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Pathophysiology > Chapter 10 - Biology Of Cancer > Flashcards

Chapter 10 - Biology Of Cancer Flashcards

1
Q

What interacts together to modify risk of developing cancer and response to treatment

A

Environment, heredity and behaviour

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2
Q

What is the leading cause of suffering and death in developed world

A

Cancer

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3
Q

Cancer is derived from what Greek word?

A

Karinoma (crab)

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4
Q

Karkinoma

A

Used “crab” to describe projections extending from tumours into adjacent tissue

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5
Q

Tumour

A

Describes a new growth or neoplasm

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6
Q

Not all tumours or neoplasms are

A

Cancer

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7
Q

well differentiated and undifferentiated are

A

Both tumours

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8
Q

Well differentiated

A

Are called and tissue structures that are like normal tissues and tend to grow and spread slowly

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9
Q

Poorly differentiated or undifferentiated tumours

A

Are made up of cells that look very abnormal and often grow and spread quickly

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10
Q

Benign tumours

A

-encapsulated
-well differentiated with organized stroma
-retain normal tissue and don’t invade beyond capsule

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11
Q

What’s an example of how benign tumours can still be dangerous

A

Benign meningioma at base of skull can compress local brain tissue

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12
Q

Malignant tumours progress to

A

Cancer

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13
Q

Malignant tumours

A

-rapid growth rate
-abnormal organization
-large stroma

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14
Q

What does it mean that malignant tumours are anaplasia

A

Loss of cellular differentiation

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15
Q

Malignant tumour: pleomorphic

A

Variability in size and shape

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16
Q

Malignant: metastasis

A

Ability to spread far beyond tissue of origin
-most deadly characteristic

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17
Q

Cellular differentiation

A

Process in which a stem cell alters from one type to a differentiated one

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18
Q

Carcinomas

A

Cancers arising from epithelial tissue

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19
Q

Adenocarcinomas

A

Cancers arising from ducal or glandular structures

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20
Q

Benign or malignant: grows slowly

A

Benign

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21
Q

Benign or malignant: not encapsulated

A

Malignant

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22
Q

Benign or malignant: invasive

A

Malignant

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23
Q

Benign or malignant: poorly differentiated

A

Malignant

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24
Q

Benign or malignant: low mitotic index

A

Benign

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25
Q

Benign or malignant: do not metastasize

A

Benign

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26
Q

Situ

A

In natural or original place

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27
Q

Carcinoma in situ

A

Preinvasive epithelial tumours of glandular or squamous cells origin

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28
Q

CIS have not

A

Broken through basement membrane or invaded surrounding stroma
-not considered malignant

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29
Q

CIS three fates

A

1.remain stable for a long time
2.progress to invasive/metastic
3.regress and disappear (immune system)

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30
Q

CIs vary

A

From low grade to high grade
-high grade lesions have highest likelihood of becoming invasive carcinoma

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31
Q

Cancer is predominantly a disease of

A

Aging

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32
Q

Multiple _____ required before cancer can develop

A

Mutations

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33
Q

Cancer mutations

A

Acquire characteristics that provide advantage over neighbouring cells

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34
Q

Common advantages of cancer cells

A

Increased growth rate and or decreased apoptosis

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35
Q

Result of mutations in cancer cells

A
  1. Decreased need for growth factors to multiply
  2. Lack contact inhibition
  3. Anchorage independence to travel through body
  4. Immortality/no apoptosis
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36
Q

Contact inhibition

A
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37
Q

Ten features of cancer

A

1.resisting cell death
2. Deregulating cellular energetic
3. Sustained proliferative signaling
4. Evading immune destruction
5. Evading growth suppressors
6. Enabling replicative immortality
7. Tumour promoting inflammation
8. Activating invasion and metastasis
9. Genomic instability
10. Inducing apoptosis

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38
Q

Cancer is a ___ disease arising from multiple ___

A

Genetic, mutations

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39
Q

Tumour microenvrioment is a ___ of cells both ___ and ___ as well as their secretions

A

Mixture, cancerous, benign

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40
Q

Stage one of cancer

A

Tumour initiation
-producing initial cancer cell
-dependant on specific mutations

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41
Q

Second stage of cancer

A

Tumour promotion
-population of cancers cells expands with diversity of phenotypes
-additional mutations

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42
Q

Stage three of cancer

A

Tumour progression
-spread of tumour to adjacent and distal items
-more mutations and changing micro environments

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43
Q

Mutations include

A

-small scale : point mutations
-large scale : translocations

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44
Q

Small scale : point mutations

A

Alteration of one or a few nucleotide base pairs
-can have profound effect on activity of resultant proteins

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45
Q

Driver mutations

A

Mutations that “drive” progression of cancer

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46
Q

Passenger mutations

A

Mutations that don’t contribute to malignant phenotype
-random events and referred to as passenger mutations

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47
Q

Large scale : chromosome translocations

A

-large changes in chromosome structure
-section of one chromosome is translocated to another chromosome

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48
Q

Large scale : gene amplification

A

Instead of normal two copies of gene, tens or even hundreds of copies are present
-gene expression of HER2 proteins

