transformation definition

A

process by which a normal cell becomes a cancer cell

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62
Q

Transformation causes malignancy

A

by progressive accumulation of genetic changes that alter basic nature of cells

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63
Q

Individual cancer cells develop

A

its own set of mutations

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64
Q

Result of individual cell mutations

A

-Gnomically heterogeneous mix of cells
-Subsets accumulate more mutations increasing the cells malignant potential

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65
Q

Cancer cells that don’t accumulate a critical set of mutations

A

lose to competition and die

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66
Q

How is cancer similar to wound healing

A

it has an initial proinflammatory response

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67
Q

cancer cell proliferation triggers

A

proinflammatory response by itself and adjacent nonmalignant cells

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68
Q

Like with wound healing mediators recruit

A

-inflammatory or immune cells (T+B, Macrophages)
-Cells associated with tissue repair (Fibroblasts, adipocytes, mesenchymal stem cells, and endothelial cells)

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69
Q

What causes abnormal wound healing

A

recruited cells form a stroma (tumor microenvironment)

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70
Q

Effect of Abnormal wound healing

A

-cancer cells increase proliferation
-become more heterogeneous (Diverse)

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71
Q

Process of abnormal wound healing

A

-great deal of cancer cell death
-surviving cells are more aggressive
-Many take of a monastic phenotype

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72
Q

Cancer cell needs uncontrolled growth through

A

sustained proliferation signals

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73
Q

sustained proliferation signals

A

-Pro-oncogene control
-oncogene mutations

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74
Q

result of sustained proliferation signals

A

blocking of body’s mechanism to stop uncontrolled growth

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75
Q

First hallmark of cancer

A

uncontrolled cellular proliferation

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76
Q

Normal cells proliferative phase

A

runs in response to growth factor

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77
Q

Growth factor

A

binds to specific receptors on cells surface and activates intracellular signaling pathways affecting DNA synthesis and cellular growth

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78
Q

Proto-oncogenes

A

normal genes that direct protein synthesis and cellular growth

79
Q

Oncogenes

A

mutated pro-oncogenes cells

80
Q

Oncogenes cells

A

-independent or normal regulatory mechanisms
-Mutations allow uncontrolled growth
-in addition various stoma cells produce their own growth factors that contribute to uncontrolled growth

81
Q

Growth receptors

A

-RAS
-P13K
-MYC
-D-cyclins

82
Q

what activates growth receptors

A

oncogenes

83
Q

Translocations cause

A

excessive inappropriate production of oncogenes

84
Q

Translocation eg. burkitts lymphoma

A

normal chromosomes get changed into Burkitt’s lymphoma which produces abnormal B cells

85
Q

Cancer cells stop tumor suppressor genes by

A

2 mutations which inactivate tumor suppressor genes

86
Q

Tumor suppressor genes in normal cells

A

-inhibit proliferation
-stop cell division when cells are damaged
-prevent mutations

87
Q

Abnormal wound healing

A

-Recruited cells form stroma
-Stroma surrounds and infiltrates tumor

88
Q

Stroma cells can make up to _of the tumor mass

A

90%

89
Q

Stroma growth is affected by

A

-rapid cancer cell proliferation
-various cell additions

90
Q

Extensive paracrine signaling affects

A

-Stromal cells
-Cancer cells

91
Q

Abnormal wound healing effect

A

-cancer cells increase proliferation
-cells become more heterogeneous (diverse)

92
Q

Abnormal cell growth process

A

-great deal of cancer cell death
-surviving cells are more aggressive
-many cells take on a metastatic phenotype

93
Q

Tumor suppressor genes are called

A

anti-oncogenes

94
Q

Tumor suppressor genes

A

Must be activated for cancer proliferation to occur

95
Q

Classic tumor suppressor gene

A

tumor-protein P53

96
Q

guardian of the genome

A

classic tumor suppressor gene P53

97
Q

P53

A

-Monitors cellular stress and activates “care taker genes” to repair genetic damage
-controls apoptosis

98
Q

Inactivation of P53

A

requires at least 2 mutations
-single mutation increases risk of children developing cancer

