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Chapter 7- Neoplasia Flashcards

1
Q

What is neoplasia?

A

New, normally abnormal growth

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2
Q

What is a neoplasm?

A

An abnormal tissue mass caused by a cell growth disorder

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3
Q

What is another name for neoplasm?

A

Tumour

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4
Q

What are the two basic components of tumours?

A
  1. Parenchyma (neoplastic cells)

2. Stroma (supporting tissue)

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5
Q

What component is tumour classification based on?

A

The parenchyma

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6
Q

What is desmoplasia?

A

Abundant collagenous stroma stimulated by tumour parenchymal cells

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7
Q

What are scirrhous?

A

Stone hard desmoplastic tumours

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8
Q

What is a polyp?

A

A neoplasm that projects above the mucosal surface

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9
Q

How can benign tumours cause morbidity and mortality?

A

Pushing on surrounding structures

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10
Q

What are the characteristics of benign tumours?

A

Localized with well circumscribed/clear borders

Doesn’t spread

Homogenous cut surface

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11
Q

What suffix designated benign tumours?

A

-oma

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12
Q

What are choristomas?

A

Masses of normal tissue in abnormal locations

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13
Q

What are hamartomas?

A

Masses of disorganized tissue indigenous to the site in which they are found

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14
Q

What are the two types of malignant tumours and what cells do they involve?

A

Sarcomas- mesenchymal cells

Carcinomas- epithelial cells

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15
Q

How do mixed tumours form?

A

A single germ cell layer differentiates into more than one cell type

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16
Q

What cell types make up a pleomorphic adenoma?

A

Epithelial and stromal

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17
Q

What characterizes a teratoma?

A

Made up of more than one germ layer

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18
Q

What are tumours categorized based on?

A

Differentiation

Local invasion

Metastasis

Rate of growth

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19
Q

What is anaplasia?

A

Lack of differentiation

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20
Q

What is pleomorphism?

A

Variability in cell size and/or shape

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21
Q

What is dysplasia?

A

Non invasive growth (no penetration of basement membrane)

Carcinoma in situ

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22
Q

What is the difference in differentiation between malignant and benign tumours?

A

Benign- well differentiated, retain functional characteristics

Mal- pleomorphic, high N:C ratio, mitoses common, loss of polarity, tumour giant cells, necrosis

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23
Q

What is the difference in local invasion between malignant and benign tumours?

A

Benign- cohesive, remain localized, often capsulated

Mal- do not remain localized

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24
Q

What is metastasis?

