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Principles of Disease-Megan > Tumour Pathology > Flashcards

Tumour Pathology Flashcards

1
Q

What is a tumour (neoplasm)

A

Abnormal growing mass of tissue

It has uncoordinated growth when compared to surrounding tissue

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2
Q

How will the removal of a stimulus causing the tumour affect its growth

A

It may continue to grow due to the irreversible change caused

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3
Q

What two groups of tumours are there

A

Benign

Malignant (cancer)

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4
Q

What are malignant tumours

A

Tumours that can invade into adjacent tissue and metastasise (spread) and grow at other sites with the body

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5
Q

State two factors which can cause cancer

A

Genetics

Environmental factors

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6
Q

What are the 5 most common types of cancer

A 
Breast
Lung
Prostate
Colon
Melanoma
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7
Q

Why is tumour classification important

A

So we can understand tumour behaviour
So we can determine the probable outcome (prognosis)
For treatment

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8
Q

What is tumour classification based on

A

Tissue of origin

Whether the tumour is benign or malignant

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9
Q

Which type of tissues can tumours originate from

A 
Epithelium
Connective tissue (mesenchyme)
Blood
Lymphoid tissue
Melanocytes
Neural tissue
Germ cells (ovary/testis)
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10
Q

What are the two main types of epithelial tumours

A

Glandular

Squamous

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11
Q

What are benign and malignant glandular epithelial tumours known as

A

Benign - Adenoma

Malignant - Adenocarcinoma

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12
Q

What are benign and malignant squamous epithelial tumours known as

A

Benign - Squamous papilloma

Malignant - Squamous carcinoma

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13
Q

In epithelial tumour nomenclature what do the benign and malignant tumours normally end in

A

Benign - oma

Malignant - carcinoma

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14
Q

What type of connective tissue tumours can occur

A

Bone
Fat
Fibrous tissue

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15
Q

What is a benign and malignant bone tumour known as

A

Benign - Osteoma

Malignant - Osteo-sarcoma

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16
Q

What is a benign and malignant fat tumour known as

A

Benign - Lipoma

Malignant - Lipo-sarcoma

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17
Q

What is a benign and malignant fibrous tissue tumour known as

A

Benign - Fibroma

Malignant - Fibro-sarcoma

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18
Q

In connective tissue tumour nomenclature what do malignant tumours normally end in

A

Sarcoma

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19
Q

What is a malignant WBC tumour known as

A

Leukaemia

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20
Q

What is a malignant lymphoid tissue tumour known as

A

Lymphoma

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21
Q

What is a benign melanocyte tumour known as

A

Naevus

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22
Q

What is a malignant melanocyte tumour known as

A

Melanoma

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23
Q

What is a tumour in the central nervous system known as

A

Astrocytoma

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24
Q

What is a tumour in the peripheral nervous tissue known as

A

Schwannoma

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25
Q

What are germ cell tumours known as

A

Teratomas

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26
Q

What is a teratoma composed of

A

Various tissues

Develops in ovaries/testies

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27
Q

Where are teratomas normally benign and where are they malignant

A

Benign - Ovaries

Malignant - Testies

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28
Q

What are the features of benign tumours

A 
Non-invasive growth pattern
Normally encapsulated
No evidence of invasion
No metastases
Cells similar to normal
Function similar to normal tissue
Rarely cause death
Are well-differentiated
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29
Q

What are the features of malignant tumours

A 
Invasive growth patterns
No capsule (or capsule breached by tumour cells)
Abnormal cells
Loss of normal function
Often evidence of spread of cancer
Cancers often poorly differentiated
Frequently cause death
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30
Q

State some properties of cancer cells

A 
Loss of tumour suppressor genes
Gain the function of oncogenes
Altered cellular function
Abnormal morphology
Cells capable of independent growth
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31
Q

Give examples of tumour suppressor genes

A

Adenomatous polyposis
Retinoblastoma
BRCA1

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32
Q

Give examples of oncogenes

A 
B-raf
Cyclin D1
ErbB2
Myc
K-ras
N-ras
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33
Q

What does the loss of cellular function cause

A

It causes the loss of cell-to-cell adhesion
Altered cell-to-matrix adhesion
Production of tumour related proteins (tumour biomarkers)

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34
Q

Give examples of types of tumour biomarkers

A

Onco-fetal proteins
Oncogenes
Growth factors and receptors
Immune checkpoint inhibitors

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35
Q

How can tumour biomarkers be benefical in the clinical setting

A

For:
Screening
Diagnosis
Prognostic (to identify patients with a specific outcome)
Predictive (to identify patients who will respond to a particular therapy)

