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Gen Path > Oncology > Flashcards

Oncology Flashcards

1
Q

What is dysplasia?

A
  • abnormality of growth
  • occurs after birth
  • there is proliferation loss, loss of regular differentiation, orderliness and cellular atypia
  • if cause is removed it can be reversed
  • commonly virally induced
  • may be precancerous
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2
Q

What are developmental malformations?

name some developmental malformations

A
  • these are present at birth, may have genetic or environmental origins and normally animal effected will have more than one
  • failure to fuse
  • failure to separate
  • failure to canalize
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3
Q

What is palatoschisis?

A
  • failure to fuse tissues so results in a cleft palate
  • normally hereditary or due to a toxin
  • animal may suffer from starvation and aspiration pneumonia
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4
Q

Cheiloschisis?

A

cleft lip

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5
Q

What is syndactyly?

A

-failure of separation of hooves

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6
Q

What is atresia?

A

failure of hollow organ to canalize

-normally named according to location (ex/ atresia ani - absence of anal opening - n hereditary in calves and pigs)

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7
Q

What is Meckel’s diverticulum?

A

failure to reabsorb the entire yolk sac
-usually causes no clinical signs but if portion of intestine because entrapped within the herniation then may result in impaction or entrapment (colic in horses)

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8
Q

What are ectopic organs?

A

a normal ORGAN that s in the wrong location

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9
Q

ectopic cordis?

A

abnormal positioning of the heart outside the thoracic cavity

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10
Q

polymelia?

A

too many limbs.

may result in difficulty giving birth to the fetus

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11
Q

polydacytly

A

extra digits

-normally causes no problems but it depends where on the limb it is located

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12
Q

adactyly

A

-failure of limbs or digits to develop

if missing all 4 limbs then tetra-amelia

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13
Q

choristoma?

give 2 examples

A

normal TISSUE in wrong location
ex/ corneal dermoids - haired skin growing on the cornea
ex/ dermoid cyst - haired cyst

can normally surgically remove them

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14
Q

hamartomas

A
  • abnormal overgrowth of a tissue in its typically location

- often microscopic at birth but then grow over time

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15
Q

What are 3 types of acquired disorders of growth?

A
  • hyperplasia (goiter)
  • metaplasia (ciliated to nonciliated epithelium)
  • dysplasia (abn orderliness of growth)
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16
Q

What is neoplasm?

What are 3 things that define it?

A
  • means new growth
    1. excessive tissue growth
    2. non responsiveness to normal control mechanisms
    3. persist even after the stimulus has been removed
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17
Q

What is cellular differentiation?

A
  • distinctive gross and histological appearance that is unique to that tissue type
  • malignant tumours are less differentiated then benign
  • with loss of differentiation, there tend to be loss of function of the organ as well
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18
Q

What is anaplasia

A
  • failure of differentiation - common for malignant tumours
  • features include poor cell differentiation, cellular and nuclear pleomorphism (nuclei of malignant neoplastic cells are darker than normal ones because they have increased DNA), mitosis occurs more often in malignant tumours and in weird forms
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19
Q

How does neoplasmic growth occur?

A
  1. increased cell proliferation
    or
  2. decreased cell apoptosis
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20
Q

What is latent period when talking about tumor growth

A
  • when the tumor is clinically undetectable for a period of time
  • normally the tumour size is very small
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21
Q

What is mitotic rate when talking about tumor growth?

A
  • higher mitotic rates are normally associated with increased cell proliferation but not always
  • neoplastic cells are abnormal, they have prolonged mitosis and they may become stalled in the mitotic process
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22
Q 
Compare benign and malignant tumors in regards to:
growth rate
mode of growth
differentiation
mitotic rate
local invasion
metastasis
A

growth rate: B -slow M - slow to rapid
mode of growth: B -expansile (blows up like a balloon), well demarcated M - expansile or infiltrative (wraps around things), poorly demarcated
differentiation: B - well differentiation M- poorly differentiated, abnormal structure
mitotic rate: B- low, normal figures M - may be high, abnormal mitotic figures
local invasion: B-absent M-present
metastasis: B-never M: occasionally

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23
Q

How are tumours generally named?

A

after the cell of origin NOT the organ that it is occurring on

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24
Q

What are some general rules for naming epithelial tumours?

