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NUR1142 > Module 3 - Chapter 10 > Flashcards

Module 3 - Chapter 10 Flashcards

1
Q

How is tumour classified?

A
  1. tissue and organ of origin
  2. extent of distribution to other sites
  3. microscopic appearance of the lesion
  4. May include critical description of its genetic changes
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2
Q

Describe Benign tumours

A
  • usually encapsulated with connective tissue, fairly differentiated, well organized stroma
  • retain recognizable normal tissue
  • do not invade beyond their capsule
  • do not spread to regional lymph nodes or distant locations
  • mitotic cells rarely present
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3
Q

How are benign tumours named

A

According to tissues from which they arise with suffix - oma

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4
Q

Describe malignant tumours

A
  • rapid growth rate
  • specific microscopic alterations (loss of differentiation, absence of normal tissue organization)
  • large darkly stained nuclei
  • mitotic cells are common
  • disorganized substantial amount of stroma
  • loss of normal tissue structure.
  • lack capsule
  • invade nearby vessels, lymphatics and surrounding structure.
  • metastasis
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5
Q

What is the hallmark of cancer cells?

A

anaplasia - loss of cells differentiation

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6
Q

Pleomorphic

A
  • marked variability of size and shape
  • characteristic of malignant cell
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7
Q

Metastasis

A

ability to spread far beyond tissue of origin

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8
Q

how does cancer cells take their name

A

from their original cell type

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9
Q

Carcinoma in Situ (CIS)

A

preinvasive tumors, glandular in origin or squamous cell in origin

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10
Q

Where does CIS occur?

A

cervix, skin, oral cavity, esophagus, and bronchus

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11
Q

in glandural epithelium, in situ lesions occur in what places?

A

stomach, endometrium, breast, and large bowel

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12
Q

Where is DCIS in the breast located?

A

It fills the mammary ducts but not progressed to local tissue invation.

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13
Q

List the 3 fates of CIS?

A
  1. can remain stable for a long time
  2. progress to invasive metastatic cancer
  3. can regress and disappear
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14
Q

High grade lesion CIS

A

highest likelihood to become invasive Ca

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15
Q

What are the 2 fundamental concepts for understanding biology of cancer?

A
  1. Cancer - complex genetic disease with multiple mutations in genetic material
  2. microenvironment of a tumour is a heterogenous mixture of cells (both cancerous and benign)
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16
Q

Tumour initiation

A
  • Process that produces initial cancer cells
  • 1st stage of cancer development
  • depends on specific mutations and characteristics of the microenvironment to influence transformation of these cells
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17
Q

Tumour Promotion

A
  • 2nd stage
  • population of cancer cells expands with diversity of cancer cell phenotypes
  • gain in function
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18
Q

What enables the process of tumour promotion?

A
  • additional mutations and changing tumour microenvironment
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19
Q

Tumour progression

A
  • spread to tumour to adjacent distal sites
  • governed by more mutations and more changes in microenvironment
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20
Q

Mutation

A

alteration in the DNA sequence affecting expression or function of a gene

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21
Q

Point mutations

A

-small-scale changes in the DNA
-alteration of one or a few nucleotide base pairs
- profound effect on the activity of resultant protein

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22
Q

Chromosomal translocation

A
  • large changes in chromosome structures
  • piece of one chromosome translocate to another
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23
Q

Gene amplification

A
  • repeated duplication of a region of a chromosome (known as a promoter sequence)
  • tens or hundreds of copies present instead of 2 copies of genes
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24
Q

What mechanisms are involved in genetic changes?