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36
Q

Give examples of some tumour biomarkers

A 
Kras - Colorectal cancer
Braf - Melanoma
EGFR - Lung cancer
PD-L1 - Lung cancer
Her2 - Breast cancer, Gastric cancer
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37
Q

Describe the morphology of cancer cells

A

The show cellular and nuclear pleomorphism (variation in size and shape)
Abnormal mitoses will often be present

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38
Q

What is tumour growth

A

A balance between cell growth and cell death

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39
Q

What is tumour angiogensis

A

Formation of new blood vessels by tumours which are required to sustain tumour growth

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40
Q

What is apoptosis

A

A mechanism of programmed single cell death in an active cell process

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41
Q

What is the role of apoptosis in tumour growth

A

Regulates tumour growth

Involved in the response to chemo and radiotherapy

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42
Q

What do blood vessels provide for tumours

A

A route for release of tumour cells into circulation

The more blood vessels that are present in a tumour equal a poorer prognosis

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43
Q

What is the fundamental property of cancer

A

Invasion

Metastasis

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44
Q

Why is the spread of cancer a major clinical problem

A

It can cause the formation of metastatic (secondary) tumours

A patients prognosis is dependent on the extent of the spread

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45
Q

How does the conversion from invasion to metastasis occur

A

Multi-step process
Involves increased matrix degradation by proteolytic enzymes
Altered cell-to-cell and cell-to-matrix adhesion

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46
Q

How can cancer spread

A

Locally
Lymphatic
Through blood
Trans-coelomic

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47
Q

How does local cancer spread occur

A

Malignant tumour invades connective tissue

Then invasion of lymph/blood vessels

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48
Q

How does lymphatic cancer spread occur

A 
Adherence of tumour cells to lymph vessels
Invasion from lymphatics
Invasion to the lymph nodes
Metastasis forms in lymph nodes
Clinical evidence of metastasis produced
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49
Q

How does blood cancer spread occur

A

Adherence of tumour cells to blood vessels
Invasion from blood vessels to tissues
Metastasis froms
Clinical evidence of metastasis produced

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50
Q

What is trans-coelomic spread

A

Special form of local spread

Tumours spread across body cavities (e.g. pleural or peritoneal)

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51
Q

Which type of tumours show trans-coelomic spread

A

Lung
Stomach
Colon
Ovary

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52
Q

What are the sites of metastasis related to

A

Not to tissue blood flow

Dependent on tumour and tissue releated factors (metastatic niche)

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53
Q

State some common sites of metastasis

A 
Liver
Lung
Brain
Bone (axial skeleton)
Adrenal gland
Omentum
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54
Q

State some uncommon sites of metastasis

A

Spleen
Kidney
Skeletal muscle
Heart

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55
Q

Where does breast cancer commonly metastasise to

A

Bone

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56
Q

Where does prostate cancer commonly metastasise to

A

Bone

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57
Q

Where does colorectal cancer commonly metastasise to

A

Liver

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58
Q

Where does ovarian cancer commonly metastasise to

A

Omentum

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59
Q

What type of cancer can the alpha-fetoprotein be a tumour biomarker for

A

Testicular teratoma

Hepatocellular carcinoma

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60
Q

What type of cancer can the carcino-embryonic antigen (CEA) be a tumour biomarker for

A

Colorectal cancer

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61
Q

What type of cancer can the oestrogen receptor be a tumour biomarker for

A

Breast cancer

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62
Q

What type of cancer can the prostate specific antigen be a tumour biomarker for

A

Prostate cancer

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63
Q

What are the local effects of benign tumours

A

Pressure

Obstruction

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64
Q

What are the local effects of malignant tumours

A

Pressure
Obstruction
Tissue destruction (ulceration/infection) Bleeding (anaemia and haemorrhage)
Pain (from pressure on nerves, perineural infiltration, bone pain from pathological fractures)
Effects of treatment

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65
Q

What are the systemic effects of cancer

A

Weight loss (cancer cachexia)
Secretion of hormones (normal and abnormal/inappropriate)
Paraneoplastic syndromes
Effects of treatment

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66
Q

When are ‘normal’ hormones produced by tumours

A

They are produced by tumours of the endocrine organ however there may be abnormal control of hormone production/secretion

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67
Q

When are ‘abnormal’/inappropriate hormones produced by tumours

A

They are produced by a tumour from an organ which doesn’t normally produce hormones

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68
Q

Paraneoplastic syndromes…

A

cannot be explained by local or metastatic effects of tumours (e.g. neuropathy or myopathy)