99
Q

Cancer wants to stop the limit to its division

A

Cancer activates telomeres to provide unlimited division

100
Q

Is there a limit to body cell division

A

yes

101
Q

What’s the limit to division called

A

Hayflick limit

102
Q

what are telomeres

A

protective caps on each chromosome

103
Q

When cells proliferate

A

telomere caps shorten each time it divides

104
Q

When telomeres run out

A

-cells can’t divide anymore
-cell death

105
Q

Telomerase

A

enzyme that maintains telomeres and stops them from shortening

106
Q

Telomerase is active

A

in ovaries and testes germ cells and stem cells

107
Q

cancer activates telomerase causes

A

unlimited telomeres

108
Q

unlimited telomeres causes

A

unlimited proliferation/immortality

109
Q

Cancer needs its own blood supply to move around the body

A

yes

110
Q

cancer making its own blood supply is called

A

angiogenesis

111
Q

Angiogenesis

A

-irregular development of vessels
-increased risk of hemorrhage

112
Q

result of angiogenesis

A

cancer has access to systemic blood system

113
Q

cancer activates production of new blood vessels

A

angiogenesis

114
Q

advanced cancer secretes

A

angiogenic factors

115
Q

GF- growth factor

A

-vascularized endothelial GF
-platelet-derived GF
-Basic Fibroblast GF

116
Q

how do vessels within tumors differ from healthy vessels

A

-irregular branching from existing capillaries
-cell contact between endothelial cells are less tight
-tumor created vessels allow passage of tumor cells

117
Q

passage of tumor cells into vascular system

A

metastasize

118
Q

less tight cell contact in tumors

A

vessels are more porous and prone to hemorrhage

119
Q

Cancer needs more building blocks to make more cells

A

programming energy meta olism

120
Q

Programming energy metabolism

A

-Warburg effect/lactic acid
-increased risk of hemorrhage
-rapid cell growth

121
Q

Reprogramming energy metabolism- Normal cells

A

-oxygen use aerobic metabolism
-limited oxygen use glycolysisd

122
Q

glycolysis produces

A

lactic acid

123
Q

Reprogramming energy metabolism- cancer cells

A

-only use glycolysis even with oxygen available
-warburg effect

124
Q

Warburg effect

A

aerobic glycolysis

125
Q

Cancer benefit of warburg effect

A

-shift in glycolysis allows continual production of lactate

126
Q

Lactate

A

used for production of lipids, amino acids, and other molecular building blocks for growth

127
Q

resisting apoptosis

A

-intrinsic/extrinsic pathways
-activate BAK
-results in blocked apoptosis

128
Q

intrinsic pathway

A

-monitors cell stress

129
Q

IP if cell can recover

A

activation of BAX

130
Q

IP if cell can’t recover

A

destroy cell with activation of BAK

131
Q

BAK and BAX

A

regulate mitochondrial release of pro-apoptotic molecules (Cytochrome c)

132
Q

Cytochrome c

A

proapoptotic molecule

133
Q

Extrinsic pathway

A

dormant till death receptor is activated (BAK)

134
Q

Both IP and EP activation cause

A

T-cells (cytotoxic) and Natural killer (NK) cells to induce apoptosis

135
Q

Apoptotic pathways in cancer

A

are dysregulated

136
Q

Mechanism for cancer to travel through the body

A

EMT

137
Q

EMT

A

the ability to metastasize

138
Q

Metastasis

A

spread of cancer cells from site of original tumor to distant tisseues and organs

139
Q

The defining characteristic of cancer

A

Metastasis

140
Q

Major cause of death from cancer

A

Metastasis

141
Q

Example of metastasis

A

Breast cancer

142
Q

Localized breast cancer

A

five year survival >90%

143
Q

Metastasized breast cancer

A

30% survival rate after 5 years

144
Q

Non-metastasized cancer

A

can often be cured by surgery, chemotherapy, and radiation

145
Q

Surgery, chemo, radiation

A

often ineffective against metastasized cancer

146
Q

Model for transition to metastasized cancer

A

EMT

147
Q

EMT

A

Epithelial-mesenchymal transition

148
Q

Carcinomas

A

From highly differentiated epithelial cells that form sheets stabilized by adhesions from neighboring cells

149
Q

Initial carcinomas

A

can complete local tumor expansion, retain epithelial characteristics that prevent disassociation from ECM

150
Q

ECM

A

extracellular matrix

151
Q

Metastasized cells must

A

dissociate from ECM

152
Q

Degree of De-differentation

A

Cells ability to differentiate and produce the phenotype that can separate from the primary to flourish in a hostile secondary site

153
Q

undifferentiated mesenchymal-like carcinoma

A

comes from the programmed transition from a partially epithelial-like carcinoma which initiates epithelial-mesenchymal transition process

154
Q

epithelial-mesenchymal transition process occurs

A

in embryonic development and wound healing

155
Q

cell separation from ECM

A

under go Anoikis

156
Q

Anoikis

A

induction of apoptosis in cells loss of ECM attachment

157
Q

Cancer cells avoid

A

Anoikis instead they enter circulation and spread

158
Q

EMT steps

A
  1. Intravasation
  2. Extravasation
  3. Survival in circulation
159
Q

Intravasation

A

Entry of tumor cells into circulation

160
Q

Intravasation occurs from

A

-Leaky angiogenesis vessels cancer created
-Spread through both vascular and lymphatic pathways

