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Gen Path Test Two > Neoplasia > Flashcards

Neoplasia Flashcards

1
Q

Which type of acquired growth disturbance is neoplastic

A

Irreversible changes

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2
Q

What is an increase in cell size resulting from increased production of cellular proteins

A

Hypertrophy

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3
Q

What is the main adaptation for cells with limited or no ability to divide

A

Hypertrophy

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4
Q

What is an increase in cell numbers caused by growth factors and hormones

A

Hyperplasia

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5
Q

What is a decrease in cell and organ size

A

Atrophy

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6
Q

Equine laryngeal hemiplasia is caused by what type of cell response

A

Atrophy

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7
Q

What is a change in the phenotype of differentiated cells

A

Metaplasia

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8
Q

T/F Metaplasia is reversible

A

True

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9
Q

What is the term for the loss of uniformity and orientation of cells

A

Dysplasia

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10
Q

What is a disorder of cell growth triggered by mutations which give the cell growth and survival advantages independent of growth regulation signals

A

Neoplasia

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11
Q

What is malignant neoplasia

A

Cancer

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12
Q

What are the two basic components of a neoplasm

A

Parenchyma and Stroma

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13
Q

What are the neoplastic cells that make up a tumor

A

Parenchyma

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14
Q

What is the reactive tissue that surrounds a tumore

A

Stroma

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15
Q

What makes up the stroma

A

Blood vessels, connective tissue, and cells from the adaptive and innate immune system

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16
Q

T/F Neoplasms have no capsule

A

F - they can sometimes have a capsule

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17
Q

What kind of neoplasm remains localized

A

Benign

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18
Q

What suffix is added to the end of a malignant neoplasia

A

-sarcoma

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19
Q

What characterizes a mixed tumor

A

The presence of two or more distinct cell types from a pluripotential clone

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20
Q

Define a pluripotent cell

A

A cell with the ability to give rise to several different cell types

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21
Q

What types of neoplasia can make up a mixed mammary tumor

A

Epithelial, myoepithelial and mesenchymal

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22
Q

What is a totipotent cell

A

A cell which has the ability to give rise to an entire new organism

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23
Q

What is a hemangioma/sarcoma

A

Tumor of the blood vessels

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24
Q

What is a meningioma/sarcoma

A

Tumor of the brain covering

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25
Q

What is leukemia

A

Cancer of hematopoietic cells, malignant by nature

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26
Q

What is lymphoma

A

Cancer of lymphoid tissue

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27
Q

What is leimyoma/sarcoma

A

Tumor of smooth muschle

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28
Q

What is rhabdoma/sarcoma

A

Tumor of striated muscle

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29
Q

What are the terms for benign and malignant squamous cell cancers

A

Squamous cell papilloma and carcinoma

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30
Q

What are the terms for cancers of the epithelial linings of glands and ducts

A

adenoma/adenocarcinoma
papilloma/papillary carcinoma
cystoadenoma/cystadenocarcinoma

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31
Q

What suffixes describe bronchial, renal and hepatic benign and malignant neoplasias

A

Benign -adenoma

Malignant -carcinoma

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32
Q

What type of tissue do transitional cell papilloma and transitional cell carcinomas affect

A

Urinary tract

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33
Q

What is the name of the benign and malignant tumors of the urinary tract

A

Transitional cell papilloma and carcinoma

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34
Q

What are the diagnostic criteria for malignancy (4)

A

Anaplasia (lack of differentiation)
Rate of growth
Local invasion
Metastasis

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35
Q

What diagnostic criteria is an unequivocal hallmark of malignancy

A

Metastasis

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36
Q

Define anaplasia

A

Lack of differentiation, cells which do not look or function like normal cells

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37
Q

What is differentiation

A

Extent to which neoplastic cells resemble and function as the normal parenchymal cells

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38
Q

What morphological features are associated with anaplasia (6)

A

Pleomorphism - variable size
Abnormal nuclear size (1:1) and shape
Increased mitoses
Atypical mitotic figures
Loss of polarity (disorganized cell growth)
Necrosis centrally due to outgrowing blood supply

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39
Q

Besides metastasis, what is the second best indicator of malignancy

A

Local proliferation, infiltration and destruction of surrounding tissue

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40
Q

Can a malignant tumor have a capsule?

A

May have a pseudocapsule in slower growing tumors, but cells can be detected invading past it.