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69
Q

Why is it better for cancer to be detected at an early stage

A

It reduces/prevents morbidity/mortality

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70
Q

How can cancer be detected at the pre-invasive stage

A

Through the identification of dysplasia/intraepithelial neoplasia

71
Q

What is dysplasia

A

A pre-malignant change

The earliest change in the process of malignancy which can be visualised

72
Q

Where can dysplasia be identified

A

Epithelium

Can progress to cancer

73
Q

State the features of dysplasia

A

Disorganisation of cells - increase nuclear size, increases mitotic activity, abnormal mitoses
Grading of dysplasia - high grade, low grade
No invasion

74
Q

What is required for the early detection of cancer

A

Effective test which is sensitive/specific and acceptable

75
Q

Give an example of a screening programme which helps to detect cancer early

A

Cervical screening programme

76
Q

What is the aim of the cervical screening programme

A

To reduce the incidence of squamous carcinoma of the cervix

77
Q

What does the cervical screening programme aim to detect

A

Dysplastic cells from squamous epithelium of the cervix

78
Q

What can cause disorders or cell growth to occur

A

Normal and abnormal cell cycles
Chemical carcinogenesis
Radiation carcinogenesis

79
Q

What does the normal cell cycle involve

A

Mitosis to cause mitotic divison

80
Q

What is mitosis

A

Mechanism of cellular replication which causes nuclear division plus cytokinesis

81
Q

What does mitotic divison produce

A

Two genetically identical daughter cells

82
Q

What is the cell cycle

A

The time interval between mitotic divisions

83
Q

What should the cell cycle be coordinated with

A

The body’s needs

Production of cell numbers and cell types is tightly controlled

84
Q

What must occur for a viable progeny to be produced

A

The cell must progress through cycle phases (DNA synthesis and mitosis) in the correct sequence

85
Q

What does quality control ensure

A

Each daughter cell receives a full chromosome complement

Mutations in DNA sequences do not pass on

86
Q

What external factors influence the cell cycle control

A

Hormones
Growth factors
Cytokines
Stroma

87
Q

What internal factors influence the cell cycle control

A

Critical checkpoints - Restriction point (R)

88
Q

What occurs prior to reaching the restriction point

A

Progress through G1 depends on external stimuli

89
Q

What occurs after the restirction point

A

Progression becomes autonomous

90
Q

What are the phases of the cell cycle

A

Quiescent, G0
Interphase (G1, S, G2)
Cell division (mitosis)

91
Q

What is the quiescent phase

A

The resting phase: cell has left the cycle and stopped dividing

92
Q

What occurs in G1

A

Cells increase in size

G1 checkpoint control mechanism ensures everything is ready for DNA synthesis

93
Q

What occurs in S phase

A

DNA replication occurs

94
Q

What occurs in G2

A

Gap between DNA synthesis and mitosis
Cell continues to grow
G2 checkpoint control mechanism ensures that everything is ready to enter the M phase

95
Q

What occurs in mitosis

A

Cell growth ceases

Metaphase checkpoint ensures cell is ready to complete division

96
Q

Where are checkpoints present in the cell cycle

A

At the end of G1
End of G2
At metaphase

97
Q

What happens if the cell size is inadequate

A

G1 or G2 arrest

98
Q

What happens if the nutrient supply is inadequate

A

G1 arrest

99
Q

What happens if essential external stimulus is lacking

A

G1 arrest

100
Q

What happens if the DNA is not replicated

A

S arrest

101
Q

What happens if DNA damage is detected

A

G1 or G2 arrest

102
Q

What happens if there is chromosome misalignment

A

M-phase arrest

103
Q

What are checkpoints

A

System of cyclically active and inactive enzymes

Catalytic sub-units activated by a regulatory sub-unit

104
Q

What is a catalytic subunit called

A

Cyclin-dependent kinases (CDKs)

105
Q

What is a regulatory sub-unit called

A

Cyclins

106
Q

What is the active catalytic subunits and regulatory sub-unit called

A

CDK/cyclin complex

107
Q

What do acitve CDK/cyclin complexes do

A

Phosphorylate target proteins

108
Q

What does the phosphorylation target proteins cause

A

The activation/inactivation of that substrate which regulate events in the next cycle phase

109
Q

How are CDKs constitutively expressed

A

In an inactive form

110
Q

How is CDK activity regulated

A 
The cyclins accumulate and are destroyed as cycle progresses
CDK inhibitors (CKIs)
111
Q