A
  1. Mutational
  2. Epigenetics
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25
Q

Give examples of mutational mechanism

A
  1. Point mutation
  2. Chromosomal translocation
  3. Gene Amplification
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26
Q

Give examples of epigenetic effects

A
  1. DNA methylation
  2. histone acetylation
  3. altered expression of non-coding RNA
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27
Q

Driver mutation

A
  • drive the progression of cancer
  • 140 different driver
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28
Q

Passenger mutations

A
  • random events, just along for the ride
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29
Q

selective advantage

A
  • clonal proliferation or clonal expansion
  • progeny can accumulate faster than its non-mutant neighbours
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30
Q

Transformation

A

Process where normal cells become a cancer cell

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31
Q

what directs transformation

A

directed by progressive accumulation of genetic changes that alters the basic nature of the cell which drives it to malignancy

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32
Q

Stroma

A

Tumour microenvironment that surrounds and infiltrate the tumour

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33
Q

What cells forms the stroma?

A

Inflammatory or immune cells such as T lymphocytes, macrophages, b lymphocytes and neutrophils. also cells associated with tissue repair (fibroblasts, adipocytes, mesenchymal stem cells, endothelial cells and pericytes)

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34
Q

What is cancer development analogous to:

A

Wound healing

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35
Q

Whey is cancer development analogous to healing?

A

initial proliferation of cancer cells and enlargement of tumor elicit the synthesis of proinflammatory mediators by the cancer cells and adjacent non malignant cells

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36
Q

What does proliferation of cancer cells and enlargement of tumor cells elicit

A

Synthesis of proinflammatory mediators by the cancer cells and adjacent non malignant cells

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37
Q

How much stromal cells make up the tumour mass?

A

90%

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38
Q

Cancer heterogeneity arises form what factors?

A

Ongoing proliferation and mutation

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39
Q

consequences of Cancer-stromal interactions

A

hallmarks of cancer

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40
Q

What are some of the hallmarks and enablers

A
  1. Primarily genomic alterations that initiate and maintain development of cancer
  2. secondary genomic change
  3. Tumour resistance to destruction
  4. activating invasion and metastasis
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41
Q

What are included in genomic alterations?

A
  1. Sustained proliferative signalling
    2.evading growth suppressors
  2. genomic instability
  3. enabling replicative immortality
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42
Q

What are included in secondary genomic change?

A

1.angiogenesis
2. reprogramming energy metabolism

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43
Q

What are included in the tumour resistance to destruction?

A
  1. resistance to apoptotic cell death
  2. tumor-promoting inflammation
  3. evading immune destruction
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44
Q

What is the first and foremost hallmark of cancer

A

Uncontrolled cellular proliferation

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45
Q

How can proliferation can be discontinued?

A

By decreased level of growth factors in the environment or inactivation of signalling pathway components.

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46
Q

Cyclins

A
  • effectively turn cell division - promising area for development of monoclonal antibodies in novel research of the treatment of cancer
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47
Q

proto oncogenes

A

Genes that encode components of receptor-mediated pathways designed to regulate normal cellular proliferation

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48
Q

oncogenes

A
  • mutated or overexpressed proto-oncogenes
  • independent of normal regulatory mechanism
  • undergo uncontrolled cell growth
  • can affect growth factor pathways
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49
Q

Autocrine stimulation

A

ability of cancer cells to secrete growth factors that stimulate their own growth

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50
Q

Oncogenes can also lead to what?

A

constant activation of the signal cascade from the cell surface receptor to the nucleus

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51
Q

Up to 1/3 of cancer have this?

A

activating mutation in the RAS gene resulting in a continous cell growth signal - even when growth factors are missing

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52
Q

What mutation is commonly observed in lung cancer

A

point mutation

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53
Q

What can point mutation results in ?

A

Continuous activation of EGF receptor tyrosine kinase

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54
Q

What changes the regulated proto-oncogene to an unregulated oncogene

A

A point mutation in RAS gene coverts it

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55
Q

What can activate oncogenes

A

Point mutations, translocations, gene amplifications

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56
Q

How can translocation activate oncogene?

A
  1. it can cause excess and inappropriate production of a proliferation factor
  2. chromosome translocation can lead to the production of novel proteins with growth promoting properties
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57
Q

BCR-ABL

A

unregulated protein tyrosine kinase that promotes growth of myeloid cells

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58
Q

Gene amplification can lead to what?

