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Pathophysiology > Chapter 10 - Biology of Cancer > Flashcards

Chapter 10 - Biology of Cancer Flashcards

1
Q

what is cancer?

A

leading cause of suffering and death in developed word.

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2
Q

what caused cancer?

A

specific and often age-related accumulation of genetic and epigenetic alterations

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3
Q

___, ___, and ____ interact to modify risk of developing cancer and response to treatment

A

environment, heredity and behavior

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4
Q

what is the study of how behaviors and environment causes changes that affect gene function

A

epigenetic

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5
Q

what does karinoma mean?

A

crab

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6
Q

what is tumuor?

A

new growth or neoplasm (new/abnormal growth)

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7
Q

cells and tissues structures that are like normal tissues and tend to grow and spread slowly?

A

well-differentiated

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8
Q

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

A

poorly differentiated or undiffrentiated

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9
Q

True or False: well-differentiated and undifferentiated are both tumuors

A

True

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10
Q

which type of tumour progresses to cancer?

A

malignant

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11
Q

loss of cellular differentiation; aka hallmark of cancer

A

anaplasia

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12
Q

what is pleomorphic? which type of tumour is this associated?

A

variability in size and shape; malignant

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13
Q

the most deadly characteristic of malignant tumuors

A

metastasis

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14
Q

what is metastasis?

A

ability to spread far beyond tissue of origin

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15
Q

these are cancers arising from epithelial tissue

A

carcinomas

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16
Q

cancers arising from ductal or glandular structures

A

adenocarcinomas

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17
Q

T or F: CIS is not considered malignant.

A

True

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18
Q

what is CIS?

A

preinvasive epithelial tumours of glandular or squamous cells origin

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19
Q

three fates of CIS?

A

remains stable for long time (1)
progress to invasive/metastatic cancers (2)
regress and disappear (3)

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20
Q

CIS vary from ___ grade to ____ grade dysplasia

A

low; high

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21
Q

which grade lesions having highest likelihood of becoming invasive carcinoma

A

high grade

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22
Q

Cancer is a predominantly a disease of ____

A

aging

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23
Q

T or F: Single mutations required before cancer can develop/

A

false; multiple mutations

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24
Q

result of multiple mutations?

A

decreased need for growth factors to multiply (1)

lack of contact inhibition (2)

anchorage independence to disseminate through body (metastasis) (3)

immortality - no apoptosis (4)

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25
Q

2 fundamental concepts of cancer:
cancer is a ___ (1) disease arising from ____ (2) mutations.

tumour environment is a ____ (3) of cells (cancerous and benign) as well as their secretions

A

genetic (1); multiple (2); mixture (3)

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26
Q

the three stages of cancer:
(1). tumour ___
(2). tumour ___
(3). tumour ___

A

initiation; promotion; progression

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27
Q

what is tumour initiation?

A
  • first stage of cancer dev
  • dependent on specific mutations
  • producing initial cancer cell
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28
Q

what is tumour promotion?

A
  • pop of cancer cell expands with diversity of phenotypes
  • additional mutations
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29
Q

what is tumour progression?

A
  • metastasis
  • more mutations and changing microenvironments
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30
Q

small-scale changes: ___ mutations

large-scale changes: ___

A

point; translocations

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31
Q

two types of small-scale:

A

driver mutations (1)

passenger mutations (2)

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32
Q

what is point mutations?

A

alteration of one or few nucleotide base pairs

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33
Q

what is driver mutations?

A

mutations that drive progression of cancer.

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34
Q

what is passenger mutations?

A

random events; mutations that don’t contribute to malignant phenotype.

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35
Q

two types of large-scale mutation?

A

chromosome translocation & gene amplification

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36
Q

what is chromosome translocations?

A
  • large change in chromosome structure
  • section of one chromosome is translocated to another chromosome
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37
Q

what is gene amplification?

A

instead of normal 2 copies of gene, tens or even hundreds of copies are present.

E.g., gene expression of HER2 proteins

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38
Q

selective advantage cancer cell has over neighboring cells

A

clonal proliferation model (CPM)

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39
Q

In CPM, cancer cells can replicate ___ than nonmutant neighbors

A

faster

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40
Q

increasingly __ cell division and ____ DNA repair mechanisms of cancer cells. This continues the accumulation of ___ throughout progression to most aggressive metastatic lesion.