161
Q

Extravasation

A

Exit of tumor cells from circulation to host tissue

162
Q

Survival in circulation

A

Platelets coat tumor providing protection (Cancer clot)

163
Q

Cancer clot

A

Platelets coating and protecting tumor cells

164
Q

Survival in new location

A

-Few cancer cells needed to establish new tumor (TICs)
-Metastasis don’t mean proliferation
-Dormancy

165
Q

TICs

A

-Tumor initiating cells
-Cancer stem cells

166
Q

Dormancy

A

Stable non-proliferating state that is reversable

167
Q

2/3 breast cancer deaths

A

occur after 5 year disease free interval

168
Q

Deceased individuals have been studied and found to have

A

dormant cancer cells even with no cancer history

169
Q

Viruses associated with cancer

A

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

170
Q

New cancer therapy

A

development of oncolytic viruses that specifically attach cancer cells

171
Q

How do cancer cells evade immune detection

A
  1. Failure to produce tumor antigen
  2. Mutation in MHC genes needed for antigen presentation
  3. Production of immunosuppressive proteins or expression of inhibitory cell surface proteins
172
Q

Normal immune system

A

protects against cancer

173
Q

Immunosuppression

A

fosters cancer

174
Q

Immune suppressed eg.

A

-Non-Hodgkin’s lymphoma
-Kaposi sarcoma
-Release of immunosuppressive factors into tumor microenvironment increase resistance of tumor to chemotherapy and radiation

175
Q

Tumor Associated Macrophages

A

Different phenotypes depending on environment

176
Q

Macrophage phenotypes

A

-Classic Macrophage (M1)
-M2
-Tumor associated macrophages (TAM)

177
Q

Classic macrophage

A

responds to inflammatory stage to perform phagocytosis

178
Q

M2

A

During healing produces anti-inflammatory mediators to suppress inflammation

179
Q

Tumor-associated Macrophage (TAM)

A

Act like M2
-block Tcells and NK cells and produce cytokines advantageous to tumor growth and spread

180
Q

Cancer Staging

A

Microscopic analysis based of presence of metastasis

181
Q

Stage I

A

No metastasis

182
Q

Stage II

A

Local invasion

183
Q

Stage III

A

spread to regional structures

184
Q

Stage IV

A

Distant metastasis

185
Q

Cancer treatments

A

-Surgery
-Radiation
-Chemotherapy

186
Q

Surgery

A

-Prevent cancer (colon polyps)
-Biopsy for diagnosis and staging
-lymph node sampling
-Palliative surgery

187
Q

Palliative surgery

A

-relieving pain
-doesn’t deal with cause of condition

188
Q

Radiation

A

-Ionizing radiation damages cancer cell’s DNA
-Goals
~eradicate cancer w/o excessive toxicity
~Avoid damage to normal structures

189
Q

Chemotherapy

A

-Takes advantage of specific vulnerabilities in target cancer cells
-Usually given in combination designed to attack cancer from many different weaknesses at the same time

190
Q

Clinical manifestations of cancer

A

-Paraneoplastic syndromes
-Pain
-Cachexia
-Leukopenia
-Infection
-Asthenia

191
Q

Paraneoplastic syndromes

A

-group of rare disorders triggered by an abnormal immune system response to a cancerous tumor
-caused by biological substances released by tumor
-may be earliest symptom of unknown cancer

192
Q

Pain

A

-little or no pain is associated with early stages of malignancy
-Influenced by fear, anxiety, sleep loss, fatigues, and physical deterioration

193
Q

Cachexia

A

Weakness and wasting of body die to severe chronic illness
-Most severe form of malnutrition

194
Q

Cachexia includes

A

-Anorexia
-Early satiety
-Weight loss
-Anemia
-Asthenia
-Taste alterations
-Altered protein, lipid, carbohydrate metabolism

195
Q

Leukopenia + Thrombocytopenia

A

-Direct tumor invasion to bone marrow causes leukopenia and thrombocytopenia

196
Q

Leukopenia

A

Reduced WBC

197
Q

Thrombocytopenia

A

Reduced platelets in blood

198
Q

Infection

A

Risk increases when absolute neutrophil and lymphocyte count falls

199
Q

Asthenia

A

Weakness, lack of energy and strength

HLSC 222 (9 decks)

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