A
  • “adenoma” if benign
  • “carcinoma” if malignant
  • “adenocarcinoma” if forming glandular structures
  • “papillomas” if growing outwards
  • polyps is small growths arising from mucous membrane
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25
Q

How do you name melanocytic tumours

A
  • “benign melanoma” or “melanocytoma”

- “malignant melanoma”

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26
Q

How do you name mesenchymal tumours?

A

-tumors within the connective tissue, bone, cartilage, hematopoietic cells, endothelium and muscle
-“oma” if benign
“sarcoma” if malignant

exceptions:

  • lymphoid tumors dont tend to have benign tumours so called lymphosacroma
  • in dogs with SQ tissue tumours, “soft tissue sarcoma” because locally invasive, tend to reoccur and are slow to metastasize
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27
Q

What are mixed tumours?

A
  • tumors that contain more than one tissue type (ex/ teratoma, which are neoplasms of the germ cells so it contains tissue from multiple embryonic layers)
  • if there is more than one TUMOR TYPE present within ONE organ or tissue then intermingle them (ex/ both malignant epithelial and mesenchymal neoplasms then called carcinosarcoma)
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28
Q

What needs to be included when making a tumour morphological diagnosis?

A

name of tumor (if known)
anatomic location
presence of metastasis and their locations

ex/ femoral osteosarcoma with multiple metastasis to the lung

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29
Q

What is tumorgenesis?

A

development of both benign or malignant tumours

-a process that involves the accumulation of non lethal genetic damage and altered gene expression

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30
Q

What are some characteristics that cause tumorgenesis to lead to tumor formation?

A
  1. increased production of normal proteins
  2. decreased number of normal proteins
  3. no production of normal proteins
  4. production of abnormal proteins
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31
Q

What are protooncogenes

A
  • normal genes in cells that enhance cell growth, proliferation, differentiation and function
  • ex/ growth factors, growth factor receptors, cell cycle checkpoint proteins, apoptosis inhibiting proteins
32
Q

what is oncogenes?

A
  • mutated counterparts of protooncogenes found in tumor cells
  • normally promote cell growth by:
  • increasing the numbers of genes within a cell
  • increasing production of a growth factor or its receptor
  • activating a receptor without its ligand present
  • unregulated activation of signal transducers
  • increasing the production of antiapoptotic proteins

-dominant mutations: only need one gene to have mutation in order to have the effect

33
Q

How is RAS involved in oncogenes?

A
  • RAS fxn is to signal growth factor receptors and increase cell proliferation when there is binding to the receptor
  • normally, protooncogene RAS binds to the receptor causing phosphorylation of GDP into GTP, allowing cell proliferation. Protooncogene RAS has intrinsic GTPase activity which converts GTP back to GDP, (dephospho rylation) stopping signal transduction for cell proliferation
  • with oncogene RAS, the GTPase activity is lost and the conversion back to GDP does not occur so there is continuous cell proliferation! NOTE: these cells are normal, there is just more of them
34
Q

Explain DNA damage and repair

A

-DNA damage is common and can be due to many causes
-just because DNA is damaged, doesn’t meant that there will be a DNA mutation because a cell has DNA repair enzymes that DNA repair genes control. These enzymes proofread the DAN and repair the damage found.
IF the damage is NOT repaired or it repair is incorrect or incomplete, then the damage is incorporated into the daughter cells and is “fixed” or permanent

NOTES: increased damage to DNA repair genes results in increase DNA mutations. If this damage happens in genes like oncogenes or tumor suppressor genes then tumor may form

35
Q

What are tumor suppressor genes? (TSG)

A

normal genes that inhibit cell proliferation and growth therefore they control the cell cycle (opposite of protooncogenes)

  • they act on the two important checkpoints within the cell cycle (G1:S and G2:M) to monitor if there is DNA damage. If there is DNA damage present, other genes will be activated to repair or destroy the cell with the DNA damage
  • two important TSG are p53 and retinoblastoma genes
36
Q

Describe p53

A
  • most important TSG
  • “guardian of the genome”
  • acts at G1:S and G2:M checkpoints to monitor for DNA damage.
  • if there is DNA damage then it activates:
    • p21 which will inhibit CDKs and causes cell arrest (at G1), activated GADD45 which repairs the DNA damage, and it activates BAX which promotes apoptosis if DNA damage cannot be repaired

-if DNA damage is repaired then cell can continue through the cell cycle

NOTE: If p53 isn’t functioning then there is nothing to detect DNA damage and the cell will grow as mutant cells, producing a malignant tumor