A

rapid; impaired; mutations

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41
Q

a process by which a normal cell becomes a cancer cell

A

transformation

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42
Q

___ ____ that do not accumulate a critical set of mutations lose to competition and die

A

cancer cells

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43
Q

T or F: each cancer develop its own set of mutations

A

true

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44
Q

Transformation is directed by ___ accumulation of ____ ____ that ____ basic nature of cell and drive it to ____

A

progressive; genetic changes; alter; malignancy

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45
Q

Cancer development is similar to ____ _____

A

wound healing

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46
Q

initial cancer cell proliferation triggers a typical ______ response by itself and ____ nonmalignant cells

A

proinflammatory; adjacent

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47
Q

wound healing, mediators recruit:
- inflammatory or ____ cells (e.g., T cells, B cells and macrophages)

  • cells associated with ___ repair like (f____, adipocytes, m____ stem cells and e____ cells
A

immune; tissue; fibroblasts, mesenchymal, endothelial

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48
Q

stroma cells make up ___% of tumour mass

A

90%

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49
Q

extensive _____ signaling among stromal and cancer cells affect both population:
(1) ____, & (2) _____

A

paracrine; secretory cell (1); adjacent target cell (2)

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50
Q

In Ab wound healing, recruited cells form a _____ (tumour microenvrionment

A

stroma

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51
Q

In ab wound healing, effect:
cancer cells ____ proliferation

becomes more ____ (diverse)

A

increase; heterogenous

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52
Q

In ab wound healing, process,
- great deal of cancer cell ___

  • surviving cells are more ____
  • many take on _____ phenotype
A

death; aggressive; metastatic

53
Q

what is the first hallmark of cancer?

A

uncontrolled cellular proliferation

54
Q

Normal cells generally only enter proliferative phases in response to ____ factors

A

growth

55
Q

what is proto-oncogenes?

A

normal genes that direct protein synthesis and cellular growth

56
Q

what are oncogenes?

A

mutated proto-oncogenes cells

57
Q

_____ produce oncogenes, which allows uncontrolled growth

A

mutations

58
Q

oncogenes are ____ of normal regulatory mechanisms

A

independent

59
Q

____ can cause excessive and inappropriate production of oncogenes

A

translocations

60
Q

translocation changes normal chromosomes into _____ lymphoma

A

Burkitt

61
Q

what does Burkitt lymphoma produces?

A

Abnormal B lymphocytes

62
Q

how do cancer cells evade growth suppressors?

A

mutation of tumour suppressor genes

63
Q

what does normal tumour suppression genes do?

A
  • inhibit proliferation
  • stop cell division when cells are damaged
  • prevent mutations
64
Q

Tumour suppressor genes (which are called ____-_____) must be _____ for cancer proliferation to occur.

A

anti-oncogenes; inactivated

65
Q

What is the classic tumour-suppressor gene?

A

tumour-protein P53

66
Q

another name for tumour protein P53

A

guardian of the genome

67
Q

what does P53 do?

A
  • monitor cellular stress and activates caretaker genes to repair genetic damage
  • also controls cellular apoptosis
68
Q

Inactivation of P53 requires at least ___ mutations

A

two

69
Q

what is Hayflick Limit?

A

the limit on cell replication imposed by shortening of telomeres in each division.

70
Q

What are the protective caps on each chromosome?

A

telomeres.

71
Q

when most cells proliferate, ______ caps ____ with each cell division

A

telomeres; shorten

72
Q

T or F: When telomeres run out, cell can no longer divide, thus cells dies.

A

True

73
Q

what is the enzyme that maintains telomeres, which don’t decrease in number with cell division

A

telomerase

74
Q

Telomerase – usually active only in _____ and ____ (germ cells) and ____ cells

A

ovaries; testes; stem

75
Q

T or F: cancer cells deactivate telomerase = unlimited telomeres

A

False; activate telomeres

76
Q

what is the result of cancer cells activating telomerase?

A

unlimited proliferation which = to immortality.

77
Q

what is angiogenesis?

A

production of new blood vessels – activated by cancer cells

78
Q

what happens if angiogenesis occurs?

A

vessels are more porous = prone to hemorrhage

irregular branching from existing capillaries

allow passage of tumour cells int vascular system = metastasize

79
Q

advanced cancers secrete ____ factors

A

angiogenic

80
Q

normal cells use ____ metabolism with O2

A

aerobic

81
Q

with limited O2, normal cells use ____ and produce ____ acid

A

glycolysis; lactic

82
Q

cancer cells use only ______ even in presence of O2. What effect is this called?

A

glycolysis; Warburg

83
Q

Warburg effect = _____ glycolysis

A

aerobic

84
Q

what is the cancer benefit of Warburg effect?

A

shift to glycolysis which allows continual production of lactate

85
Q

what pathway is relatively dormant until death receptor is activated. What death receptor is needed?

A

extrinsic; BAK

86
Q

T or F: The activation of both extrinsic and intrinsic pathways = T cells and NK cells induce apoptosis

A

true

87
Q

Apoptotic pathways are ______ in cancers

A

dysregulated

88
Q

T or F: Cancer cells do not undergo programmed apoptosis

A

True

89
Q

Metastasis is the defining characteristic of cancer and the major cause of _____ from cancer.

