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Veterinary Pathology > Post Term Test 2 - Cancer > Flashcards

Post Term Test 2 - Cancer Flashcards

1
Q

how do neoplastic cells BEHAVE BADLY (6)

A

expansion
tissue injury
pain
invasion
metastasis
secretion

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2
Q

Hyperplastic vs Benign vs Malignant - Cellular Differentiation

A

Hyperplastic: normal gradient/cells
Benign: usually well differentiated
Malignant: poorly differentiated, anaplastic

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3
Q

Hyperplastic vs Benign vs Malignant - Mitotic Activity

A

Hyperplastic: variable; typically low
Benign: usually low
Malignant: often high

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4
Q

Hyperplastic vs Benign vs Malignant - Rate of growth/Reversible or irreversible

A

Hyperplastic: reversible
Benign: slow, irreversible
Malignant: rapid, irreversible

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5
Q

Hyperplastic vs Benign vs Malignant - Necrosis

A

Hyperplastic: none
Benign: usually minimal
Malignant: often high

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6
Q

Hyperplastic vs Benign vs Malignant -Tissue demarcation

A

Hyperplastic: blends with normal
Benign: expansive, discrete
Malignant: poorly demarcated; locally invasive

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7
Q

Hyperplastic vs Benign vs Malignant - Heterogeneity

A

Hyperplastic: none
Benign: minimal
Malignant: more

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8
Q

Hyperplastic vs Benign vs Malignant - Aneuploidy

A

Hyperplastic: none
Benign: low
Malignant: more

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9
Q

Hyperplastic vs Benign vs Malignant - paraneoplastic syndrome

A

Hyperplastic: none
Benign: variable
Malignant: variable

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10
Q

Hyperplastic vs Benign vs Malignant - recurrence after removal

A

Hyperplastic: none
Benign: rare
Malignant: frequent

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11
Q

Hyperplastic vs Benign vs Malignant - Propensity to progress if not removed

A

Hyperplastic: none
Benign: low
Malignant: high

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12
Q

name some examples of local injury

A

ulceration, infection, perforation, hemmorrhage, nerve damage, restricted motion

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13
Q

T/F invasion and local spread is always malignant

A

T

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14
Q

what is one way that cancerous cells can change phenotype and why is it beneficial

A

epithelial to mesenchymal -> the latter has fewer cell-cell junctions/contact inhibition and more ECM matrix adhesion/protease expression -> better invasion

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15
Q

what is the fertile soil concept of tumor metastasis

A

going from one region of the organ to another because it can grow well there (ex. from one ovary to the other via the peritoneal cavity)

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16
Q

Uterine carcinoma tends to produce what characteristic that can be appreciated grossly

A

Secretes growth factors (ex. TGFβ) that induce fibrosis; tumors are schirrhous

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17
Q

what is paraneoplastic syndrome

A

when tumours produce excessive amounts of functional proteins in an unregulated manner (think endocrine disease-causing tumours)

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18
Q

what is elevated with some paraneoplastic syndromes and can indicate neoplasia

A

elevated Ca2+

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19
Q

What underpins neoplastic behaviour on a molecular level (7)

A
  • activated oncogenes
  • functional harmful molecules
  • matrix proteinases
  • angiogenic factors
  • ECM factors (ex. TGFβ -> scarring)
  • cell adhesion molecules
  • resistance factors
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20
Q

T/F necrotic tumors are easier to kill than non-necrotic tumours

A

F

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21
Q

a tumor that outgrew its own blood supply takes on what gross appearance

A

umbilicated; has a central, red depression

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22
Q

name two examples of angiogenic growth factors

A

VEGF, bFGF

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23
Q

Sutent (Sunitinib) does what

A

inhibits angiogenesis

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24
Q

what are the 6 hallmarks of cancer

A

sustained proliferative signalling
evade growth suppressors
activate invasion and metastasis
evade cell death
induce angiogenesis
enable replicative immortality

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25
Q

what are two enabling characteristics of cancer

A

genome instability and mutation
tumor promoting inflammation

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26
Q

oncogenes are __________ in cancers whereas TSGs are _____________in cancers

A

activated; inactivated

27
Q

oncogenes

A

mutated genes that produce proteins with increased growth stimulatory or cell survival functions

28
Q

tumor suppressor genes

A

genes typically involved in genomic stability and apoptosis, or that counteract oncogenes, that become mutated

29
Q

what is c-kit

A

a membrane receptor for growth factors; targeted in some cancer therapies

30
Q

what are two examples of oncogenes

A

mutated c-kit; mutated tyrosine kinase receptors

31
Q

Herceptin (Trastumuzab) targets

A

ErbB2 receptor (tyrosine kinase)

