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Z MD1 Respiratory block > Cancer > Flashcards

Cancer Flashcards

1
Q

How do tumour cells degrade ECM

A

secrete metaloproteases to break down collagen

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2
Q

what treatments target the tumour cells genome instability and mutation

A

PARP inhibitors

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2
Q

Staging system of tumours

A

TNM T - T0-T4 = indicates increasing size and/or local extent of the primary tumour N - N0-N3 = regional lymph node metastases M - Mo-M1 = absence or presence of distant metastases X - unable to be assessed or unknown

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3
Q

the tumours microenvironment is important for what?

A
  • important for establishment and growth of metastases
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3
Q

how do mutations in cells occur for cancer

A
  • carcinogenic agents: microbes, radiation, chemicals - inherited - normal mistakes in normal DNA replication that is not repaired - sustained cell proliferation from any cause can increase risk
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3
Q

once a diagnosis of malignancy is made, we need to know what extra stuff?

A

specific tumour type and subtype (cell lineage) grade stage presence of lymphovascular invasion

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4
Q

What is the general function of p53

A

regulates the expression of cell cycle factors (the guardian of the genome)

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5
Q

what histological feature is typical of epithelial tumours

A

keratinization

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5
Q

a mutation in an oncogene leads to

A

uncontrolled accerlerated growth

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5
Q

What does p53 specifically do?

A

Responds to mutations/cellular stress and directs the cell to: - undergo apoptosis - arrest cell cycle - DNA repair - differentiation - sequescence

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5
Q

mechanisms that regulate TSG expression

A
  • miRNA - methylation
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5
Q

What treatment targets the replicative immortality of tumour cells

A

Telemoerase inhibitors

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6
Q

death often results from malignant tumour due to:

A
  • cachexia - secondary infection related to poor nutrition, effects of treatment - damage to vital organ or system by either primary or secondary tumour
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7
Q

What class of genes are BRCA1 and BRCA2

A

DNA repair genes

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7
Q

Difference between mutation and polymorphisms

A

Mutation - change in DNA away from normal (rare and abnormal varient) Polymorphism - sequence variation that is common in the population (no single allele is recognised as the standard sequence)

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7
Q

Telomeres and cancer?

A

Some tumour cells reactivate telomerase - thus starving off mitotic catastrophe and achieving immortality

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8
Q

definition of neoplasia

A

excessive and unregulated cell proliferation

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8
Q

adeno: squamous: leiomyo: osteo:

A

adeno: glandular squamous: squamous cell Leiomyo: Smooth muscle Osteo: osteoblastic

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8
Q

Questions you must ask yourself when diagnosing a lesion

A

Neoplastic or non-neoplastic Begnign or malignant Epithelial, mesenchymal? Primary versus metastatic

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9
Q

which cancers can lead to inappropriate ADH syndrome

A

SCC

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9
Q

how can lung cancer predispose to lung infection

A

cancer blocks the bronchus –> leading to pneumonia, collapse or bronchiectasis in the distal lung as you cannot clear the alveoli

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10
Q

what is the difference between histopathology and cytology

A

cytology - don quite see the relationship between cells as easily

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12
Q

6 main hallmarks of cancer

A
  • sustaining proliferative signaling - evading growth suppressors - activating invasion and metastasis - enabling replicative immortality - inducing angiogenesis - resisting cell death
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12
Q

What treatments target the tumour cell resistance of cell death

A

pro-apoptotic BH3 mimetics

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13
Q

At what stage of tumour growth is the rate of growth the fastest

A

when the tumour is vascularised but with no necrosis

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13
Q

main types of lung cancer in order

A

adenocarcinoma, Small cell carcinoma, squamous cell carcinoma, large cell carcinoma

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15
Q

where does neoplasia normally start?

A

in stem cells or progenitor cells

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17
Q

suffix for a benign tumour

A

oma

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17
Q

what is a premalignant lesion?

A

cells that are not yet malignant but there is a reasonable chance of them becoming malignant

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18
Q

how do cancer cells evade apoptosis

A
  • reduced CD95 level (Fas receptor) - inactivation of death-induced signaling complex by FLICE protein - up-regulation of BCL2 - reduced levels of pro-apoptotic BAX resulting from loss of p53 - loss of APAF-1 - upregulation of inhibitors of apoptosis
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20
Q

mutations that cause cancer occur in which types of genes (broadly)