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49
Q

Clonal proliferation model

A

Selective advantage cancer cell has over neighbouring cells
-replicate faster than non mutant neighbours

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50
Q

What leads to accumulation of mutations

A

Rapid cell division and impaired DNA repair

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51
Q

Inactivation of APC

A

Cell seems normal but is predisposed to proliferate excessively

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52
Q

Mutation activation of K-ras

A

Cell begins to proliferate too much but is otherwise normal

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53
Q

Loss of DCC + over expression of COX-2

A

Cell proliferates more rapidly
-undergoes structural changes

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54
Q

Loss of TP53 + activation of telomerase

A

Cell grows uncontrollably and looks obviously abnormal

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55
Q

Transformation

A

Process by which a normal cell becomes a cancer cell

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56
Q

Transformation is directed by

A

Progressive accumulating of genetic changes that alter basic nature of cell
-drives it to malignancy

57
Q

Each cancer may develop its own set of

A

Mutations

58
Q

Cancer that does not accumulate critical set of mutations

A

Lose to competition and dies

59
Q

Initial pro inflammatory response

A

-triggers typical prinflammatory response by itself and non malignant cells

60
Q

Mediators that are recruited by initial pro inflammatory response

A

-inflammatory immune cells : T, B and macrophages
-tissue repair : fibroblasts, adipocytes, mesenchymal, endothelial

61
Q

Extensive paracrine signals affects

A

Both stroma and cancer cell populations

62
Q

Stroma

A

-Surrounds and infiltrates tumour
-make up 90% of tumour mass

63
Q

Stroma not just affected by rapid cancer cell proliferation but

A

Various cell additions stroma

64
Q

Cancer cells ___ proliferation and become

A

Increase
-more heterogenous

65
Q

Cancer becoming more heterogenous and diverse =

A

Higher rate of cancer cell death
-surviving cells more aggressive
-metastatic phenotype

66
Q

How does the cancer cell: sustain proliferation signals

A

-pro-oncogene control
-blocking body’s mechanism to stop uncontrolled growth

67
Q

First hallmark of cancer

A

Uncontrolled cellular proliferation

68
Q

Normal cells only enter proliferative phases in response to

A

Growth factor
-which bind to specific receptors on cell surface, activating pathways—> activate DNA synthesis and cellular growth

69
Q

Proto-oncogenes

A

Normal genes that direct protein synthesis and cellular growth

70
Q

Oncogenes

A

Mutated proto-oncotgene cells
-independant
-uncontrolled growth
-produce their own growth factors

71
Q

Growth receptors: RAS, P13K, MYC, D-cyclins are activated by

A

Cancer oncogenes

72
Q

Translocations can cause

A

Excessive production of oncogenes

73
Q

Burkitt lymphoma produces

A

Abnormal B lymphocytes

74
Q

How does the cancer cell: evading growth suppressor

A

-two mutations required
-inactivation of tumour suppressor genes

75
Q

Evading growth suppressors —> mutation of

A

Tumour suppressor genes

76
Q

Normal tumour suppressor gene function

A

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

77
Q

Tumour suppressor genes must be

A

Inactivated for cancer proliferation to occur

78
Q

Classic tumour suppressor gene

A

Tumour protein P53
-guardian of the genome

79
Q

P53

A

-monitors cellular stress and activates caretaker genes to repair genetic damage
-control apotposis

80
Q

Inactivation of P53 requires at least

A

Two mutations
-inc cancer risk in offspring

81
Q

How does the cancer cell: limited cellular division

A

Activates telomerase to provide unlimited tickets to divide

82
Q

Hayflick limti

A

Most body cells are not immortal and can only divide a limited number of times

83
Q

Telomeres

A

Protective caps on each chromosome

84
Q

What happens to telomere during proliferation

A

The caps shorten with each division

85
Q

When telomeres run out

A

The cell can no longer divide, and it die

86
Q

Telomerase

A

Enzyme that maintains telomeres
-don’t decrease in number with cell division

87
Q

Telomerase is usually only active in

A

Ovaries and testes, and stem cells

88
Q

Cancer cells activate telomerase =

A

Unlimited telomeres

89
Q

Unlimited proliferation =

A

Immortality

90
Q

How does the cancer cell: get its own blood supply for movement

A

-angiogenesis
-irregular development of vessels
-risk of hemorrhages
-access to systemic blood system

91
Q

Angiogenesis

A

Cancer cells can activate production of new blood vessels

92
Q

Advanced cancers secrete ____ factors

A

Angiogenic

93
Q

Vessels formed within tumours

A

Perform irregular branching from existing capillaries
-less tight, more porous=hemorrhage
-allow passage of tumour cells=metastasize

94
Q

How does the cancer cell: program energy metabolism

A

-Warburg effect/lactic acid
-inc risk of hemorrhage
-rapid cellular growth

95
Q

Energy metabolism in normal cells

A

-oxygen=aerobic metabolism
-limited oxygen=glycolysis=lactic acid

96
Q

Energy metabolism in cancer cells

A

Adequate oxygen=use only glycolysis

97
Q

Warburg effect

A

Glucose—>glycolysis—>pyruvate—>lactate
Aerobic glycolysis

98
Q

Benefit for cancer using the Warburg effect

A

-shift to glycolysis allows continual production of lactate
-lactate used for production of lipids, nucleoside, aa for building blocks = rapid growth