A

increased expression of an oncogene - in some cases, medication-resistance genes

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59
Q

Tumour-suppressor genes or antioncogenes

A
  • regulate cell cycle
  • inhibit proliferation from growth signals
  • stop cell division with damage cells
  • prevent mutations
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60
Q

What needs to happen in tumour suppressor gene for cancer to occur?

A

both copies of tumour suppressor genes must undergo mutations

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61
Q

What is the normal function of caretaker genes:

A

Maintain DNA and chromosome stability

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62
Q

What is the mutation effect with caretaker genes?

A

Chromosomes instability leads to increased rates of mutation

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63
Q

What is the normal function of dominant oncogenes?

A

Encode proteins that promote growth

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64
Q

What is the mutation effect on dominant oncogenes

A

Overexpression or amplification causes gain of function

65
Q

What is the normal function of tumour suppressors (recessive oncogenes)

A

Encode protein that inhibit proliferation and prevent or repair mutations

66
Q

What is the mutation effect on tumour suppressors?

A

Loss on function of both alleles increases cancer risk

67
Q

What inherited mutation can predispose a family member to cancer?

A

Mutation in tumour suppressor gene because it only takes a single additional mutation in any other cell (somatic cell mutation) to completely inactivate the tumour-suppressor gene

68
Q

What is the gene associated with retinoblastoma?

A

RB1

69
Q

What’s the gene associated with Li-Fraumeni syndrome?

A

p53 (TP53)

70
Q

What is the gene associated with familial melanoma?

A

P16INKa (CDKN2A)

71
Q

What is the gene associated with neurofibromatosis?

A

Neurofibromin(NF1)

72
Q

What is the gene associated with familial adenomatous polyps?

A

APC

73
Q

What is the gene associated with breast cancer?

A

BRCA1

74
Q

RB

A
  • tumor suppressor gene
  • monitors antigrowth cellular signals
  • block activation of the growth and division phase in the cell.
  • puts a brake on cell division
  • key regulator of cellular metabolism
75
Q

What happens when RB is mutated

A

persistent call growth

76
Q

antiproliferative activity of RB depends of what factor?

A

degree of protein phospholyration

77
Q

What happens with the process of RB protein phosphorylation?

A

Protein inactivates the RB gene –> allows cells to enter cell cycle with increased production of transcription factors and corresponding production of DNA.

78
Q

What happens if there is hypophosphorylation

A
  • cell growth inhibition because of increased binding of RB to transcription factors and resultant inhibition of the cell cycle.
79
Q

What increases phosphorylation?

A

growth factors kinases which results in RB inactivation

80
Q

Approximately what percentage of children with retinoblastoma have inheritable form

A

50%

81
Q

TP53

A
  • guardian of genome
  • monitors intracellular signals related to stress and activates caretaker genes
82
Q

What can stress activate?

A

Stress can activate kinases

83
Q

Many types of cellular stress can produce what (can be detectable by P53)

A

Intracellular signals

84
Q

What happens when stress activates kinases?

A

phosphorylate p53 into an active suppressor of cell division and activator of caretaker genes.

85
Q

What is some of the functions of caretaker genes?

A
  • encode proteins that repair damaged DNA
86
Q

What does P53 protein control

A

P53 protein controls initiation of cellular senescence or apoptosis and suppresses cell division until DNA repair or correction is complete

87
Q

Loos of function of TP53 or caretaker genes can lead to ?

A

increased mutation rates and cancer

88
Q

inheriting mutated TP 53 increases risk of cancer at early aga by how much?

A

25 fold

89
Q

Malignancies related to TP 53 may include:

A

Breast Cancer,
Brain Tumors
Acute Leukemia
Soft tissue sarcoma
bone sarcoma
adrenal cortical carcinoma

90
Q

Whatare other inheritable mutations in tumous supressor genes?