What CDK inhibitors (CKIs) families are there and how do they work

A

INK4A
CIP/KIP
Bind to cyclin/CDK complexes

112
Q

Describe the INK4A family

A

They bind to CDK4 and 6 to prevent association of these CDKs with their cyclin regulatory proteins

113
Q

How is the cell cycle regulated

A

An extracellular growth signal activates cyclin D
This combines with CDK4 to form a cyclin D-CDK4 complex
The complex inhibits p21 and activates E2F
The activation of E2F responsive genes occurs through phosphorylation and deactivation of RB
This causes Cyclin E to combine with CDK2 to form cyclin E-CDK2 complex
And cyclin A to combine with CDK2 to form cyclin A-CDK2 complex

114
Q

What does the cyclin E-CDK2 control

A

G1/S checkpoint

115
Q

What does the cyclin A-CDK2 control

A

G2/M checkpoint

116
Q

Describe the retinoblastoma gene

A

It encodes a 110 kDa phosphoprotein (pRb) expressed in almost every cell of the human body
pRb is hypophosphorylated and phosphorylation increases as cells progress through the cell cycle
Active cyclin D/CDK complexes will phosphorylate pRb

117
Q

What is the function of hypophosphorylated/active Rb

A

Inactivates E2F so puts a brake to the cell cycle

118
Q

What is the function of phosphorylated/inactive pRb

A

Loses affinity for E2F

119
Q

What is the main target for pRb

A

E2F transcription factor as E2F is a potent stimulator of cell cycle entry

120
Q

What will free E2F transcription factors do

A

Activate vital target genes

121
Q

What causes carcinogenesis

A

Mutation of genetic material that upsets the normal balance between proliferation and apoptosis (cell death)

122
Q

What leads to tumours

A

Uncontrolled proliferation of cells

123
Q

What types of mutations can cause a cell to lose control of proliferation

A

Mutations in genes regulating cell division, apoptosis and DNA repair

124
Q

What can lead to carcinogenesis

A

Non-lethal genetic damage

125
Q

Where can non-lethal genetic damage arise from

A 
Environmental agents (e.g. chemicals, radiation and oncogenic viruses)
Inherited
126
Q

Describe chemical carcinogenesis

A

Purine and pyrimidine bases in DNA are critically damaged by various oxidizing and alkylating agents
The chemical carcinogens or their active metabolites react with DNA forming covalently bound products (DNA adducts)
Adduct formation at particular chromosome sites causes cancer

127
Q

What is a critical cellular target for radiation damage

A

Purine and pyrimidine bases in DNA

128
Q

When is radiation carcinogenic

A

High-energy radiation if received in sufficient doses (e.g. from ultraviolet radiation, X-rays, Gamma radiation)

129
Q

Which type of genes are mutated in cancer

A

Genes that regulate the cell cycle

130
Q

Which regulatory pathways tend to be disrupted in cancer

A

The cyclin D-pRb-E2F pathway

p53 pathway

131
Q

What happens when pRB is inactive or absent

A

It causes the cell cycle break to be released

132
Q

Where are cancers most likely to be dysregulated

A

G1-S

133
Q

Which genes tend to have mutations that cause dysregulation at G1-S

A

Rb
CDK4
cyclin D
p16

134
Q

What is the function of p53

A

To maintains genomic integrity

135
Q

What does increased levels of p53 in damaged cells cause

A

Induces cell cycle arrest at G1
Facilitates DNA repair
If damage is severe it causes p53-induced apoptosis

136
Q

What occurs in cells with mutated p53

A

They do not G1 arrest or repair damaged DNA

Genetically damaged cells will proliferate and form malignant neoplasms

137
Q

State some factors which affect carcinogenesis

A

Geographic and environmental factors
Age
Heredity

138
Q

What are proto-oncogenes

A

Normal genes that promote normal cell growth and mitosis

Normal genes coding for normal proteins that regulate growth

139
Q

What are tumour suppressor genes

A

Genes that discourage cell growth, or temporarily halt cell division to carry out DNA repair

140
Q

What type of genes are classed as tumour-suppressor genes

A

Genes negatively regulating mitosis - Rb
Genes regulating apoptosis
Genes regulating DNA repair

141
Q

What is the key event in tumour formation

A

Uncontrolled cell proliferation via cell cycle dysregulation via loss of tumour suppressor gene function

