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RUSVM Pathology I > Neoplasia 2 > Flashcards

Neoplasia 2 Flashcards

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1
Q

Neoplasia is a result of an abnormality involved the ________________

A

Cell cycle

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2
Q

Abnormalities in genes controlling what part of the cell cycle can result in neoplasm

A

DNA repair
growth signaling
Growth-inhibition signaling
Evasion of apoptosis

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3
Q

Defective DNA repair leads to __________

A

Genetic instability

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4
Q

Abnormal cell cycle checkpoints and abnormal responses to DNA damage are due to what

A

Defective DNA repair

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5
Q

A normal gene that regulates cell proliferation

A

Proto-oncogene

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6
Q

Protocol-oncogenes regulate?

A

Growth factors
Signal transducers
Transcription factors
Cell cycle component

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7
Q

_____________produced oncoproteins

A

Oncogenes

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8
Q

Are proto-oncogene mutations to oncogenes dominant or recessive?

A

Dominant

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9
Q

___________ gene encodes a receptor tyrosine kinase with growth factor ligand

A

Ckit

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10
Q

What mutation is common in canine mast cell tumors

A

Ckit (oncogene)

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11
Q

Are mutations in tumor suppressor genes dominant or recessive?

A

Recessive

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12
Q

What usually inhibits cell proliferation, and when absent will lead to growth that is insensitive to inhibition

A

Tumor suppressor genes

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13
Q

Are mutations in a protoncogene OR a tumor suppressor gene inherited in the germ line

A

Tumor suppressor gene

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14
Q

What does p53 encode??

A

DNA binding protein that stimulates many genes involved in arresting cell cycle, and stimulating DNA repair and apoptosis

Eg CDK inhibitor

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15
Q

What are normal triggers for apoptosis

A

DNA damage
Loss of essential nutrients/growth factors
Binding of “death factors”
Cytotoxic lymphocytes

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16
Q

Are mutations that allow evasion of apoptosis dominant for recessive

A

Can be either

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17
Q

What is the Rb gene and what is its normal function

A

Tumor suppressor gene

Required for G1/S transition in the cell cycle

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18
Q

Are neoplasms clonal or polyclonal?

A

Clonal

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19
Q

How do neoplasms become heterogenous if they are clonal?

A

Genetic instability

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20
Q

What the tumor cell progression an the effect therapy will have on these cells?

A

Clonal neoplasm -> genetic instability leading to multiple clones -> progression to malignant clone -> overgrowth of malignant cells

Treatment -> selection and growth of resistant cells

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21
Q

What is tumor invasion ?

A

Malignant tumors do not respect anatomical boundaries

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22
Q

What must cells do be be invasive?

A

Overcome passive growth-> loss of contact inhibition

Loosen cell junctions

Penetrate BM and ECM (enzymatic destruction of collagenase and matrix metalloproteinases)

Migrate actively -> stimulated by growth factors and cleavage products of ECM

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23
Q

Loosening of intracellular junctions is caused by decreased expression of _________

A

Cadherins

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24
Q

Cleavage of matrix components produces substances that have what kind of properties