37
Q

Describe retinoblastoma gene (RB)

A
  • another cell cycle regulatory tumor suppressor gene
  • prevents DNA replication because it keeps the DNA in a coiled form. In order to replicate the DNA, it has to be unlocked from the RB gene
  • if there is a loss of function with the RB gene, then there is the production of an aggressive tumour in the eye, in both familial and sporadic forms

NOTE: this is a recessive mutation so both alleles need to be effected to get RB

38
Q

Describe the familial form of RB

A

-one of the 2 alleles from the parent (1 allele from each parent) is mutated and non functional. Therefore, if the second allele becomes mutated then the function of the entire gene is lost and a tumor develops
=> one hit

39
Q

Describe the sporadic form of RB

A

-both alleles are normal and both require a mutation before the function is lost
=> two hits

40
Q

Describe epigenetic changes

A
  • heritable changes in gene expression without DNA sequence alterations
  • most common form in cancer is DNA methylation
41
Q

Describe DNA methylation in epigentic changes

A
  • it is the addition of a methyl group in CPG islands, which prevents the transcription of the gene
  • it is a normal method of regulation of gene expression
  • if hypomethylation = increase gene activation
  • if hypemethylation = decreased gene activation
42
Q

what is imprinting?

Describe it

A
  • normal suppression of maternal or paternal allele of a gene in somatic cells by DNA methylation
  • if imprinting is lost, then there is DNA hypomethylation and both alleles become active
  • in other tumours the promoter regions of tumor suppressor cells is hypermethylated so there is decreased expression of regulatory genes
43
Q

Describe microDNA

A

-microDNA genes code for short pieces of RNA.
-they bind to complementary strands of mRNA and prevent the translation (because it is destroying it), therefore acting as gene expression regulation
-can act as oncogenes or suppressor genes:
oncogenes: if the target RNA is a TSG mRNA, then binding to it and preventing its translation will result in the prevention of product molecule being formed. there will be less TSG there fore it is acting as an oncogene
TSG: if the target RNA is from an oncogene, the microRNA will stop its function and it will act as a TSG

44
Q

What are the 3 chemical models of tumorigenesis?

A
  1. initiation
  2. promotion
  3. progression

-initiation needs to occur first and then promotion in order for a tumor to form because the promotion allows the mutated cell to proliferate. You can have a gap right after the initiation because that is permanent but the promotion is not so don’t want big gaps between them

45
Q

Describe initiation of tumorigenesis

A
  • it is the primary event
  • it irreversibly causes DNA damage from a single exposure to a carcinogen.
  • in order for it to become permanent, the cell and DNA needs to go through the cell cycle
46
Q

Describe promotion of tumorigenesis

A
  • it is a secondary event
  • it does NOT cause DNA damage but it creates an environment where mutated cells have an advantage over non mutated cells
  • it is reversible and it promotes cell proliferation
  • it needs to be applied chronically or multiple times
47
Q

Describe progression of tumorigenesis

A

-when you have an cell that goes through initiation and promotion, it is forming a preneoplastic benign tumor. progression accumulates the DNA damage and gene expression alteration until a malignant tumour forms

48
Q

What is tumor heterogeneity?

A

when a neoplasm clone is better adapted and will develop mutations that will benefit it and allow it to survive else where…compared to the original neoplasm

49
Q

Describe metastisis

A
  • happens when colonies of tumours take up residence at a location away from their original location (parent tumor)
  • only happens with malignant tumours
  • it is an important reason why treatment doesn’t work and the result is death
  • where the tumor spreads is not random…different tissues provide different environments for tumor growth so the tumor chooses where is the best. Some factors that determine the environment are particular receptors, adhesion molecules or chemokines -> some tumours express chemokine receptors on their surface so they go to locations with high amount of appropriate chemokines
50
Q

Name and describe some routes of metastasis

A
  1. transcoelomic: spread by seeding the neoplasm cells to serosal surfaces. Often has fluid accumulation; carcinomas do this
  2. Lympatic vessels: lymphatics don’t have a basement membrane so they are easier to gain access to. carcinomas do this - spread through lymphatic system. tend to spread to regional lymph nodes first
  3. Hematogenous: carcinomas spread through the vascular and lymphatic system (through the veins because they are thinner walled so easier to invade). Normally they stop at the first capillary bed that they encounter. common sites and lungs and liver
51
Q