32
Q

Lapatinib targets

A

downstream tyrosine phosphorylation of the ErbB2 receptor

33
Q

T/F oncogenes may undergo translocations to become activated

A

T

34
Q

what is the classic example of oncogene translocations in cancer

A

chronic myeloid/myelogenous leukemia (CML)

35
Q

what goes Gleevec (imatinib) target (3)

A

tyrosine kinase domain of abl, c-kit, and PDGF-R

36
Q

what is a classic tumor suppressor gene product

A

p53 (involved in cell cycle checkpoints and initiation of apoptosis)

37
Q

patients with DNA mismatch repair defects are susceptible to

A

colon polyps -> cancer

38
Q

how does heterozygosity play a role in oncogenesis

A

if people are born heterozygous for a TSG allele and then lose that copy, they are more prone to progress to malignancy

39
Q

how does PTEN work as a TSG

A

it dephosphorylates tyrosine kinase receptors (ex. c-Met), which inhibits downstream signalling

40
Q

what is a key factor for combating colon carcinogenesis

A

remove the polyp before it becomes malignant; if malignant you will leave cells behind

41
Q

transition of a large colon adenoma to a carcinoma is mediated by what molecular factor

A

p53 mutation and loss of 18q

42
Q

___________heterogeneity leads to ____________ heterogeneity

A

genotypic; phenotypic

43
Q

heterogeneity leads to what practical problems (4)

A

diagnostic markers
chemotherapeutic regimens (drug resistance)
mutation-specific drugs
evasion of immune system

44
Q

how can we identify poorly differentiated tumors? how can this be a problem?

A

immunohistochemistry; can be an issue if the tumor is heterogeneous for expression of markers

45
Q

what is an endothelial cell marker

A

CD31

46
Q

what are the two ways that cancer cells can sustain proliferative signalling

A
  1. do not require GF for signalling
  2. make their own GF
47
Q

what is a marker for cancer stem cells

A

CD133

48
Q

T/F tumours require cancer stem cells to form a new tumour

A

T

49
Q

what are 2 key factors that make cancer stem cells hard to treat

A
  1. low proliferation rate
  2. low uptake of drugs

Consequence: drug and radiation resistant

50
Q

T/F cancer stem cells express unique stem cell markers

A

F; often express normal markers

51
Q

how can giving anti-oxidants actually increase the incidence of cancer

A

cancer cells produce high ROS, which can kill them; antioxidants produced by the cell deal with this but only partially balance the oxidative stress, which means the cancer cells survive and have more ROS-mediated mutagenic events

52
Q

most cancer mortality is due to

A

metastasis

53
Q

T/F for some cancers there are primary tumor gene expression signatures that can predict their likelihood to metastasize

A

T

54
Q

what is the term for spread into body cavities by entering the pleural, peritoneal, pericardial or subarachnoid spaces

A

transcelomoic

55
Q

what are the 8 steps in the metastatic cascade

A
  1. detach (from primary tumor)
  2. invade (local stroma)
  3. intravasate (go into local lymphatics/bvs)
  4. survive (in circulation)
  5. arrest (in capillaries or venules)
  6. extravasate (go into parenchyma)
  7. adapt to or subvert (environment)
  8. proliferate (to form new tumor)
56
Q

why is inflammation associated with cancer (4)

A
  1. cytokines
  2. angiogenic factors
  3. high proliferation
  4. produce ROS - predisposes to mutation
57
Q

how do cancer cells avoid immune destruction (3)

A
  1. stop producing antigen in a subset of cells (immuno-editing)
  2. mutate or stop expressing MHC
  3. produce immunosuppressive cytokines
58
Q

list whether the following factors increase or decrease the risk of cancer:
- decreasing age
- high calorie, low fibre diets
- obesity
- reproductive status (spayed/neutered)
- exposure to chemical carcinogens
- ionizing and UV radiation

A
  • decreases
  • increases
  • increases
  • decreases
  • increases
  • increases
59
Q

what are 4 oncogenic viruses

A

papillomaviruses
herpesviruses
hepadnaviruses
retroviruses

60
Q

avian leukosis virus causes

A

bursa lymphoma

61
Q

marek’s disease (herpesvirus) causes

A

lymphoma infiltrate in liver

62
Q

T/F there can be transmission of live neoplastic cells

A

T (can occur in tasmanian devils, in dogs)

63
Q

T/F after a tumor has undergone treatment, it cannot be reliably graded but can be reliably staged

A

F; cannot be reliably graded OR staged

Veterinary Pathology (7 decks)

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