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Pathology > Chapter 7- Neoplasia > Flashcards

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
Q

What is the most reliable feature for tumour differentiation?

A

Metastasis

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26
Q

What types of tumours does metastasis occur in?

A

Only malignant

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27
Q

What are the different ways cancer can be disseminated?

A
  1. Lymphatic spread
  2. Direct seeding of body cavities and surfaces (open space with no physical barriers)
  3. Hematogenous spread (veins invaded)
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28
Q

What type of tumours initially spread via lymphatics?

A

Carcinomas

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29
Q

What spaces are combining seeding during tumour dissemination?

A

Peritoneal, pleural, pericardial, subarachnoid, joint spaces

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30
Q

What are the most common sites of hematogenous tumour spread?

A

Lung and liver

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31
Q

How does growth rate differ between benign and malignant tumours?

A

Benign- slow and progressive

Mal- erratic

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32
Q

What different risk factors affect the development of cancer?

A

Environmental

Age

Acquired predisposing conditions

Genetic predisposition

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33
Q

What is the dominant risk factor for most cancers?

A

Environment

34
Q

Why do most carcinomas occur later in life?

A

Accumulation of somatic mutations and decline in immune surveillance

35
Q

What types of acquired predisposing conditions can lead to the development of cancer?

A

Chronic inflammation

Precursor lesions (eg. dysplasia)

Immunodeficiency states

36
Q

Why is chronic inflammation associated with the development of cancer?

A

Produces a favourable environment

GF release, increases stem cells

ROS

Mediators cause cell survival

Metaplasia

37
Q

What types of precursor lesions may lead to cancer?

A

Chronic inflammation with metaplasia

Noninflammatory hyperplasia

Benign neoplasms

38
Q

What types of genetic predispositions can lead to the development of cancer?

A

Autosomal dominant mutations (tumour suppressor genes)

Defective DNA repair syndromes

Familial cancers

39
Q

What is Lynch syndrome?

A

Inactivation of DNA mismatch repair gene

40
Q

What does Lynch syndrome predispose a patient to?

A

Colon cancer

Endometrial cancer

41
Q

What underlies carcinogenesis?

A

Non-lethal genetic damage

Cells continue to acquire mutations as they won’t die

42
Q

What are the different classes of regulatory genes?

A

Proto-oncogenes- regulate cell growth and differentiation

Tumour suppressor genes- slow/stop cell division

Apoptotic regulating genes

DNA repair genes

43
Q

What alterations are required for malignant transformation?

A

Self sufficiency in growth signals

Insensitivity to growth inhibitory signals

Evasion of apoptosis

Limitless replicative potential

Sustained angiogenesis

44
Q

How is self sufficiency in growth signals achieved by cancer cells?

A

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
Q

What mutations do tumour cells use to escape from senescence (become insensitive to inhibitory signals)?

A

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
Q

What causes a germ line P53 mutation?

A

Li Fraumeni syndrome

47
Q

Overexpression of what protein allows cancer cells to evade apoptosis?

A

BCL2

48
Q

How does BCL2 prevent apoptosis?

A

Limits cytochrome C release from mitochondria

49
Q

How is limitless replicative potential achieved by tumour cells?

A

Inappropriate telomerase activity allows cells to continuously divide

50
Q

Why is angiogenesis required for malignant transformation?

A

Without blood vessel growth, tumours would only reach 1-2mm

Leaky vessels allow for metastatic potential

51
Q

What is the major driving force in angiogenesis of malignant transformation?

A

Hypoxia

52
Q

What normally prevents metastasis?

A

Cell detachment from E cadherin normally causes cell death

53
Q

What mutations lead to genomic instability and increase the risk for carcinogenesis?

A

Mismatch repair- micro-satellite instability

Nucleotide excision repair

Recombination repair- hypersensitivity to agents that damage DNA

54
Q

What type of mutation is hereditary nonpolyposis colon cancer syndrome associated with?

A

Mismatch repair

55
Q

What is nucleotide excision repair responsible for?

A

Correct IV light pyrimidine dimer formation

56
Q

What do defects on nucleotide excision repair lead to?

A

Skin cancer

57
Q

What is the Warburg effect?

A

Tumours use glycolysis for energy even when adequate oxygen is available for oxidative phosphorylation

Results in required carbon intermediates

58
Q

What can cause the dysregulation of cancer associated genes?

A

Chromosomal changes

Epigenetic changes

miRNA

59
Q

How does Philadelphia chromosome (t(9:22)) affect the development of cancer?

A

Results in constitutive kinase activity

60
Q

How are tumour cells recognized and destroyed by host defences?

A

MHC I cells present tumour Ags to and activate CD8 CTLs

61
Q

How do tumour cells evade host defences?

A

Selective outgrowth of Ag negative variants

Loss/reduced expression of histocompatibility genes

Secretion of factors that suppress the immune response

62
Q

How do inflammatory reactions modify the microenvironment to make it beneficial to cancer?

A

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
Q

What is anoikis?

A

Epithelial cell detachment from the basement membrane resulting in cell death

64
Q

What can prevent the anoikis of tumour cells?

A

Macrophages bound to the cells

65
Q

What proteins remodel the ECM to activate invasion and metastasis?

A

Proteases

66
Q

What are the three types of carcinogenic agents?

A

Chemical

Radiant energy

Oncogenic viruses and other microbes

67
Q

How do chemical carcinogens exert their effects?

A

Initiation- irreversible genome changes

Promotion- tumour formation in previously initiated cells

68
Q

What is the difference between direct and indirect chemical carcinogens?

A

Direct- reactive without metabolism

Indirect- require metabolic conversion

69
Q

How does UV light lead to the development of skin cancer?

A

Dimer formation

70
Q

How does radiant energy lead to the development of cancer?

A

Free radical generation

71
Q

What type of UV light is associated with melanoma? Non-melanoma skin cancer?

A

Melanoma- intense intermittent light

Non-melanoma- cumulative

72
Q

What are some examples of oncogenic viruses and the cancers they cause?

A

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
Q

What characteristics of tumours affect their morbidity and mortality?

A

Location and impingement on other structures

Functional activity

Bleeding and infection

Symptoms from rupture or infarction

Cachexia

Paraneoplastic syndrome

74
Q

What is cachexia?

A

Loss of body fat and muscle (wasting away)

75
Q

What is paraneoplastic syndrome?

A

Mimicry of metastatic disease

Symptoms can’t be explained by tumour location or hormones normally produced

76
Q

What does grading determine?

A

Degree of differentiation

77
Q

What is staging based on?

A

TNM system

T= primary tumour (size and structure)

N= lymph node involvement

M= metastases

78
Q

What is used for the laboratory diagnosis of cancer?

A

Histo/cyto

IHC- cell surface markers

Flow cytometry- blood based

Molecular- FISH (chromosomal changes)

Tumour markers- screening

79
Q

What is the most important component of lab diagnosis of cancer?

A

Histo/cyto

80
Q

What types of cancer is IHC useful for?

A

Poorly differentiated (can determine site of origin)

81
Q

What does FISH detect?

A

Chromosomal changes

82
Q

What are some examples of tumour markers?

A

PSA- prostate

CEA- colon, pancreatic, stomach, breast

AFP- liver and testicular

Pathology (25 decks)

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