A

WT1 gene - Wilms Tumour
NF1 gene - Neurofibromatosis
APC gene - familial polyposis coli or adenomas of the colon

91
Q

Genomic instability:

A

increased tendency of alterations (mutability) in the genome during the life cycle of cells.

92
Q

What can cause level of genomic instability and risk for developing cancer?

A
  • Inherited and acquired mutations in caretaker genes
93
Q

Acquired mutations in the guardians of the genome (e.g. TP53) results in?

A

increasing accumulation of mutations in the overall DNA as a whole.

94
Q

xeroderma pigmentosum

A
  • defect in the repair of DNA pyrimidine dimers - caused by UV light - increases risk for cancer
95
Q

epigenetic silencing

A
  • modulation of gene function
  • can cause genomic instability
96
Q

oncomirs

A

miRNAs that stimulate cancer development and progression

97
Q

What does miRNA do?

A
  • regulate diverse signalling pathways
  • decrease the stability and expression of other genes by pairing with mRNA and decreasing the efficiency of translation
98
Q

BRCA1 and BRCA2

A
  • Tumour suppressor genes and caretaker genes - repair double stranded DNA breaks
99
Q

Approximately what percentage of women generally will develop breast CA in their lifetime?

A

11%

100
Q

What is the percentage of individuals with BRCA1and BRCA2 who will develop breast cancer.

A

47-66% with high risk BRCA1 mutation and 40 -57 % with BRCA2 mutation will develop breast CA by age 70

101
Q

Ovarian cancer occurs in approximately what percentage of the population

A

1.2%

102
Q

about what percentage of women with an inherited mutation in BRCA1 and about what percentage with a mutation in BRCA2 will develop ovarian cancer by age 70

A

but about 35 to 46% of women with an inherited mutation in BRCA1 and about 13 to 23% with a mutation in BRCA2 will develop ovarian cancer by age 70

103
Q

Immortality

A

Hallmark of cancer cells in that they seem to have an unlimited lifesapn and will continue to divide for years under appropriate lab conditions

104
Q

Hayflick limit

A

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

105
Q

senescence

A

cease dividing

106
Q

Telomeres

A
  • a major block to unlimited cell division
  • protected ends or caps of repeating hexanucleotides on each chromosomes.
107
Q

Telomerase

A

enzymes that places and maintains telomeres

108
Q

Where are telomerase active?

A

germ cells, ovaries, testes, an din stem cells

109
Q

What happens when nongerm cells begin to proliferate abnormally

A

telomere caps shorten with each cell division.

110
Q

What does short telomere caps do:

A

Normally signal the cell to cease cell division. If the telomeres become critically small, the chromosomes become unstable and fragment and cells die.

111
Q

T or F: Cancer cells are very heterogenous

A

T

112
Q

What happens when cancer cells reach a critical age?

A

Cancer cells activate telomerase to restore and maintain their telomeres which allows for continous division

113
Q

What is required to trigger for re-expression of telomerase activity?

A

expression of specific oncogenes such as RAS and MYC, loss of function of certain suppressor genes such as p53 and RB.

114
Q

Restoaration of telomerase activity occurs in about what percentage of cancers?

A

90%

115
Q

The remaining cancers appear to recruit or originate from ?

A

stem cells - cancer stem cells that maintain telomerase activity characteristically found in somatic stem cells.

116
Q

angiogenesis or neovascularization

A

process of establishing new blood vessels within tissue undergoing repair

117
Q

What does angiogenic factors and angiogenic inhibitors normally do?

A

Normally control development of new vessels.

118
Q

H1F-1A (Hypoxia-inducible factor-1)

A

Oxygen sensitive transcription factor - major regulator of angiogenesis in normal tissue.

119
Q

What leads to increased expression of HIF-1α–regulated angiogenic factors and increased vascularization.

A

Inactivation of tumour-suppressor genes (e.g., p53) or increased expression of oncogenes (e.g., HER2)

120
Q

What is increased expression of HIF-1α also is related to

A

is related to increased resistance to chemotherapy, increased tumour cell glycolysis, increased metastasis, and a poor prognosis.