A

Growth promoting, angiogenic, and chemotactic

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25
Where are growth factors that stimulate migration derived from?
Tumors cells and/or degraded ECM
26
What is the metastatic cascade?
Clonal expansion-> metastatic subclone -> adhesion and invasion of BM -> pass through ECM -> intravasation -> interact with lymphoid cells -> form tumor cell embolus (wth platelets) -> adhesion of BM -> extravasation -> metastatic deposit -> angiogenesis -> growth
27
Can a tumor progress without angiogenesis ?
No Limited to 1-2mm diameter without new blood vessels
28
How do tumor cells recruit endothelial cells and promote angiogenesis ?
Release of vascular endothelial growth factor (VEGF)
29
What are the pathways of spread of tumors
Tanscoelomic Hematogenous Lymphatic
30
What is transcoelomic spread and what cancers is this common in?
Seeding of body cavities and surfaces -> On surface of organs have fewer atomically barriers Mesothelioma, ovarian adenocarcinoma
31
What is hematogenous spread and what tumors is this most common in?
Invasion of veins (usually not arteries = thicker wall) Sarcoma
32
What is lymphatic spread and what tumors use this route?
In lymphatic-> patterned dictated by lymphatic drainage but lymphatic tumors do not arise orderly. Carcinoma
33
If metatatic spread is hematogenous or lymphatic where do the metastasis often arise?
In the first capillary bed encountered Lungs(many tumors) Liverr(enteric tumors)
34
Prostate and mammary carcinoma metastasis have organotrophism for ____________
Bone
35
Pulmonary carcinoma in cats has metastatic organotropism for ___________
Digits
36
T/F: neoplasms are irreversible proliferation but have the ability to regress
T
37
_______________ are proteins and carbohydrates expressed on tumor cell surface
Tumor antigens
38
Immune system is capable of recognizing self-antigens expressed on tumor cells and attacking these cells
Immunosurveillance
39
What is the most effective anti-tumor defense?
CD8+ cytotoxic Tcell
40
CD8+ Tcells recognize what tumor antigens?
Product of oncogenes or mutated tumor suppressor gene Mutated self protein Overexpressed or aberrantly expressed self protein Oncogenic virus proteins
41
What immuno-evasive mechanisms can a tumor cell have
Alter MHC expression Loss or masking tumor-specific antigens Tolerance (antigen shared with normal tissue) Immunosuppression -> Fas ligand stimulate apoptosis of binding Tcells
42
How can DNA be altered to generate an neoplasm?
Mutation Chromosomal alterations Epigenetic changes (heritable change in gene expression resulting from something other than DNA sequence)
43
What are the two sources of altered DNA
Inherited in germ line Acquired somatic mutation
44
What is a germline mutation/
Mutation passed on in ova or sperm
45
Familial cancer syndrome are most likely due to mutations in what types of genes
Recessive genes Tumor suppressor genes Gene involved in DNA repair
46
T/F: aquired somatic mutations are passed in germline
False
47
What are acquired somatic mutations?
Spontaneous mutations (accumulate over lifetime)
48
What are causes of altered DNA?
``` Spontaneous Radiation Chemical carcinogens Oncogenic virus Hormonal ```
49
What are the two types of radiation and what damage do they cause to DNA
Ionizing -> strand breaks Ultraviolet -> pyrimidine dimers
50
What are the mechanisms of injury of chemical carcinogens?
Genotoxic -> directly damage DNA Cytotoxic -> increased cell proliferation due to cell injury Mitogenic -> increased cell proliferation without cell injury
51
What is a classic veterinary medicine example of a chemical carcinogens?
Bracken fern Aflatoxin Dioxins, Nitrosamines, Polycyclic aromatic hydrocarbons (cigarette smoke)
52
How do oncogenic viruses interrupt host cell genes?
Insert their own oncogene (eg papilloma virus ) Insertional mutagenesis (eg retroviruses) Immunosuppression
53
How do papilloma viruses cause neoplasia
E6/E7 proteins from papilloma virus inactivate p53 and other tumor suppressor genes => loss of cell cycle control
54
How can hormones cause carcinogenesis ?
Stimulation and growth of target organ
55
How can chronic inflammation cause carcinogenesis
Inflammatory cytokines producing cell proliferation (not well understood) Eg Spirocerca lupi/ Biliary infection by liver fluke/ Helicobacter
56
What are the mechanisms of host damage of a neoplasm
Direct - tissue destruction Paraneoplasic (indirect)
57
Indirect and usually remote effects caused by tumor cell products rather than the primary tumor and its metastases
Paraneoplasic syndromes
58
When does tumor necrosis occur?
Secondary to inflammation of tumor Trauma Tumor outgrows blood supply
59
What is cancer cachexia
Progressive loss of body fat and lean body mass accompanied by profound weakness, anorexia, and anemia
60
What is the difference between cachexia and starvation
Cachexia => Lose both fat and muscle, but metabolic rate does not decrease Decreased metabolic rate in starvation
61
what is the pathogenesis of cancer cachexia
TNF, IL1, IL6, and IFNy =>systemic inflammation - > anorexia - > impaired digestion - > metabolic/endocrine changes
62
T/F: cachexia cannot be reversed with extra nutrient support
T
63
What is ectopic hormone production?
Non-endocrine neoplasms produce hormonally active substances not normally found in tissue
64
Production of parathyroid hormone -like protein by neoplasm is an example of what? And what does it lead to?
Edocrinopathy -> ectopic hormone production Hypercalcemia of malignancy
65
90% of hypercalcemia of malignancy in dogs is due to what type of tumor?
Apocrine gland acendocarconoma of the anal sac
66
Hypertrophic osteopathy in cats and dogs is associated with what neoplasm
Space-occupying thoracic lesions Presents clinically with lameness
67
What diagnostic method is faster, cheaper and less invasive then histology
Cytologic diagnosis
68
A subset of mesenchymal neoplasm that appear as round cells on cytology
Round cell tumors Shame on your cow, if you didnt get this.
69
What are the round cell tumors ?
``` Plasma cell tumor Histiocytoma Mast cell tumor Lymphoma Transmissible venereal tumor ```
70
How do you decide if your biopsy should be incisional vs excisional ?
Incisional - diagnosis might affect surgical plan Excisional - diagnosis will not affect surgical plan
71
What are the criteria for malignancy
Degree of differentiation Invasion Mitotic rate Features of anaplasia
72
What are the features of anaplasia
``` Pleomorphism Anisokaryosis/anisocytosis Hyperchromasia High N:C ratio Prominent nuceloli ```
73
What stain should be used for diagnosis of mast cell tumor
Toluidine blue
74
What is Fontana Masson's stain used for?>
Accentuate melanin in amelanotic melanoma
75
What is histopathologic grading used for?
Designate now abnormal the cells are Prognostic factor/indicator to predict behaviour and inform treatment
76
Method that uses dye-labeled antibodies to detect various proteins expressed by a neoplasm
Immunohistochemistry
77
An immunohistochemistry that is positive for vimentin means?
Mesenchymal cells -> sarcoma
78
An immunohistochemistry that is positive for cytokeratin mean?
Epithelial -> carcinoma
79
How can we use clonality assays to determine between hyperplasia and neoplasm
High clonality -> neoplastic Low clonality -> hyperplasia/inflammation
80
What is staging?
Indication of extend of tumor growth and spread Prognostic factor Uses: - size - depth of invasion - involvement of regional lymph nodes - extent of distant metastasis

RUSVM Pathology I (17 decks)

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