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
what are two enabling characteristics of cancer
genome instability and mutation tumor promoting inflammation
26
oncogenes are __________ in cancers whereas TSGs are _____________in cancers
activated; inactivated
27
oncogenes
mutated genes that produce proteins with increased growth stimulatory or cell survival functions
28
tumor suppressor genes
genes typically involved in genomic stability and apoptosis, or that counteract oncogenes, that become mutated
29
what is c-kit
a membrane receptor for growth factors; targeted in some cancer therapies
30
what are two examples of oncogenes
mutated c-kit; mutated tyrosine kinase receptors
31
Herceptin (Trastumuzab) targets
ErbB2 receptor (tyrosine kinase)
32
Lapatinib targets
downstream tyrosine phosphorylation of the ErbB2 receptor
33
T/F oncogenes may undergo translocations to become activated
T
34
what is the classic example of oncogene translocations in cancer
chronic myeloid/myelogenous leukemia (CML)
35
what goes Gleevec (imatinib) target (3)
tyrosine kinase domain of abl, c-kit, and PDGF-R
36
what is a classic tumor suppressor gene product
p53 (involved in cell cycle checkpoints and initiation of apoptosis)
37
patients with DNA mismatch repair defects are susceptible to
colon polyps -> cancer
38
how does heterozygosity play a role in oncogenesis
if people are born heterozygous for a TSG allele and then lose that copy, they are more prone to progress to malignancy
39
how does PTEN work as a TSG
it dephosphorylates tyrosine kinase receptors (ex. c-Met), which inhibits downstream signalling
40
what is a key factor for combating colon carcinogenesis
remove the polyp before it becomes malignant; if malignant you will leave cells behind
41
transition of a large colon adenoma to a carcinoma is mediated by what molecular factor
p53 mutation and loss of 18q
42
___________heterogeneity leads to ____________ heterogeneity
genotypic; phenotypic
43
heterogeneity leads to what practical problems (4)
diagnostic markers chemotherapeutic regimens (drug resistance) mutation-specific drugs evasion of immune system
44
how can we identify poorly differentiated tumors? how can this be a problem?
immunohistochemistry; can be an issue if the tumor is heterogeneous for expression of markers
45
what is an endothelial cell marker
CD31
46
what are the two ways that cancer cells can sustain proliferative signalling
1. do not require GF for signalling 2. make their own GF
47
what is a marker for cancer stem cells
CD133
48
T/F tumours require cancer stem cells to form a new tumour
T
49
what are 2 key factors that make cancer stem cells hard to treat
1. low proliferation rate 2. low uptake of drugs Consequence: drug and radiation resistant
50
T/F cancer stem cells express unique stem cell markers
F; often express normal markers
51
how can giving anti-oxidants actually increase the incidence of cancer
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
most cancer mortality is due to
metastasis
53
T/F for some cancers there are primary tumor gene expression signatures that can predict their likelihood to metastasize
T
54
what is the term for spread into body cavities by entering the pleural, peritoneal, pericardial or subarachnoid spaces
transcelomoic
55
what are the 8 steps in the metastatic cascade
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
why is inflammation associated with cancer (4)
1. cytokines 2. angiogenic factors 3. high proliferation 4. produce ROS - predisposes to mutation
57
how do cancer cells avoid immune destruction (3)
1. stop producing antigen in a subset of cells (immuno-editing) 2. mutate or stop expressing MHC 3. produce immunosuppressive cytokines
58
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
- decreases - increases - increases - decreases - increases - increases
59
what are 4 oncogenic viruses
papillomaviruses herpesviruses hepadnaviruses retroviruses
60
avian leukosis virus causes
bursa lymphoma
61
marek's disease (herpesvirus) causes
lymphoma infiltrate in liver
62
T/F there can be transmission of live neoplastic cells
T (can occur in tasmanian devils, in dogs)
63
T/F after a tumor has undergone treatment, it cannot be reliably graded but can be reliably staged
F; cannot be reliably graded OR staged