121
Q

matrix metalloproteinases (MMPs; e.g., MMP-9)

A

zinc-dependent proteases that digest the surrounding extracellular matrix (ECM)

122
Q

What is the difference between metabolism with noncancerous cell and cancerous cell?

A

Non- malignant: With adequate O2 - generates ATP using OXPHOS –> generates 36 ATP. If hypoxic, cells perform glycolysis –> generates 2 ATP per molecules per molecule of glucose (by product - lactic acide and pyruvate)

Malignant: does not use OXPHOS even with O2- reprogrammed to glycolysis (aerobic glycolysis) (Warburg effect)

123
Q

A shift from OXPHOS to glycolysis allows what?

A

allows lactate and other products of glycolysis to be used for more efficient production of lipids, nucleosides, amino acids, and other molecular building blocks needed for rapid cell growth.

124
Q

Explain Reverse Warburg Effect

A
  • CA cells continue using OXPHOS to generate ATP
  • Manipulates CAF (cancer-associated fibroblasts) by inducing oxidative stress to undergo aerobic glycolysis and secrete metabolites (lactate and pyruvate) –> cancer cells can use in Krebs cycle to feel OXPHOS and produce ATP
  • secondary consequence of above process - induction of autophagy –> consumption of CAF and release of materials needed by CA cells for synthesis of new organelles
124
Q

What promotes aerobic glycolysis?

A

oncogenes and mutated tumour suppressor

125
Q

What increases transport of glucose into the cytoplasm?

A

Upregulation of glucose transporter 1 (GLUT1) und er the control of oncogenes (RAS, MYC), mutant tumour suppressors (TP53)

126
Q

Apoptosis

A
  • Programmed cell death
  • mechanism where cells can self-destruct under condition of tissue modeling or as a protection against aberrant cell growth that may lead to malignancy
127
Q

What are the 2 pathways that may trigger apoptosis?

A
  1. Intrinsic pathway (mitochondrial pathway) monitors cellular stress
  2. Extrinsic pathway - activated through a plasma membrane receptor complex linked to intracellular activators of apoptosis.
128
Q

Give examples of cellualr stress:

A

Cellular stress may include DNA damage, genomic instability, aberrant proliferation, loss of adhesion to ECM or to adjacent cells, and other causes and characteristics of abnormal cellular physiology;

129
Q

What family of genes regulate apoptosis?

A

Bcl-2

130
Q

What does Bcl-2 family of genes do?

A
  • Regulates apoptosis and encodes for proteins that function in the mitochondrial membrane to either stimulate (BAX, BAK) or inhibit (Bcl-2 protein) apoptosis.
  • Both groups regulate mitochondrial release of proapoptotic molecSules (e.g. cytochrome c)
131
Q

What regulates the expression of the BAX gene and what is it involved in?

A

TP53 gene, involved in P53-mediated apoptosis.

132
Q

Phosphorylation of TP53 induces what?

A

transcription of proapoptotic factors and BAX/BAK proteins.

133
Q

When does extrinsic pathway become non-dormant?

A

When death receptor is activated

134
Q

What is the principal apoptotic receptor?

A

Fas/CD95

135
Q

What suppresses activation of apoptosis during DNA damage?

A
  • Loss of function mutations to the TP53
  • dysregulated balance between pro and antiapoptotic molecules
136
Q

Excess expression of other antiapoptotic members of the Bcl-2 family also may provide increased resistance to ?

A

chemotherapeutic medications, many of which act through induction of apoptosis.

137
Q

downregulation of caspases or production of caspase inhibitors helps with what?

A

resistance to apoptosis

138
Q

What is an important factor in the development of cancer?

A

Chronic inflammation

139
Q

What organs appear to be more suscptible to the oncogenic effects of chronic inflammation?

