Neoplasia 1 Flashcards

1
Q

Where is the word neoplasia derived from?

A

Greek - ‘neo’ = new, ‘plasia’ = growth or formation

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2
Q

Definition of neoplasia

A

uncoordinated growth of cells that persists after the initial stimulus is removed

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3
Q

Description of normal cell growth

A

coordinated, controlled, responsive to stimuli, self-limiting, well-differentiated

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4
Q

Description of neoplastic growth

A

autonomous growth that escapes normal regulatory mechanisms

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5
Q

What is the result of neoplasia?

A

abnormal tissue masses (tumours/neoplasms)

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6
Q

What are the 2 types of neoplasia?

A

benign or malignant

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7
Q

What are the cells of benign neoplasms like?

A

well-differentiated cells that resemble the tissue of origin (e.g. if benign neoplasm is in epithelia, cells look like epithelial cells)

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8
Q

What is the growth rate of benign neoplasms?

A

slow growth

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9
Q

Metastasis definition

A

the spread of cancer cells from the primary tumour site to other parts of the body (via circulatory/lymphatic system)

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10
Q

Can benign neoplasms metastasise?

A

no metastasis - local expansion rather than invasion

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11
Q

What structural feature of benign neoplasms prevent invasion of surrounding tissue?

A

the borders are well defined - often encapsulated

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12
Q

Are benign neoplasms life-threatening?

A

no unless in critical location

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13
Q

Examples of benign neoplasms in oral cavity

A

fibroma, lipoma, papilloma

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14
Q

What are the cells of malignant neoplasms like?

A

often poorly differentiated and variable/poor histological resemblance to normal tissue (look like stem cells rather than original tissue)

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15
Q

What is the growth rate of malignant neoplasms?

A

rapid, uncontrolled growth

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16
Q

Can malignant neoplasms metastasise?

A

yes due to poorly defined borders

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17
Q

What does the absence of defined borders in malignant neoplasm allow?

A

Enables infiltrative growth and invasion of surrounding tissue

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18
Q

Can malignant neoplasms be life-threatening?

A

malignant neoplasms are often fatal is untreated

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19
Q

Is there a potential for recurrence after removing a benign neoplasm?

A

No - benign tumours are encapsulated so all the cells are removed

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20
Q

Is there a potential for recurrence after removing a benign neoplasm?

A

yes - cells may escape removal and reform tumour

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21
Q

Examples of malignant neoplasms in the oral cavity

A

squamous cell carcinoma, mucoepidermoid carcinoma, salivary gland carcinoma

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22
Q

What is the frequency of necrosis occurring in benign neoplasms?

A

rarely occurs

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23
Q

What is the frequency of necrosis occurring in malignant neoplasms?

A

common

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24
Q

Which type of neoplasm commonly exhibits ulceration?

A

malignant neoplasm (rare in benign)

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25
Q

Where does ulceration commonly occur in malignant neoplasms?

A

skin or mucosal surfaces

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26
Q

What is the direction of benign neoplastic growth on skin or mucosal surfaces?

A

often exophytic (projects outwards from surface - lump/ulcer may be present)

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27
Q

What is the direction of malignant neoplastic growth on skin or mucosal surfaces?

A

often endophytic (invades inwards)

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28
Q

Anaplasia definition

A

loss of cellular differentiation and reversion to a more primitive, stem-cell like form that often has an increased capacity for rapid cell division

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29
Q

Which type of neoplasia has anaplastic cells?

A

malignant neoplasms

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30
Q

What changes do malignant cells undergo?

A

anaplasia, nuclear changes and cellular changes

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31
Q

What are the nuclear changes that malignant cells undergo?

A

enlarged nuclei (high nucleus : cytoplasm ratio), hyperchromasia (so darkly staining), abnormal chromatin pattern, prominent nucleoli

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32
Q

What cellular changes occur in malignant cells?

A

pleomorphism, abnormal mitotic figures, loss of polarity

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33
Q

Pleomorphism definition

A

variation in size and shape (of cell/nuclei)

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34
Q

What feature of a cell when disrupted can lead to loss of polarity?

A

cytoskeleton (maintains cell shape and structure)

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35
Q

Cell polarity definition

A

the intrinsic asymmetry observed in cells (shape, structure, cellular organisation)

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36
Q

What is the importance of cell polarity in epithelial cells?

A

cell polarity allows the formation of defined apical and basal membranes in epithelial cells

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37
Q

What process is loss of cell polarity often associated with?