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41
Q

Define metastasis

A

Spread of a tumor to sites physically discontinuous with original site

42
Q

What are the pathways of metastasis (3)

A

Direct seeding
Lymphatic spread
Hematogenous spread

43
Q

What type of metastasis is most typical of carcinomas

A

Direct seeding

44
Q

What type of metastasis is most typical of sarcomas

A

Hematogenous spread

45
Q

How does hematogenous spread usually occur

A

Thin walled veins most easy to invade, tumors settle in capillary bed they first encounter

46
Q

What are the two primary sites for hematogenous spread of malignancy

A

Lung and liver

47
Q

What is the most common initial pathway of spreading for carcinomas

A

Lymphatic

48
Q

What normal regulatory genes are the principle target for cancer-causing mutations (4)

A

Protooncogenes
Tumor suppressor genes
Apoptosis regulating genes
DNA repair genes

49
Q

What kind of mutation are those in protooncogenes

A

Gain of function

50
Q

What kind of mutation are those in tumor suppressor genes

A

Loss of function

51
Q

What kind of mutation are those in apoptosis regulating genes

A

Loss or gain of function

52
Q

What kind of mutation are those in DNA repair genes

A

Loss of function

53
Q

What are genes that promote autonomous growth in cancer cells

A

Oncogenes

54
Q

What are oncoproteins

A

Abnormal proteins encoded by oncogenes that inactivate regulation to lead to proliferation

55
Q

What types of things can be protooncogenes (5)

A 
Growth factors
Growth factor receptors
Nuclear regulatory proteins
Signal transduction proteins
Cell cycle regulators
56
Q

Describe the protooncogenesis of a specific growth factor receptor

A

Tyrosine kinase mutations lead to continuous signals to divide

57
Q

What way can cancer avoid growth inhibition

A

Tumor suppressor gene inhibition

58
Q

Name two tumor suppressor genes

A

RB- retinoblastoma- hypophosphorylated state leads to inhibition of division (if RB is phosphorylated, cell division may proceed)
p53- guardian of the genome- monitors for signals and accumulates to bind DNA and causes arrest/repair/apoptosis

59
Q

Describe how RB functions

A

RB is a tumor suppressor gene. Stimulation of p16 inactivates cyclinD and CDK4 which hypophosphorylate RB to inhibit cell division.

60
Q

What actions can cancer cells use to inhibit RB

A

Loss of the p16 inhibitor leads to lack of inhibition of cyclingD/CDK4
Gene amplification of cyclinD and CDK4 allows greater concentrations to overcome their inhibition
Direct binding by viral oncoproteins to inhibit

61
Q

Describe how p53 is involved in cancer (2)

A

Mutations in this gene which lead to inability to guard the genome
Inactivation by viral oncoproteins

62
Q

T/F Intact tumor suppressor genes in a cell will shut down an oncogene

A

True

63
Q

Describe the altered cellular metabolism of cancers

A

High glucose consumption

Conversion of glucose to lactose via fermentation even in high oxygen situations

64
Q

What is the Warburg effect

A

Conversion to a cell whose phenotype of metabolism is aerobic glycolysis in cancer

65
Q

Why does the Warburg effect occur

A

Cancer cells need production of cellular proteins which cannot be made with oxidative phosphorylation

66
Q

What is the most common method of avoiding apoptosis in cancer (also name its signal)

A

Incapacitation of intrinsic (mitochondrial) pathway to apoptosis via decreased C95

67
Q

What stimulates vessel growth in cancers

A

Angiogenic switch

68
Q

Define neoangiogenesis

A

Stimulation of vessel outgrowth from existing capillaries to supply nutrients and growth factors

69
Q

What effect does neoangiogenesis have on cancer

A

Leaky connections of new vessels allow for access by tumor and increased potential for metastasis

70
Q

What factors of transcription are upregulated by cancer for angiogenesis

A

VEGF (and B-FGF)

71
Q

What is a common target in cancer treatment affecting blood supply to tumors

A

VEGF (factor which induces angiogenesis)

72
Q

What are the 4 theories of metastasis

A

Non-metastatic tumor acquires metastatic variants which go on to metastasize
Tumors begin with metastatic capabilities
Metastatic tumor develops new metastatic variants which go on to metastasize
Stromal response surrounding tumor allows metastatic variants to exploit conditions

73
Q

What are the four main components of the metastatic cascade

A
  1. Loosening of intracellular junctions
  2. Degradation of ECM
  3. Attachment to ECM
  4. Migration and invasion
74
Q

