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
What is leukemia
Cancer of hematopoietic cells, malignant by nature
26
What is lymphoma
Cancer of lymphoid tissue
27
What is leimyoma/sarcoma
Tumor of smooth muschle
28
What is rhabdoma/sarcoma
Tumor of striated muscle
29
What are the terms for benign and malignant squamous cell cancers
Squamous cell papilloma and carcinoma
30
What are the terms for cancers of the epithelial linings of glands and ducts
adenoma/adenocarcinoma papilloma/papillary carcinoma cystoadenoma/cystadenocarcinoma
31
What suffixes describe bronchial, renal and hepatic benign and malignant neoplasias
Benign -adenoma | Malignant -carcinoma
32
What type of tissue do transitional cell papilloma and transitional cell carcinomas affect
Urinary tract
33
What is the name of the benign and malignant tumors of the urinary tract
Transitional cell papilloma and carcinoma
34
What are the diagnostic criteria for malignancy (4)
Anaplasia (lack of differentiation) Rate of growth Local invasion Metastasis
35
What diagnostic criteria is an unequivocal hallmark of malignancy
Metastasis
36
Define anaplasia
Lack of differentiation, cells which do not look or function like normal cells
37
What is differentiation
Extent to which neoplastic cells resemble and function as the normal parenchymal cells
38
What morphological features are associated with anaplasia (6)
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
39
Besides metastasis, what is the second best indicator of malignancy
Local proliferation, infiltration and destruction of surrounding tissue
40
Can a malignant tumor have a capsule?
May have a pseudocapsule in slower growing tumors, but cells can be detected invading past it.
41
Define metastasis
Spread of a tumor to sites physically discontinuous with original site
42
What are the pathways of metastasis (3)
Direct seeding Lymphatic spread Hematogenous spread
43
What type of metastasis is most typical of carcinomas
Direct seeding
44
What type of metastasis is most typical of sarcomas
Hematogenous spread
45
How does hematogenous spread usually occur
Thin walled veins most easy to invade, tumors settle in capillary bed they first encounter
46
What are the two primary sites for hematogenous spread of malignancy
Lung and liver
47
What is the most common initial pathway of spreading for carcinomas
Lymphatic
48
What normal regulatory genes are the principle target for cancer-causing mutations (4)
Protooncogenes Tumor suppressor genes Apoptosis regulating genes DNA repair genes
49
What kind of mutation are those in protooncogenes
Gain of function
50
What kind of mutation are those in tumor suppressor genes
Loss of function
51
What kind of mutation are those in apoptosis regulating genes
Loss or gain of function
52
What kind of mutation are those in DNA repair genes
Loss of function
53
What are genes that promote autonomous growth in cancer cells
Oncogenes
54
What are oncoproteins
Abnormal proteins encoded by oncogenes that inactivate regulation to lead to proliferation
55
What types of things can be protooncogenes (5)
``` Growth factors Growth factor receptors Nuclear regulatory proteins Signal transduction proteins Cell cycle regulators ```
56
Describe the protooncogenesis of a specific growth factor receptor
Tyrosine kinase mutations lead to continuous signals to divide
57
What way can cancer avoid growth inhibition
Tumor suppressor gene inhibition
58
Name two tumor suppressor genes
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
Describe how RB functions
RB is a tumor suppressor gene. Stimulation of p16 inactivates cyclinD and CDK4 which hypophosphorylate RB to inhibit cell division.