A

Spread of tumour to sites physically discontinuous with the primary tumour

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25
What is the most reliable feature for tumour differentiation?
Metastasis
26
What types of tumours does metastasis occur in?
Only malignant
27
What are the different ways cancer can be disseminated?
1. Lymphatic spread 2. Direct seeding of body cavities and surfaces (open space with no physical barriers) 3. Hematogenous spread (veins invaded)
28
What type of tumours initially spread via lymphatics?
Carcinomas
29
What spaces are combining seeding during tumour dissemination?
Peritoneal, pleural, pericardial, subarachnoid, joint spaces
30
What are the most common sites of hematogenous tumour spread?
Lung and liver
31
How does growth rate differ between benign and malignant tumours?
Benign- slow and progressive Mal- erratic
32
What different risk factors affect the development of cancer?
Environmental Age Acquired predisposing conditions Genetic predisposition
33
What is the dominant risk factor for most cancers?
Environment
34
Why do most carcinomas occur later in life?
Accumulation of somatic mutations and decline in immune surveillance
35
What types of acquired predisposing conditions can lead to the development of cancer?
Chronic inflammation Precursor lesions (eg. dysplasia) Immunodeficiency states
36
Why is chronic inflammation associated with the development of cancer?
Produces a favourable environment GF release, increases stem cells ROS Mediators cause cell survival Metaplasia
37
What types of precursor lesions may lead to cancer?
Chronic inflammation with metaplasia Noninflammatory hyperplasia Benign neoplasms
38
What types of genetic predispositions can lead to the development of cancer?
Autosomal dominant mutations (tumour suppressor genes) Defective DNA repair syndromes Familial cancers
39
What is Lynch syndrome?
Inactivation of DNA mismatch repair gene
40
What does Lynch syndrome predispose a patient to?
Colon cancer Endometrial cancer
41
What underlies carcinogenesis?
Non-lethal genetic damage Cells continue to acquire mutations as they won’t die
42
What are the different classes of regulatory genes?
Proto-oncogenes- regulate cell growth and differentiation Tumour suppressor genes- slow/stop cell division Apoptotic regulating genes DNA repair genes
43
What alterations are required for malignant transformation?
Self sufficiency in growth signals Insensitivity to growth inhibitory signals Evasion of apoptosis Limitless replicative potential Sustained angiogenesis
44
How is self sufficiency in growth signals achieved by cancer cells?
Proto-oncogene conversion to oncogene Autocrine production of GFs Constant activation of GF receptors Signal transducing proteins are locked into signal transmission Cyclins and CDK mutations result in a loss of cell cycle control
45
What mutations do tumour cells use to escape from senescence (become insensitive to inhibitory signals)?
RB mutations- cells bypass the G1/S checkpoint P53 mutation- neither repair or apoptosis is activated Adenomatous polyposis coli/beta catenin pathway mutations- growth signals in WNT pathway are no longer down regulated
46
What causes a germ line P53 mutation?
Li Fraumeni syndrome
47
Overexpression of what protein allows cancer cells to evade apoptosis?
BCL2
48
How does BCL2 prevent apoptosis?
Limits cytochrome C release from mitochondria
49
How is limitless replicative potential achieved by tumour cells?
Inappropriate telomerase activity allows cells to continuously divide
50
Why is angiogenesis required for malignant transformation?
Without blood vessel growth, tumours would only reach 1-2mm Leaky vessels allow for metastatic potential
51
What is the major driving force in angiogenesis of malignant transformation?
Hypoxia
52
What normally prevents metastasis?
Cell detachment from E cadherin normally causes cell death
53
What mutations lead to genomic instability and increase the risk for carcinogenesis?
Mismatch repair- micro-satellite instability Nucleotide excision repair Recombination repair- hypersensitivity to agents that damage DNA
54
What type of mutation is hereditary nonpolyposis colon cancer syndrome associated with?
Mismatch repair
55
What is nucleotide excision repair responsible for?
Correct IV light pyrimidine dimer formation
56
What do defects on nucleotide excision repair lead to?
Skin cancer
57
What is the Warburg effect?
Tumours use glycolysis for energy even when adequate oxygen is available for oxidative phosphorylation Results in required carbon intermediates
58
What can cause the dysregulation of cancer associated genes?
Chromosomal changes Epigenetic changes miRNA
59
How does Philadelphia chromosome (t(9:22)) affect the development of cancer?
Results in constitutive kinase activity
60
How are tumour cells recognized and destroyed by host defences?
MHC I cells present tumour Ags to and activate CD8 CTLs
61
How do tumour cells evade host defences?
Selective outgrowth of Ag negative variants Loss/reduced expression of histocompatibility genes Secretion of factors that suppress the immune response
62
How do inflammatory reactions modify the microenvironment to make it beneficial to cancer?
Release of GFs (promote proliferation) Removal of growth suppressors (eg. proteases) Enhanced resistance to cell death Angiogenesis induction Activation of invasion and metastasis Evading immune destruction (immunosuppressive environment)
63
What is anoikis?
Epithelial cell detachment from the basement membrane resulting in cell death
64
What can prevent the anoikis of tumour cells?
Macrophages bound to the cells
65
What proteins remodel the ECM to activate invasion and metastasis?
Proteases
66
What are the three types of carcinogenic agents?
Chemical Radiant energy Oncogenic viruses and other microbes
67
How do chemical carcinogens exert their effects?
Initiation- irreversible genome changes Promotion- tumour formation in previously initiated cells
68
What is the difference between direct and indirect chemical carcinogens?
Direct- reactive without metabolism Indirect- require metabolic conversion
69
How does UV light lead to the development of skin cancer?
Dimer formation
70
How does radiant energy lead to the development of cancer?
Free radical generation
71
What type of UV light is associated with melanoma? Non-melanoma skin cancer?
Melanoma- intense intermittent light Non-melanoma- cumulative
72
What are some examples of oncogenic viruses and the cancers they cause?
HTLV-1- T cell leukaemia/lymphoma (CD4) HPV- cervical cancer via inhibition of RB, P53 and CDK inhibitors EBV- Burkitt lymphoma, B cell and Hodgkin lymphoma, nasopharyngeal carcinoma Hep C- hepatocellular carcinomas via P53 inactivation H. pylori- gastric cancer and MALToma
73
What characteristics of tumours affect their morbidity and mortality?
Location and impingement on other structures Functional activity Bleeding and infection Symptoms from rupture or infarction Cachexia Paraneoplastic syndrome
74
What is cachexia?
Loss of body fat and muscle (wasting away)
75
What is paraneoplastic syndrome?
Mimicry of metastatic disease Symptoms can’t be explained by tumour location or hormones normally produced
76
What does grading determine?
Degree of differentiation
77
What is staging based on?
TNM system T= primary tumour (size and structure) N= lymph node involvement M= metastases
78
What is used for the laboratory diagnosis of cancer?
Histo/cyto IHC- cell surface markers Flow cytometry- blood based Molecular- FISH (chromosomal changes) Tumour markers- screening
79
What is the most important component of lab diagnosis of cancer?
Histo/cyto
80
What types of cancer is IHC useful for?
Poorly differentiated (can determine site of origin)
81
What does FISH detect?
Chromosomal changes
82
What are some examples of tumour markers?
PSA- prostate CEA- colon, pancreatic, stomach, breast AFP- liver and testicular

Pathology (25 decks)

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