A

epithelial-to-mesenchymal transition (EMT)

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38
Q

What happens during epithelial-to-mesenchymal transition (EMT)?

A

epithelial cells lose their polarity and acquire mesenchymal characteristics which promotes cell migration and invasion

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39
Q

How are benign tumours named?

A

cell/tissue of origin + suffix ‘-oma’

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40
Q

How are malignant tumours named?

A

cell/tissue of origin + either carcinoma / sarcoma

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41
Q

When would a malignant neoplasm have ‘carcinoma’ as a suffix?

A

if the malignancy is of epithelial origin

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42
Q

When would a malignant neoplasm have ‘sarcoma’ as a suffix?

A

if the malignancy is of mesenchymal origin

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43
Q

Name of benign neoplasm of surface epithelium

A

papilloma

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44
Q

Name of malignant neoplasm of surface epithelium

A

squamous cell carcinoma

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45
Q

Name of benign neoplasm of glandular epithelium

A

adenoma

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46
Q

Name of malignant neoplasm of glandular epithelium

A

adenocarcinoma

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47
Q

Name of benign neoplasm of fibrous tissue

A

fibroma

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48
Q

Name of malignant neoplasm of fibrous tissue

A

fibrosarcoma (connective tissue is of mesenchymal origin)

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49
Q

Name of benign neoplasm of adipose tissue

A

lipoma

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50
Q

Name of malignant neoplasm of adipose tissue

A

liposarcoma

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51
Q

Name of benign neoplasm of cartilage

A

chondroma

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52
Q

Name of malignant neoplasm of cartilage

A

chondrosarcoma

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53
Q

Name of benign neoplasm of bone

A

osteoma

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54
Q

Name of malignant neoplasm of bone

A

osteosarcoma

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55
Q

Where are epithelial tumours derived from?

A

epithelial tissues

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56
Q

Examples of epithelial tumours

A

squamous cell carcinoma, basal cell carcinoma

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57
Q

Where are mesenchymal tumours derived from?

A

connective tissues

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58
Q

Examples of mesenchymal tumours

A

osteosarcoma, chondrosarcoma, liposarcoma

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59
Q

Where are hematopoietic tumours derived from?

A

blood forming tissues

60
Q

Examples of hematopoietic tumours

A

leukaemia, lymphoma

61
Q

Where are neural tumours derived from?

A

Neural tissues

62
Q

Examples of neural tumours

A

neurofibroma, schwannoma

63
Q

Where are mixed tumours derived from?

A

more than one tissue type

64
Q

Example of mixed tumour

A

pleomorphic adenoma of salivary glands

65
Q

What are the different types of genetic alterations?

A

point mutations, chromosomal translocations, gene amplifications, deletions

66
Q

What happens during a point mutation?

A

one nucleotide/base is swapped

67
Q

What happens during chromosomal translocations?

A

part of a chromosome breaks and is reattached to a different chromosome (can lead to overexpression)

68
Q

What happens during gene amplifications?

A

multiple copies of a gene is produced (leads to overexpression)

69
Q

What does the accumulation of genetic alterations result in?

A

uncontrolled proliferation, resistance to apoptosis, ability to invade and metastasise

70
Q

What are the key genes that can lead to cancer if affected?

A

DNA repair genes, oncogenes, tumour suppressor genes

71
Q

Definition of oncogenes

A

genes that promote cell growth and division

72
Q

How do oncogenes exist initially before they are overexpressed/mutated?

A

proto-oncogenes

73
Q

What are proto-oncogenes?

A

normal cellular genes that regulate cell growth

74
Q

What are the main functions of oncogenes?

A

promote cellular proliferation, survival and migration

75
Q

What are the mechanisms that activate oncogenes from proto-oncogenes?

A

chromosomal translocation, point mutations, gene amplification, insertion of promoter/enhancer

76
Q

How may chromosomal translocation of the oncogene cause its activation?

A

the oncogene can be translocated from an untranscribed site to a position adjacent to an actively transcribed gene (e.g. Ig gene in B cell) which leads to inappropriate transcription of oncogene

77
Q

Example of neoplasia where chromosomal translocation involving an oncogene is the cause

A

Burkitt lymphoma (increased B cells)

78
Q

How can a point mutation within the oncogene lead to activation?

A

substitution of a single base is translated into an amino acid substitution resulting in a hyperactive oncogene

79
Q

How can gene amplification of the oncogene lead to neoplasia?