60
What actions can cancer cells use to inhibit RB
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
Describe how p53 is involved in cancer (2)
Mutations in this gene which lead to inability to guard the genome Inactivation by viral oncoproteins
62
T/F Intact tumor suppressor genes in a cell will shut down an oncogene
True
63
Describe the altered cellular metabolism of cancers
High glucose consumption | Conversion of glucose to lactose via fermentation even in high oxygen situations
64
What is the Warburg effect
Conversion to a cell whose phenotype of metabolism is aerobic glycolysis in cancer
65
Why does the Warburg effect occur
Cancer cells need production of cellular proteins which cannot be made with oxidative phosphorylation
66
What is the most common method of avoiding apoptosis in cancer (also name its signal)
Incapacitation of intrinsic (mitochondrial) pathway to apoptosis via decreased C95
67
What stimulates vessel growth in cancers
Angiogenic switch
68
Define neoangiogenesis
Stimulation of vessel outgrowth from existing capillaries to supply nutrients and growth factors
69
What effect does neoangiogenesis have on cancer
Leaky connections of new vessels allow for access by tumor and increased potential for metastasis
70
What factors of transcription are upregulated by cancer for angiogenesis
VEGF (and B-FGF)
71
What is a common target in cancer treatment affecting blood supply to tumors
VEGF (factor which induces angiogenesis)
72
What are the 4 theories of metastasis
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
What are the four main components of the metastatic cascade
1. Loosening of intracellular junctions 2. Degradation of ECM 3. Attachment to ECM 4. Migration and invasion
74
What leads to loosening of intracellular junctions
E-cadherin junction breakdown or complete loss of expression
75
What leads to degradation of ECM in metastasis (2)
Tumor cell protease secretion and loss of ECM proteins like collagen
76
What ways are cancers able to evade immuno system (4)
Growth of Ag-negative variants Reduction of MHC expression Production of immunosuppressive/regulatory molecules
77
What is APC
Adenomatous polyposis coli - single mutant allele inheretance leading to colorectal cancer
78
What differentiates the two types of carcinogens
Direct and indirect acting and the need for metabolism to convert them to action
79
What are the steps of chemical carcinogenesis
Initiation- exposure of cell to carcinogen and cause of permanent DNA damage Promotors- induce tumors to arise from initiated cells
80
What is the mechanism of UV radiation damage
Formation of pyrimidine dimers not allowing normal DNA dimer pairing, failure of nucleotide excision repair allows mutation to persist
81
What is the mechanism of Feline Leukemia Virus
Insertional mutagenesis by virus inserting on c-myc protooncogene (also flv, fit) altering cell cycle regulation
82
What is the mechanism of HPV
Overexpression of E6 and E7 viral oncoproteins which increase cell proliferation- not insertional
83
What conditions caused by viral infection lead to increased risk of cancer
High free radical environment from immune response Elevated DNA synthesis Chronic tissue damage and inflammation and repair response
84
What is cachexia
Progressive loss of body fat and lean body mass due to increased BMR in cancer
85
What are the mechanisms of cachexia (3)
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
Name three paraneoplastic syndromes
Hypercalcemia Hypertrophic osteoarthropathy Endocrinopathy
87
Describe mechanisms of hypercalcemic paraneoplastic syndrome
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
What conditions in dogs and cats lead to hypercalcemia
Dogs- T-cell lymphoma, parathyroid adeno/carcinomas, bone tumors, multiple myeloma Cats- lymphoma, squamous cell and pulmonary carcinomas
89
Describe hypertrophic osteoarthropathy
Development of exostosis along long bones secondary to pulmonary tumors (and occasionally bladder tumors)
90
Describe endocrinopathy and give an example
Ectopic hormone production by tumors as a paraneoplastic syndrome (ex. testicular sertoli cell tumor producing estrogens)
91
Name the four diagnostic methods of cancer
Histological Flow Immunohistochemistry Molecular analysis/PCR
92
What is grading of tumors based on
Degree of differentiation Number of mitoses Architectural features
93
What are the two mast cell tumor grading schemes
Patnaik- (1-3) | Kiupel - Low/high
94
What are the parameters used it Patnaik mast cell tumor grading
Number of cells, mitoses, anisocytosis, pleomorphism, granules, multinucleation, etc
95
What are the relative survival rates for each of the Patnaik Mast Cell Tumor grades
1- 93% 2- 50/50 3- 6%
96
What parameters are used to grade Kiupel Mast Cells
Mitoses, multinucleation, bizarre nuclei, karyomegaly
97
What is STS
Canine soft tissue sarcoma - wide group of similar slow-growing tumors
98
How is cancer staged?
T- T0 (in situ) T1-4 in terms of size N- nodes involvement M metastases
99
What mediates hypercalcemia in apocrine gland adenocarcinoma of the anal sac
PTHrP
100
What proteins mediate cancer cachexia?
TNFa and proteolysis inducing factor
101
Small thymus in 3 day old foal
Hypoplasia
102
What discurbances of growth do Sertoli cell testicular tumors induce in prostatic epithelium
Metaplasia