What leads to loosening of intracellular junctions

A

E-cadherin junction breakdown or complete loss of expression

75
Q

What leads to degradation of ECM in metastasis (2)

A

Tumor cell protease secretion and loss of ECM proteins like collagen

76
Q

What ways are cancers able to evade immuno system (4)

A

Growth of Ag-negative variants
Reduction of MHC expression
Production of immunosuppressive/regulatory molecules

77
Q

What is APC

A

Adenomatous polyposis coli - single mutant allele inheretance leading to colorectal cancer

78
Q

What differentiates the two types of carcinogens

A

Direct and indirect acting and the need for metabolism to convert them to action

79
Q

What are the steps of chemical carcinogenesis

A

Initiation- exposure of cell to carcinogen and cause of permanent DNA damage
Promotors- induce tumors to arise from initiated cells

80
Q

What is the mechanism of UV radiation damage

A

Formation of pyrimidine dimers not allowing normal DNA dimer pairing, failure of nucleotide excision repair allows mutation to persist

81
Q

What is the mechanism of Feline Leukemia Virus

A

Insertional mutagenesis by virus inserting on c-myc protooncogene (also flv, fit) altering cell cycle regulation

82
Q

What is the mechanism of HPV

A

Overexpression of E6 and E7 viral oncoproteins which increase cell proliferation- not insertional

83
Q

What conditions caused by viral infection lead to increased risk of cancer

A

High free radical environment from immune response
Elevated DNA synthesis
Chronic tissue damage and inflammation and repair response

84
Q

What is cachexia

A

Progressive loss of body fat and lean body mass due to increased BMR in cancer

85
Q

What are the mechanisms of cachexia (3)

A

High TNFa and IL6 in tumors
Breakdown of skeletal muscle via proteolysis inducing factor (PIF) from tumor cells
Lipid mobilization factor (LMF) from tumor cells leads to FA oxidation

86
Q

Name three paraneoplastic syndromes

A

Hypercalcemia
Hypertrophic osteoarthropathy
Endocrinopathy

87
Q

Describe mechanisms of hypercalcemic paraneoplastic syndrome

A

PTHrP- expression of PTH-like substance from cancers like anal gland apocrine carcinoma
PTH- produced by adenocarcinomas and carcinomas
Bone resorption from invasion or indirect cause

88
Q

What conditions in dogs and cats lead to hypercalcemia

A

Dogs- T-cell lymphoma, parathyroid adeno/carcinomas, bone tumors, multiple myeloma
Cats- lymphoma, squamous cell and pulmonary carcinomas

89
Q

Describe hypertrophic osteoarthropathy

A

Development of exostosis along long bones secondary to pulmonary tumors (and occasionally bladder tumors)

90
Q

Describe endocrinopathy and give an example

A

Ectopic hormone production by tumors as a paraneoplastic syndrome (ex. testicular sertoli cell tumor producing estrogens)

91
Q

Name the four diagnostic methods of cancer

A

Histological
Flow
Immunohistochemistry
Molecular analysis/PCR

92
Q

What is grading of tumors based on

A

Degree of differentiation
Number of mitoses
Architectural features

93
Q

What are the two mast cell tumor grading schemes

A

Patnaik- (1-3)

Kiupel - Low/high

94
Q

What are the parameters used it Patnaik mast cell tumor grading

A

Number of cells, mitoses, anisocytosis, pleomorphism, granules, multinucleation, etc

95
Q

What are the relative survival rates for each of the Patnaik Mast Cell Tumor grades

A

1- 93%
2- 50/50
3- 6%

96
Q

What parameters are used to grade Kiupel Mast Cells

A

Mitoses, multinucleation, bizarre nuclei, karyomegaly

97
Q

What is STS

A

Canine soft tissue sarcoma - wide group of similar slow-growing tumors

98
Q

How is cancer staged?

A

T- T0 (in situ) T1-4 in terms of size
N- nodes involvement
M metastases

99
Q

What mediates hypercalcemia in apocrine gland adenocarcinoma of the anal sac

A

PTHrP

100
Q

What proteins mediate cancer cachexia?

A

TNFa and proteolysis inducing factor

101
Q

Small thymus in 3 day old foal

A

Hypoplasia

102
Q

What discurbances of growth do Sertoli cell testicular tumors induce in prostatic epithelium

A

Metaplasia

Gen Path Test Two (4 decks)

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