A

death

90
Q

T or F: Cancer that has not mestastized can often be cured by a combination of surgery, chemotherapy and radiation

A

true

91
Q

T or F: Same therapies are frequently effective againts metastasized cancer

A

False; ineffective against metastasized

92
Q

How do cancer cells develop ability to metastasize?

A

epithelial-mesenchymal trasition (EMT)

93
Q

To metastasize, cancer cells must dissociate from _____

A

ECM

94
Q

Carcinomas originate from highly _____ _____ cells that form structured sheets stabilized by multiple adhesions to neighboring cells.

A

differentiated epithelial

95
Q

EMT – achieved with a programmed transition from a ____ epithelial- like carcinoma to a more _______ mesenchymal-like carcinoma.

This step is initiation of _____-mesenchymal transition process

A

partially; undifferentiated; epithelial

96
Q

EMT occurs normally in ____ development and wound ____ healing

A

embryonic; wound

97
Q

what happens to normal cells when separated from their ECM?

A

normal cells undergo Anoikis – induction of apoptosis in cell’s loss of ECM

98
Q

T or F: Cancer cells avoid anoikis by entering circulation and spread

A

True

99
Q

what are the three steps of EMT?

A

(1) Intravasation - entry of tumor cells into circulation

(2) extravasation – exit of tumor cells from circulation to host tissue

(3) survival in circulation – platelets coat tumor = provide protection

100
Q

what does platelets coat tumor do? and what stage of EMT you can find them?

A

provide protection; aka cancer clot. Stage 3 of EMT: survival in circulation

101
Q

In terms of survival in new loc, only a ____ cancer cells required to establish a tumour in new loc.

A

few

102
Q

what do you call to cancer cells establish in new location?

A

tumour initiating cells (TIC) or cancer stem cells

103
Q

T or F: metastasis does guarantee proliferation.

A

FALSE; it doesnt guarantee.

104
Q

what is dormancy?

A

a stable non-proliferating state that is reversible.

105
Q

how many of the breast cancer deaths occur after a 5 year disease-free interval?

A

2/3

106
Q

T or F: studies of deceased individuals with no history of cancer have dormant cancer cells.

A

True

107
Q

what are the viruses associated with cancer?

A

HPV, EBV, & Hepatitis B and C

108
Q

what is a new cancer therapy?

A

dev of oncolytic viruses that specifically attack cancer cells

109
Q

cancer cells avoid immune detection and destruction using 3 mechanisms:

A

failure to produce tumor antigen (1), mutation in MHC genes (2) & production of immunosuppressive proteins or expression of inhibitory cell surface proteins

110
Q

T or F: normal immune system protects against cancer

A

true

111
Q

T or F: immunosuppression fosters cancer

A

True

112
Q

Ways on how immunosuppression fosters cancer?

A

(1) Non-hodgkin’s lymphoma (10x)
(2) Kaposi sarcoma (1000X)
(3) Release of immunosuppressive factors into tumour microenvironment increases resistance of tumour to chemo and radiotherapy

113
Q

What are the different phenotypes of macrophages?

A

M1, M2 & TAM

114
Q

What is M1?

A

classic macrophage (M1) responds to inflammatory stage to perform phagocytosis

115
Q

during healing, what does M2 produces? And what does it do?

A

anti-inflammatory mediators, which suppress inflammation

116
Q

what does TAM (tumour-associated macrophages) do?

A

perform like M2; TAM block T cells and NK cells and produce cytokines advantageous to tumour growth and spread

117
Q

what are the 4 stages based on presence of metastasis?

A

Stage 1: no metastasis
Stage 2: local invasion
Stage 3: spread to regional structures
Stage 4: distant metastasis

118
Q

what are some cancer treatment?

A

surgery, radiation & chemotherapy

119
Q

what is paraneoplastic syndromes?

A

group of rare disroders that are triggered by an ab immune system response to a cancerous tumour.

120
Q

____ or ____ pain is associated with early stages of malignancy

A

little; no

121
Q

weakness and wasting of body due to severe chronic illness

A

cachexia syndrome

122
Q

what is cachexia syndrome?

A

most severe form of malnutrition (1)

includes anorexia, early satiety, weight loss, anemia, asthenia, taste alteration, altered protein, lipid and carbo metabolism

123
Q

what is asthenia?

A

weakness; lack of energy and strength

124
Q

What causes when there is a direct tumour invasion of bone marrow?

A

leukopenia and thrombocytopenia

125
Q

what is leukopenia?

A

reduced WBC in blood

126
Q

what is thrombocytopenia?

A

blood platelet count too low

127
Q

its a risk that increases when absolute neutrophil and lymphocyte counts fall

A

infection

128
Q
A

Pathophysiology (20 decks)

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