A

cell proliferation apoptosis DNA repair

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20
Q

definition of a malignant tumour

A

locally invasive, destructive growth, often poorly circumscribed

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20
Q

which cancers can lead to hypoglycaemia

A

ovarian cancer fibroma

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21
Q

EGFR mutations are particularly present in which population

A

young, non or light smoking female Asians with low-stage disease

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22
Q

What treatment targets the sustained proliferative signalling of tumour cells

A

EGFR inhibitors

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24
Q

What are the 2 hallmarks of emerging tumour development

A

deregulating cellular energetics Avoiding immune destruction

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25
Q

What are the 2 characteristics enabling tumour formation

A

Genome instability and mutation Tumour-promoting inflammation

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27
Q

main defining features of a benign tumour

A
  • well circumscribed - local - usually well differentiated cells (look similar to mature cells) - unable to metastasise
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28
Q

Leading cancer that causes death in Victoria

A

Lung cancer

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29
Q

alternative names for premalignant lesion

A

dysplasia intraepithelial neoplasia

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29
Q

What are the oncogenic factors that can result in abnormal cell proliferation

A

the growth factor The receptor The proteins involved in signal transduction Cell cycle regulators

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31
Q

what does anaplastic mean

A

completely undifferentiated cell

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33
Q

examples of TSGs

A

P53 Rb APC PTEN

35
Q

common sites of metastases

A

brain, liver, lung, colon

37
Q

how does metastases spread

A
  • lymphatics - haematogenous - transcoelomic (along pericardial, pleural or peritoneal cavities)
37
Q

What is a homogenous stained region of a chromosome

A

Where there is many copies of the same gene on one chromosome leading to amplification of the expressed protein

37
Q

order of the histopathological changes seen up until invasive lung carcinoma

A
  • goblet cell hyperplasia - reserve cell hyperplasia - squamous metaplasia - squamous dysplasia - carinoma in situ - invasive carcinoma
38
Q

clinical presentation of lung tumour

A

Cough Haemoptysis Wheeze Dyspnoea Pneumonia Pancoasts syndrome

40
Q

a mutation in a TSG leads to

A

Uncontrolled continuous growth

40
Q

histopathological features of squamous cell carcinoma

A

shows stratified squamous and keratinized whirls, often with a lot of eosinophilic cytoplasm

41
Q

how is grading of a tumour decided

A

determined by the extent to which the tumour cells resemble their normal counterparts histologically (well differentiated, moderately differentiated, poorly differentiated, aplastic)

42
Q

histopathological features of adenocarcinoma

A

cells try and form a lumen like gland

43
Q

function of shortened teleomeres

A

eventually activate cell cycle checkpoings, leading to senescene and placing a limit on the number of divisions a cell may undergo

44
Q

what does tumour stroma consist of?

A

fibroblasts, ECM, endothelial cells, immune cells, soluble molecules

44
Q

definition of loss of heterozygosity

A

loss of normal function of one allele of a gene in which the other allele was already inactivated

45
Q

Function of miRNA

A

Non coding ss RNA that function as negatie regulators of genes

47
Q

main defining features of a malignant tumour

A
  • frequently induce desmoplasia in stroma as they invade - sometimes necrosis (from tumour outgrowing blood supply) - variable differentiation: well, moderate, poor or anaplastic - potential to metastasise
48
Q

what do traditional chemotherapy drugs aim to do

A

interfere with cell division - including normal cells

49
Q

features of cytological atypia

A
  • larger nuclei - pleomorphic nuclei - coarser nuclear chromatin - hyperchromatic nuclei - larger more prominent nucleoli - more mitotic activity with abnormal mitotic figures
51
Q

definition of a benign tumour

A

local expansile, generally slow growing, often (not always) well circumscribed (+- encapsulated)

52
Q

Definition of oncogene

A

mutant versions of proto-oncogenes that function autonomously without requirements for normal growth-promoting signals

53
Q

Which hormone imbalance leads to cushings syndrome

A

ACTH

55
Q

Definition of proto-oncogene

A

Normal cellular genes whose products promote cell proliferation

56
Q

histopathological features of small cell carcinoma

A

cells are small (not particularly pleomorphic), very different looking to normal cancer cells

57
Q

what do targeted therapies for cancer do?