List the steps involved in tissue invasion by the tumor

A
  1. detatchment
  2. degradation of basement membrane
  3. attachement to the basement membrane
  4. migration
52
Q

Describe what happens with detatchement

A
  • the tumor has to detach from its neighbouring cells.
  • to do so, it needs to interrupt the E cadherins which keep the cells attached.
  • the expression of E cadherin molecules is lower in carcinomas, which decreases the adhesion between the surrounding the cells and the tumor cell
53
Q

Describe what happens with degradation of the basement membrane

A
  • the tumor cells secrete proteolytic enzymes, called Type IV collagenase, which breaks down the type IV collagen in the basement membrane, providing a path for the tumor cells to follow
  • this path will help the cells move towards the blood vessels
54
Q

Describe what happens with the tumor cells attaching to the basement membrane

A

-there are multiple receptors (like laminin and fibronectin receptors) that are on the surface of the tumour cells, which allow the cells to bind to constituent components (laminin and fibronectin) of the extracellular matrix

55
Q

Describe what happens with migration

A

-fibronectin receptors on tumour cells bind to fibronectin in the ECM and migration that is induced by autocrine production of growth factor allows the tumour cells to migrate to the vessel

56
Q

Explain stroma and how it interacts with neoplasia

A
  • stroma is the non neoplastic connective tissue and blood supply that supports and supplies the neoplasm
  • they interact by exchanging signalling molecules (growth factors, cytokines and inflammatory mediators). these molecules are important for mediating growth rate, differentiation and behaviour of both cell types
  • tumours produce PDGF, which stimulate the surrounding nonneoplastic fibroblasts to increase the production of collagen, which will produce scirrhous reaction around the tumour
  • tumour like cells may also stimulate the surrounding cells to release cytokines to enhance the tumour proliferation and molity
57
Q

What is angiogensis and explain its importance with neoplasia

A
  • angiogenesis is the formation of new blood vessels
  • it is important once the tumour gets big enough so it can supply the tumour with nutrients and oxygen to help it develop
  • the tumour will secrete VEGF, which will stimulate new blood vessel production
  • the tumor will also down regulate thrombospondin, which normally suppresses the growth of new blood vessels

-normally, p53 would down regulate VEGF and up regulate thrombospondin but if p53 is absent then not only will the genetic function be altered, but blood vessel formation will be too

NOTE: the blood vessels that are formed are abnormal because they are more tortuous, dilated and more permeable than norma. this makes it easier for the tumour cells to metastasize

58
Q

what is carcinomatosis

A

when more than one carcinomas develop simultaneously but they all come from the same primary source

59
Q

how is tumour immunity different than normal immunity?

A
  • neoplastic cells are abnormal
  • the cells express proteins that are not normally expressed on the surface and they fail to express proteins that are normally expressed. => this leads to interactions with host immunity
  • it can help us Dx neoplasms earlier (ex/ PSA is increased by protstatic carcinoma. if we monitor PSA levels in blood early then we are able to detect if a tumour is developing)
60
Q

How does our innate immune system respond to tumours

A
  • NK cells and macrophages do not require antigen specific dendritic cells to destroy tumour cells
  • NK cells kill tumour cells that don’t have MHC on their surface by stimulating apoptosis in the cells
  • macrophages, when stimulated by interferon gamma (produced by T lymphocytes and NK cells) induce tumour cell destruction
61
Q

How does the acquired immune system respond to tumours?

A
  • dendritic cells get antigens from intact or dying tumour cells and link them to Class 1 or 2 MHC
  • CD8 t cells recognize MHC1 on surface of neoplastic cells
  • CD4 helper T cells recognize MHC2
  • B lymphcytes produce antibodies to tumour antigens that activate MAC
62
Q

name and describe some methods of tumours cells evading the immune system

A
  1. sarcoid down regulate MHC1 expression on their surface so that CD8 t cells are unable to destruct them
  2. down regulation of MHC2 so that it can evade CD4 t cells
  3. production of Decoy receptor 3, which induced macrophage differentiation to a type that suppresses the immune response and promotes angiogenesis. this causes apoptosis of dendritic cell (ex/ binds to Fas ligand but nothing happens)
  4. transforming growth factor a inhibits lymphocyte and macrophage proliferation
  5. destruction of T lymphocytes that express Fas ligand on their surface, inducing apoptosis
63
Q

What are some therapies that are used by the immune system to destroy tumours?