142
Q

What types of mutations can mimic the effect of pRB loss

A

Mutational activation of cyclin D or CDK4

Mutational inactivation of CDKIs also drive proliferation

143
Q

How can mutations of anti-oncogenes occur

A

From:
Sporadic mutations
Inherited mutations

144
Q

How do inherited anti-oncogene mutations arise

A

One defective inherited copy of pRb

Somatic point mutation of other copy

145
Q

How do sporadic anti-oncogene mutations arise

A

2 mutations occur in a single cell

146
Q

How many allelic copies must be mutated to give rise to cancer

A

Both

147
Q

What types of syndromes can be involved in causing cancer

A

Heredity - accounts for 5-10% of all cancers

Inherited cancer syndromes
Familial cancers
Autosomal recessive syndromes of defective DNA repair

148
Q

What are inherited cancer syndromes

A

A strong family history of uncommon site-specific cancers

An autosomal dominant inheritance of a single mutant gene

149
Q

Give examples of inherited cancer syndromes

A 
Familial retinoblastoma
Familial adenomatous polyposis of colon
Multiple Endocrine Neoplasia 
Neurofibromatosis
Von Hippel-Lindau Syndrome
150
Q

What is the risk with familial retinoblastoma

A

Carriers have 10000x risk of bilateral retinoblastoma

Increased risk of second cancers (e.g. bone sarcomas)

151
Q

What is the risk with familial adenomatous polyposis of colon

A

100% risk of colon cancer by age 50 years

152
Q

What are the signs of familial cancers

A

Family clustering of cancers but individual predisposition unclear
Multifactorial inheritance
Early age of onset
Multiple/bilateral tumours

153
Q

Give examples of familial cancers

A

Some Breast cancers
Some Ovarian cancers
Non-FAP colon cancers

154
Q

Describe the APC gene

A

Function: signal transduction
Somatic mutation causes: gastric, colon, pancreas, melanoma
Inherited mutation causes: FAP colon cancer

155
Q

Describe the p53 gene

A

Function: cell cycle/apoptosis
Somatic mutation causes: most cancers
Inherited mutation causes: li-fraumeni syndrome (multiple carcinomas and sarcomas)

156
Q

Describe the Rb gene

A

Function: cell cycle regulation
Somatic mutation causes: retinoblastoma, colon, lung and breast carcinomas
Inherited mutation causes: retinoblastoma and osteosarcoma

157
Q

Describe the p16 (INK4a) gene

A

Function: Inhibits CDKs
Somatic mutation causes: pancreatic, oesophageal carcinomas
Inherited mutation causes: maligant melanomas

158
Q

Describe BRCA 1/2

A

Function: DNA repair

Inherited mutation causes: breast and ovarian cancer

159
Q

What are oncogenes derived from

A

Proto-oncogenes

160
Q

How can oncogenes be activated

A

By:
Alteration of proto-oncogene structure
Dysregulation of proto-oncogene expression

161
Q

What does the dysregulation of proto-oncogene expression cause

A

Gene amplification

Overexpression

162
Q

What does the alteration of proto-oncogene structure cause

A

Point mutations

Chromosome rearrangements + translocations

163
Q

What can oncogenes produce

A

Active oncoprotein products

164
Q

What type of oncoprotein products are there

A 
Growth Factors
Growth Factor Receptors
Proteins involved in Signal Transduction
Nuclear Regulatory Proteins
Cell Cycle Regulators
165
Q

What does the proto-oncogene sis activate

A

PDGF causing overexpression

Cancers caused: astrocytoma, osteosarcoma

166
Q

What does the proto-oncogene erb-B2 activate

A

EGF-receptors family causing amplification

Cancers caused: breast, ovarian, lung, stomach

167
Q

What does the proto-oncogene ras activate

A

GTP-binding causing point mutation

Cancers caused: lung, colon, pancreas, leukaemia

168
Q

What does the proto-oncogene myc activate

A

Transcriptional activators causing translocation

Cancer caused: Burkitt’s lymphoma

169
Q

What does the proto-oncogene cyclin D activate

A

Cyclins causing translocation and amplification

Cancers caused: mantle cell lymphom, breast, liver, oesophageal

170
Q

What does the proto-oncogene CDK4 activate

A

CDK causing amplification

Cancers caused: melanoma, sarcoma

171
Q

What mechanisms can be used for viral carcinogenesis

A

Virus genome inserts near a host proto-oncogene
Viral promoter or other transcription regulation elements cause proto-oncogene over-expression
Retroviruses insert an oncogene into host DNA causing cell division

172
Q

Which DNA viruses are known to cause cancer in humans

A

HPV (cervical cancer)
Hepatitis B (liver cancer)
EBV (Burkitt lymphoma)

173
Q

How many genetic aberrations do sporadic cancers obtain

A

Multiple

The abnormalities accumulate with time

Principles of Disease-Megan (41 decks)

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