A

Some examples are: the gastro-intestinal [GI] tract, prostate, thyroid gland

140
Q

Individuals who have suffered with ulcerative colitis for 10 years or more have up to a ______increase in the risk of developing colon cancer

A

30 fold increase

141
Q

What is strongly associated with gastric carcinoma and important cause of PUD and associated with mucosa-associated lymphoid tissue lymphomas (MALT)?

A

H.Pylori

142
Q

When does h.pylori infection usually occur?

A

During childhood

143
Q

Which socioeconomic class does H.Pylori disproportionately affects

A

lower socioeconomic classes

144
Q

Prolonged chronic inflammation with H.Pylori can lead to:

A

increased gastric acid secretion, atrophic gastritis, and duodenal ulcers, or benign cellular proliferation that can, in a small fraction of individuals, progress to dysplastic changes and, finally, gastric adenocarcinoma.

145
Q

How can H.pylori change cellular biology?

A

It can directly and indirectly produce genetic and epigenetic changes in cells of infected stomachs, including mutations in TP53 and alterations in the methylation of specific genes.

146
Q

What can prevent cancer in relation to H.Pylori?

A

Eradication of H. pylori from infected individuals before the development of dysplasia

147
Q

MALT lymphomas associated with chronic H. pylori infections may depend on what factors?

A

chronic inflammation and antigenic stimulation associated with infections, and therefore, treatment with antibiotics may be useful, even in cases of early lymphoma.

148
Q

Explain what happens when cells with malignant phenotypes develop in relation to inflammation

A
  • cancer cells disrupt the environment, initiate/enhance inflammation –> recruit local and distant cells (macrophages, lymphocytes, and others involved in inflammation–>function to eliminate infection turns to initiating and directing healing.
  • tumour manipulates recruited cells of inflammatory response from rejection response to wound healing and tissue regeneration
  • The change in response include induction of cellular proliferation, neovascularization, local immune supression in the damaged tissue
  • This benefits cancer progression
  • increases resistance to chemotherapy
149
Q

Give one key cell that promote tumour survival

A

TAM - tumour associated macrophage

150
Q

Tumours commonly produce these and are chemotactic factors for monocytes and macrophages

A

cytokines and chemokines

151
Q

Give examples of chemotactic factors for monocytes/macrophages?

A
  • CSF-1 colony-stimulating factor-1
  • CCL2 macrophage chemotactic protein-1
152
Q

Levels of CCL2 in human breast cancer and cancers of the esophagus are related to these factors

A

the degree of macrophage infiltration and progression of the tumour.

153
Q

Presence of this can correlate with a worse prognosis.

A

TAMs

154
Q

What does TAMs appear to phenotypically mimic?

A

TAMs appear to phenotypically mimic the M2 phenotype.

155
Q

What is the primary macrophage in the inflammatory response -is responsible for removal and destruction of infectious agents.

A

proinflammatory macrophage (M1)

156
Q

This phenotype of macrophage produces anti-inflammatory mediators to suppress ongoing inflammation and induce cellular proliferation, angiogenesis, and wound healing

A

M2

157
Q

Explain some of the function of TAMs

A
  • have diminished cytotoxic response and develop the capacity to block Tc-cell and NK-cell functions
  • TAMs secrete cellular growth factors (e.g., TGF-β and fibroblast growth factor-2 [FGF-2]) that favour tumour cell proliferation, angiogenesis, and tissue remodelling, similar to their activities in wound healing.
  • produce cytokines that are advantageous for tumour growth and spread.
  • They also secrete angiogenesis factors (e.g., VEGF) that induce neovascularization and MMPs that degrade intercellular matrix.
  • The overall effect is increased tumour growth, invasion of the blood vessels, increased oxygen to the tumour, and invasion through the degraded matrix into the local tissue.
158
Q

Explain CAF - cancer associated fibrobalsts

A
  • synthesize the ECM that surrounds and permeates the tumour
  • Cytokines and growth factors stored in the matrix, as well as growth factors, metalloproteases, proteoglycans, and other molecules secreted by CAFs contribute greatly to cancer progression, local spread, and metastasis.

NUR1142 (112 decks)

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