A
  1. production of monoclonal antibodies to tumour antigens
  2. toxin coupled monoclonal antibodies (toxin is bound to the tumour specific antigens)
  3. vaccination against oral melanomas in dogs
64
Q

What are some direct effects that tumours have on the host?

A
  • displacement of tissues, which can be fatal if the tissue is confined in a certain area
  • normal structures can be damaged, like rupturing the intestine
  • hemangiosarcoma on right auricle of heart
65
Q

What are some indirect effects that tumours have on host

A
  1. Cachexia
  2. Endocrinopathies
  3. hypercalcemia of malignancy
  4. skeletal abnormalities
  5. vascular and hematopoietic syndromes
  6. neurologic syndromes
  7. gastrointestinal ulceration
  8. feline pancreatic carcinoma
66
Q

Describe Cachexia

A
  • exhibit a lot of weight loss, with a loss of both muscle and fat
  • happens because of anorexia, impaired digestion of nutrients, increased metabolic demands because of the tumor, nutrient loss
  • increasing the calorie intake will not do the trick
67
Q

Describe Endocrinopathies

A
  • tumours in the endocrine organs produce normal hormones but the hormone production is not controlled
  • ex/ excess thyroid hormone production (hyperthyroidism) or excess cortisol production (from pituitary or adrenal tumour)
  • ex/ pheochromocytoma - increased release of epinephrine in an uncontrolled way. causes high HR, excited behaviours
68
Q

Describe hypercalcemia of malignancy

A
  • syndrome produces a parathyroid hormone related protein (PTH-Pr), which has identical effects to PTH
  • it is produced by lymph sarcomas and apocrine gland adrencarcinomas of the anal sac
  • hypercalcemia produced because there is increased Ca release and reabsorption from the bones and intestine, respectively and increased reabsorption from the kidneys
  • clinical signs include muscle weakness, cardiac arrythmias, anorexia, vomiting, renal failure
69
Q

describe skeletal abnormalilties

A
  • hypertrophic osteopathy -> periosteal new growth associated with thoracic masses
  • excessive bone growth production on long bones
70
Q

describe vascular and hematopoietic syndromes

A
  • increased levels of eosinophils and neutrophils in the blood (in non hematopoietic cancers)
  • anemia of chronic diseases - over time become anemic because of the decreased bone marrow production because of the tumours
  • erythrocytosis with renal cancers because abnormal production of erythropoietin
  • thrombocytopenia can be common in tumours because of DIC
  • hyperviscoscity of blood leading to platelet dusfunction, CHF and neurological signs because of excessive immunoglobulin production. seen with plasma cell sarcomas
71
Q

Describe Neurologic syndromes

A

-ex/ myasthenia gravis causes nerve transmission failure and leads to weakness and dysphagia

72
Q

describe gastrointestinal ulceration

A
  • associated with histamine release from mast cell tumour granules
  • histamine induces increased gastric acid production from parietal cells. this in combination with vascular damage produces gastric ulceration
73
Q

Describe feline pancreatic carcinomas

A
  • with liver metastasis
  • sometimes associated with alopecia
  • tends to be symmetrical alopecia of limbs and ventrums caused by excessive grooming, which also removes the stratum corneum causing it to have a glistening skin appearance
  • assocaited with pancreatic carcinomas
74
Q

Name and briefly describe some diagnostic methods

A
  1. histopathology (H and E staining)
  2. special stains are used to highlight features of certain tumours to help determine what type of tumour it is
  3. immunohistochemistry -expression of antigens help identify type of timor
  4. PCR
75
Q

explain tumour grading

A
  • used after you identify what type of tumor it is
  • helps to classify the tumour to help predict its behaviour
  • usually used with soft tissue sarcomas and mast cell tumours
  • grade 1 - most differentiates, best prognosis
  • grade 3 - least differentiated, poor prognosis
76
Q

Explain tissue staging

A

-indication of how large the tumour is and how far it spread
-helps form a therapeutic plan and assist in determining the prognosis
-TNM :
size of tumour (T)
lymph node involvement (N)
presence of metastasis (M)

77
Q

Explain surgical margins

A
  • used to see if you have removed all of the tumour (excisional biopsy)
  • see if surgical margins are clean or dirty. if they are dirty then they are for sure dirty but if they are clean then it doesn’t mean that they are for sure clean because you can’t test the whole tissue sample because it would take forever

Gen Path (10 decks)

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