A

multiple excess copies of the oncogene are inserted stimulating cellular proliferation

80
Q

How may the insertion of a promoter/enhancer activate oncogenes?

A

insertion of promoter or enhancer sequence proximal to oncogene actives its expression

81
Q

Examples of oncogenes (inactive in health)

A

RAS (signal transduction), MYC (transcription factor), HER2/neu (growth factor receptor), BCL-2 (inhibits apoptosis)

82
Q

Definition of tumour suppressor genes

A

genes that inhibit inappropriate cell division and suppress growth

83
Q

What are the functions of tumour suppressor genes?

A

cell cycle regulation, apoptosis induction, DNA damage repair, maintain genomic stability

84
Q

How are tumour suppressor genes inactivated?

A

two hit hypothesis - both alleles (on both chromosomes) must be inactivated - tumour suppressor gene can still function is only one chromosome is affected

85
Q

What is the consequence of tumour suppressor genes being inactivated?

A

loss of cell cycle control leading to uncontrolled proliferation, genomic instability

86
Q

Examples of tumour suppressor genes

A

Tp53, RB (retinoblastoma gene)

87
Q

What is the cause of DNA mutations/damage?

A

cariogenic stimuli

88
Q

Function of TP53 gene

A

‘guardian of the genome’ - maintains genome stability via the synthesis of p53

89
Q

What happens to cells with DNA mutations that have a normal p53?

A

cell is arrested in G1 until the damage is repaired or apoptosis occurs if the damage is too severe

90
Q

What happens in cells that have a DNA mutation and a defective p53 (due to TP53 mutation)?

A

no repair or apoptosis occurs and the cell proceeds to S phase. DNA damage is propagated to daughter cells, uncontrolled proliferation to form tumour

91
Q

What are retinoblastomas?

A

malignant tumours derived from the retina that occur almost exclusively in children

92
Q

What are the two types of retinoblastomas?

A

inherited and sporadic retinoblastoma

93
Q

Which was the first tumour suppressor gene identified?

A

retinoblastoma gene (RB)

94
Q

What is the function of a normal retinoblastoma gene?

A

controls progression from G1 to S phase of cell cycle, bind and inactivates transcription factors (E2F family), prevents uncontrolled cell division

95
Q

What must occur for retinoblastoma to take place?

A

both RB alleles must be inactivated (two-hit hypothesis)

96
Q

What happens during retinoblastoma?

A

there is a loss of cell cycle control leading to uncontrolled proliferation

97
Q

Which type of retinoblastoma is more common?

A

inherited retinoblastoma (one allele is already impaired)

98
Q

Which type of retinoblastoma has a high risk for bilateral retinoblastoma?

A

inherited retinoblastoma (high possibility of at least one mutation occurring in any cell)

99
Q

Which type of retinoblastoma causes unilateral retinoblastoma?

A

sporadic retinoblastoma

100
Q

What happens in inherited retinoblastoma?

A

one of the paired RB1 genes is already mutated/absent. So mutation/loss of the remaining RB1 allele in any retinal cell will lead to retinoblastoma. Likely to occur more than once (high risk of bilateral retinoblastoma)

101
Q

What happens in sporadic retinoblastoma?

A

mutations/deletions of both RB genes in the same cell or its daughters must occur (very rare and is unilateral - almost impossible for process to occur in both eyes!)

102
Q

Carcinogens definition

A

agents that initiate or promote cancer development

103
Q

What are the categories of carcinogens?

A

chemical, physical and biological carcinogens

104
Q

Examples of chemical carcinogens

A

tobacco, asbestos, benzene

105
Q

Examples of physical carcinogens

A

UV radiation, ionizing radiation

106
Q

Examples of biological carcinogens

A

HPV, HBV, H. pylori

107
Q

What tumour is associated with polycyclic aromatic hydrocarbons?

A

skin (mineral oil exposure) and lung cancer (smoking)

108
Q

What tumour is associated with aromatic amines?

A

bladder cancer (in rubber and dye workers)

109
Q

What tumour is associated with alkylating agents?

110
Q

What tumour is associated with vinyl chloride?

A

liver angiosarcoma

111
Q

Which biological carcinogen is associated with cervical and oropharyngeal carcinoma?

A

human papillomavirus

112
Q

Which biological carcinogen is associated with nasopharyngeal cancer?

A

epstein-barr virus

113
Q

What is carcinogenesis?