99
Q

How does the cancer cell: resisting apoptosis

A

-intrinsic/extrinsic pathway
-activate BAK
-apoptosis blocked

100
Q

Apoptosis intrinsic pathway

A

Monitors cellular stress
-cell recovers = activated BAX
-cell needs to be destroyed = activated BAK

101
Q

Both BAX and BAK regulate

A

Mitochondrial release of pro-apoptotic molecules
-cytochrome c

102
Q

Apoptosis extrinsic pathway

A

Relatively dormant until death receptor BAK is activated

103
Q

Activation of both intrinsic and extrinsic apoptosis pathways causes

A

T cells and natural killer cells to induce apoptosis

104
Q

How does the cancer cell: EMT

A

The ability to metastasize

105
Q

Cancer that has not metastasized can be

A

Cured, by a combination of surgery, chemotherapy and radiation

106
Q

Cancer that has metastasized can

A

Find the same therapies ineffective

107
Q

Epithelial mesenchymal transition (textbook)

A
108
Q

Initial carcinomas can adequately complete local tumour expansion but still

A

Retain epithelial like characteristics that prevent dissociation from ECM
-must dissociate from ECM to metastasize

109
Q

How do cancer cells dissociate from ECM

A

-need greater degree of de-differentiation, to produce phenotype to separate from primary tumour
-turn into undifferentiated mesenchymal like carcinoma

—> initiates epithelial mesenchymal transition process

110
Q

EMT occurs normally in

A

embryonic development and wound healing

111
Q

Normal cells when separated from ECM.. BUT cancer cells..

A

Undergo anoikis—>apoptosis

Avoid anoiki—>enter circulation and spread

112
Q

Intravasation

A

Entry of tumour cells into circulation
-through the vessel the cancer has created
-spreads through vascular and lymphatic pathways

113
Q

Extravasation

A

Exit of tumour cells from circulation to host tissue

114
Q

Survival in circulation

A

Platelets coat tumour = provide protection called a cancer clot

115
Q

Cancers survival in new location

A

only need a few cancer cells -> tumour initiating cells or cancer stem cells

116
Q

Dormancy

A

Stable non proliferating state that is reversible

117
Q

Viruses associated with cancer

A

HPV, EBV, HEP B + C

118
Q

new cancer therapy

A

Development of oncolytic viruses that specifically attack cancer cells

119
Q

Cancer cells avoid immune detection and destruction using three mechanisms

A
  1. Failure to produce tumour antigen
    2.mutation in MHC genes needed for antigen presenting
  2. Production of immunosuppressive proteins or expression of inhibitory cell surface proteins
120
Q

Immunosuppressive fosters cancer (2)

A

-non Hodgkin’s lymphoma x10
-kaposi sarcoma x1000

121
Q

Release of im o suppressive factors into tumour micro environment increases

A

Resistance of tumour to chemotherapy and radiotherapy

122
Q

Classic macrophage (M1)

A

Responds to inflammatory stage to preform phagocytosis

123
Q

M2 macrophage

A

Appears during healing, to produce anti inflammatory mediators that suppres inflammation

124
Q

Tumour associated macrophages (TAM)

A

Preform similar to M2
-block T cell and NK cells and produce cytokines for tumour growth and spread

125
Q

Cancer/metastasis stage one

A

No metastasis

126
Q

Cancer/metastasis stage two

A

Local invasion

127
Q

Cancer/metastasis stage three

A

Spread to regional structure

128
Q

Cancer/metastasis stage four

A

Distant metastasis

129
Q

Cancer treatment: surgery

A

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

130
Q

Cancer treatment: radiation

A

Ionizing radiation damages cancer cells DNA
-eradicate cancer without excessive toxicity
-avoid damage to normal structures

131
Q

Cancer treatment: chemotherapy

A

Takes advantage of specific vulnerabilities in target cancer cells
-combinations designed to attack cancer from many different weakness at a same time

132
Q

Paraneoplastic syndrome

A

Group of rare disorders that are triggered by abnormal immune system response to cancerous tumour

133
Q

Paraneoplastic syndrome caused by

A

Biological substances released by tumour
-earliest symptom of unknown cancer

134
Q

Cancer pain

A

Little or no pain is associated with early stages
-influenced by fear, anxiety, sleep loss, physical deterioration

135
Q

cachexia syndrome

A

Weakness and wasting of body due to severe chronic illness
-malnurition

136
Q

Leukopenia and thrombocytopenia

A

Direct tumour invasion to bone marrow
-reduced WBC
-reduced platelets in blood
(Respectively)

137
Q

Cancer infection levels

A

Risk increases when absolute neutrophil and lymphocyte counts fall

138
Q

Asthenia

A

Weakness lack of energy and strength

Pathophysiology (20 decks)

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