A

block the growth of cancer cells by interfering with the function of specific molecules resulting from genetic alterations that drive carcinogenesis and tumour growth

58
Q

which cancers can lead to hypercalcaemia

A

SCC breast carcinoma renal cell carcinoma adult T cell leukaemia/lymphoma

60
Q

histopathological features of neoplasia

A

cytological atypia and architectural disorganisation

61
Q

what histological feature is typical of adenocarcinoma

A

cells trying to form lumina (look like glands)

62
Q

2 ways cytology can be gained

A

fine needle aspiration exfoliative cytology

63
Q

what does staging incorporate

A
  • the size or depth of invasion - local extent of primary tumour and location - extent of metastases
64
Q

2 specific mutations that lead to non-small cell carcinomas (primarily adenocarcinoma)

A

EGFR ALK

66
Q

definition of dysplasia

A

abnormality of development, alteration in size, shape and organisation of cells

67
Q

What is the cause for familial predisoposition to developing tumours

A

the individual inherits one defective copy of TSG and loose the second one through somatic mutation

68
Q

small cell carcinoma is an example of what

A

neuroendocrine carcinoma

70
Q

what is the cause for familial retinoblastoma

A

Germiline mutation of one allele of the retinoblastoma (RB1) gene, and a mutation of the other allele later gives rise to clinical cancer at very young age

71
Q

What are the 4 classes of normal regulatory genes that are the prinicpal targets of genetic damage leading to tumour formation

A

-growth promoting proto-oncogenes - growth-inhibiting tumour suppressor genes - genes that regulate programmed cell death - genes involved in DNA repair

72
Q

factors secreted by tumour cells to allow angiogenesis

A

VEGF

73
Q

what treatments target angiogenesis of tumour cells

A

inhibitors of VEGF signalling

74
Q

macroscopic look of lung carcinoma

A

pale mass, irregular, may be associated with a bronchus, may be necrotic

75
Q

suffixes for a malignant tumour

A

carcinoma: epithelial sarcoma: mesenchymal

76
Q

definition of oncoproteins

A

proteins encoded by oncogenes

77
Q

which cancers can lead to polycythaemia

A

renal carcinoma hepatocellular carcinoma

79
Q

main cancers of paediatrics

A
  • certain leukemias - certain brain tumours - neuroblastoma - Wilm’s tumor - certain lymphos - rhabdomyosarcoma - retinoblastoma - certain bone cancers
80
Q

what treatment targets the deregulating cellular energetics of tumour cells

A

Aerobic glycolysis inhibitors

82
Q

Number of alleles needed to be affected with oncogenes and TSGs

A

Oncogenes - only 1 allele needs to be mutated TSG - both alleles need to be mutated

83
Q

2 main categories of targeted therapy for cancer

A
  • small molecules that inhibit growth factor Rs or tyrosine kinase - monoclonal antibodies that target specific proteins or receptors
84
Q

What treatment targets the activation of invasion and metastasis

A

inhibitors of HGF/c-Met

85
Q

How does bone pain occur from metastases

A

Related to hypercalcaemia

86
Q

What treatment targets the tumour promoting inflammation

A

selective anti-inflammatory drugs

87
Q

which hormone imbalance leads to hypoglycaemia in cancers

A

insulin

88
Q

which cancers can lead to Cushing’s sundrome

A

SCC pancreatic cancer

89
Q

How many of the major classes of normal regulatory genes need to be involved in the initation of a tumour

A

All 4 in most cases

90
Q

Staging of a tumour cell refers to

A

the progression of the malignancy in terms of local spread and metastasis

91
Q

Types of mutations involved in cancer

A
  • errors in DNA replication not repaired - point mutations - amplification of oncogenes - chromosomal rearrangements
93
Q

what is does the grade refer to in malignant tumours

A

the differentiation of the cells within the tumour

94
Q

a grade 3 tumour usually refers to

A

in situ carcinoma

96
Q

Examples of oncogenes

A

Her2-neu Ras Myc

97
Q

4 things that need to occur for metastasis

A
  1. Detachment of tumour cells from each ther 2. Degradation of ECM 3. Attachment to novel ECM components 4. Migration of tumour cells
98
Q

What treatment targets the evasion of growth suppression of tumour cells

A

cyclin-dependent kinase inhibitors

99
Q

when are polyps associated with cancer

A

glandular dysplastic lesions arising from lining epithelial often form polyps

100
Q

how does EGFR mutation predispose you to non small cell carcinoma

A

increase the EGFR tyrosine kinase domain activity leading to hyperactivation of downstream signalling pathways

102
Q

How can polymorphisms increase the risk of cancer

A

May be associated with differences in cell response to cytotoxicity due to changes in how much of the SNPd protein is expressed, or a change in its stability

103
Q

What treatment targets tumour cell immune destruction avoidance

A

anti-CTLA4 mAb

104
Q

Which hormone imbalance leads to hypercalcaemia in cancers

A

PTH related protein

105
Q

histopathological features of large cell carcinoma

A

large atypical cells, sheets of atypical cells which are not differentiated (no keratinization, glands, mucus), but still epithelial

106
Q

grading of dysplasia

A

mild,moderate or severe 1, 2 or 3

107
Q

which hormone imbalance leads to polycythaemia in cancers

A

erythropoeitin

Z MD1 Respiratory block (11 decks)

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