A

the multi-step process of cancer development

114
Q

What are the steps in the theory of carcinogenesis?

A
  1. initiation
  2. promotion
  3. progression
115
Q

What happens during the initiation step of carcinogenesis?

A

carcinogen causes an irreversible alteration in DNA (of relevant genes e.g. oncogene/tumour suppressor gene)

116
Q

What happens during the promotion stage of carcinogenesis?

A

a promoter stimulates proliferation of initiated cells via clonal expansion to form a benign tumour (reversible process)

117
Q

What happens during the progression stage of carcinogenesis?

A

additional mutations are acquired which increases malignant potential and develops invasive and metastatic capabilities

118
Q

Definition of latency period

A

time between exposure to carcinogen and development of cancer

119
Q

How does cellular senescence normally work?

A

each time a cell divides, the telomeres become shorter until the chromosome is too short and the cell can no longer divide.

120
Q

What are the 3 genetic mechanisms in carcinogenesis?

A
  1. expression of telomerase
  2. loss/inactivation of both TSG copies
  3. activation of oncogenes
121
Q

How does telomerase expression contribute to carcinogenesis?

A

telomerase prevents telomeric shortening with each cell division hence preventing cellular senescence, making the cell immortal

122
Q

How does inactivation of tumour suppressor genes contribute to carcinogenesis?

A

the loss of TSG function permits mutations (DNA repair is impaired) and removes inhibitory growth control

123
Q

How does the activation of oncogenes contribute to carcinogenesis?

A

results in cell proliferation via autocrine growth stimulation

124
Q

Epigenetics definition

A

the study of changes in organisms caused by modification of gene expression rather than an altered gene code

125
Q

How do epigenetic mechanisms contribute to carcinogenesis?

A

either normally repressed genes are abnormally expressed or normally active genes are repressed (silenced)

126
Q

What are the 3 epigenetic mechanisms that contribute to carcinogenesis?

A
  • hypermethylation
  • histone modifications
  • microRNA
127
Q

How may hypermethylation contribute to carcinogenesis?

A

gene silencing results from the hypermethylation of promotor DNA sequences

128
Q

How can histone modification contribute to carcinogenesis?

A

histone modifications usually to histone tails can alter chromatin structure leading to gene up- or downregulation

129
Q

How does microRNA contribute to carcinogenesis?

A

increased microRNA leads to reduced mRNA translation and protein expression whereas decreased microRNA enhances protein expression

130
Q

What is microRNA?

A

short sequences of inhibitory RNA that binds to mRNA transcripts

131
Q

What are some host factors that can contribute to carcinogenesis?

A

race/ethnicity, diet and obesity, constitutional factors (sex, inherited risks..), transplacental exposure, premalignant lesions

132
Q

What are premalignant lesions of the oral cavity referred to as?

A

Oral Potential Malignant Disorders (OPMD)

133
Q

Examples of premalignant lesions of the oral cavity

A

leukoplakia, erythroplakia, oral submucous fibrosis

134
Q

Definition of leukoplakia

A

white patch that cannot be characterised clinically or pathologically as any other disease

135
Q

What is the malignant transformation rate of leukoplakia?

136
Q

Definition of erythroplakia

A

red patch that cannot be characterised clinically or pathologically as any other disease

137
Q

What is the malignant transformation rate of erythroplakia?

138
Q

What is oral submucous fibrosis characterised by?

A

fibrosis and restricted mouth opening

139
Q

What is associated with causing oral submucous fibrosis?

A

areca nut/betel quid chewing

140
Q

How is the risk of cancer of premalignant lesions predicted?

A

checking for dysplasia in biopsy of premalignant lesion

141
Q

What are the factors affecting tumour growth?

A

cell proliferation rate, cell death rate (apoptosis), angiogenesis, stromal interactions

142
Q

How does angiogenesis affect tumour growth?

A

blood vessels supply nutrients and oxygen, provides route for metastasis

143
Q

What is the growth pattern for benign tumours?

A

expansile growth (pushes surrounding tissues aside, encapsulated, distinct border)

144
Q

What is the growth pattern for malignant tumours?

A

infiltrative growth (invasion of surrounding tissues, irregular/ill-defined borders, destruction of normal architecture)

145
Q

How is growth rate / aggression of a tumour estimated clinically?

A

using tumour doubling time

146
Q

What is meant by tumour heterogeneity and clonal evolution?

A

diverse cell populations in tumours, selection pressures leads to emergence of aggressive clones, has implications for treatment resistance