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principles of disease > tumour pathology week 6 > Flashcards

tumour pathology week 6 Flashcards

1
Q

what is aetiology

A

what causes disease

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2
Q

what is pathogenesis

A

how a disease develops and progresses

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3
Q

what is neoplasia

A

the uncontrolled, abnormal growth of cells or tissues in body

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4
Q

what is classification of tumours based on

A
  • tissue of origin

- benign vs. malignant

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5
Q

nomenclature of epithelial tumours

A 
glandular
benign: adenoma
malignant: adenocarcoma
squamous
benign: squamous papilloma 
malignant: squamous carcinoma
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6
Q

nomenclature of connective tissue tumours

A 
bone
benign = osteoma
malignant = osteosarcoma 
fat 
benign = lipoma
malignant - liposarcoma 
fibrous tissue 
benign = fibroma
malignant = fibrosarcoma
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7
Q

nomenclature of tumours of blood cells

A

white blood cells
malignant = leukaemia
- no known benign tumours of WBC
- no known tumours of red blood cells

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8
Q

nomenclature of tumours of lymphoid tissue

A

malignant = lymphoma

- no known benign tumours of lymphoid tissue

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9
Q

nomenclature of tumours of melanocytes

A 
benign = naevus 
malignant = melanoma
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10
Q

nomenclature of neural tissue

A

central nervous system = astrocytoma

peripheral nervous system = shwannoma

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11
Q

nomenclature of germ cells tumours

A
  • germ cells (testes/ovaries)
  • teratomas
  • tumour can be composed of various tissue because they are stem cells
  • ovarian teratomas usually benign
  • testicular teratomas usually malignant
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12
Q

what are some features of benign tumours

A
  • non-invasive growth pattern
  • usually encapsulated
  • no evidence of invasion
  • no metastases
  • cells similar to normal
  • ‘well differentiated’
  • function similar to normal tissue
  • rarely cause death
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13
Q

what are some features of malignant tumours

A
  • invasive growth pattern
  • no capsule or capsule breached by tumour cells
  • cells abnormal
  • ‘poorly differentiated’
  • loss of normal function
  • often evidence of spread of cancer
  • frequently cause death
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14
Q

what are some properties of cancer cells

A
  1. loss of tumour suppressor genes (BRCA1, Rb)
  2. gain of function of oncogenes (B-raf, cyclin D1)
  3. altered cellular function
  4. abnormal morphology
  5. cells capable of independent growth
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15
Q

what happens to cellular function in cancer

A
  • loss of cell to cell adhesion
  • altered cell to cell matrix adhesion
  • production of tumour related proteins
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16
Q

what are tumour biomarkers

A
  • any properties of cancer cells that can be exploited clinically
  • Onco-foetal proteins (present in foetus, switched off post natal, switched on again in tumours), oncogenes, growth factors and receptors, immune checkpoint inhibitors
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17
Q

what are some examples of clinically useful predictive biomarkers

A 
Kras = colorectal cancer 
Braf = melanoma
EGFR = lung cancer 
PD-L1 = lung cancer 
Her2 = breast cancer, gastric cancer
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18
Q

what is morphology of cancer

A
  • histology of cancer
  • cellular and nuclear pleomorphism
  • mitoses present and often abnormal
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19
Q

what is tumour growth a balance of

A
  • cell growth and cell death

- angiogenesis and apoptosis

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20
Q

what is tumour angiogenesis

A
  • new blood vessel formation by tumours
  • required to sustain tumour growth
  • provides route for release of tumour cells into circulation
  • more blood vessels in a tumour = poorer prognosis
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21
Q

what is apoptosis

A
  • mechanism of programmed single cell death
  • active cell process
  • regulates tumour growth
  • involved in response to chemo and radio therapy
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22
Q

how does metastasis begin

A
  • increased matrix degradation by proteolytic enzymes

- altered cell-to-cell and cell-to-matrix adhesion

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23
Q

what are the modes of spread of cancer

A
  1. local spread (spread into adjacent structures, invasion)
  2. lymphatic spread
  3. blood spread
  4. trans-coelomic spread (through body cavities)(lung, stomach, colon and ovary cancers)(e.g. pleural or peritoneal cavities)
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24
Q

what does site of metastasis depend on

A
  • doesn’t depend on blood flow
  • depends on both tumour and tissue related factors
  • metastatic niche
25
Q

what are some common sites of metastasis

A
  • liver
  • lung
  • brain
  • bone (axial skeleton)
  • adrenal gland
  • omentum(layer of adipose tissue in abdomen)/peritoneum(tissue that lines abdominal walls)
26
Q

what are some uncommon sites of metastasis

A
  • spleen
  • kidney
  • skeletal muscle
  • heart
27
Q

where do breast tumours normally metastasise to

A

bone

28
Q

where does prostate cancer normally metastasise to

A

bone

29
Q

where does colorectal cancer normally metastasise to

A

liver

30
Q

where does ovarian cancer noramally metastasise to

A

omentum(layer of adipose tissue in abdomen)/peritoneum(tissue that lines abdomen)

31
Q

what are the local effects of benign tumours

A
  • pressure

- obstruction

32
Q

what are the local effects of malignant tumours

A
  1. pressure
  2. obstruction
  3. tissue destruction - ulceration/infection
  4. bleeding - anaemia, haemorrhage
  5. pain - pressure on nerves, perineurial infiltration (tumour infiltrates along nerves), bone pain from pathological fractures
  6. effects of treatment
33
Q

what are the systemic effects of malignant tumours

A
  1. weight loss - cancer cachexia
  2. secretion of hormones - normal (e.g. tumour in gland secreting), abnormal/inappropropriate (tissue that doesn’t normally secrete is secreting)
  3. paraneoplastic syndroms
  4. effects of treatment
34
Q

what is dysplasia

A
  • pre-malignant change
  • earliest change in the process of malignancy that can be visualised
  • identified in epithelium
  • no invasion
  • can progress to cancer
35
Q

what are some features of dysplasia

A
  1. disorganisation of cells - increased nuclear size, increased mitotic activity, abnormal mitoses
  2. grading of dysplasia - high/low (high = more risk in shorter time)
  3. no invasion
36
Q

an adenoma is what type of tumour

A

benign tumour of glandular epithelium

37
Q

an adenocarcinoma is what type of tumour

A

malignant tumour of glandular epithelium

38
Q

what are the phases of the cell cycle

A
  • G1
  • S
  • G2
  • mitosis
39
Q

what can result in G1 arrest

A
  • inadequate nutrient supply
  • external stimulus lacking
  • abnormal cell size
  • DNA damage detected
40
Q

what can result in G2 arrest

A
  • abnormal cell size

- DNA damage detected

41
Q

what can result in S phase arrest

A

DNA not replicated

42
Q

what can result in M phase arrest

A

chromosome misalignment

43
Q

how are cyclin-dependent kinases activated

A

by cyclins to form CDK/cyclin complex

44
Q

what do CDK/cyclin complexes do

A
  • different CDK/cyclin complexes operate at sequential stages of the cycle
  • active CDK/cyclin complexes phosphorylate target proteins
  • phosphorylation results in the activation/inactivation of these proteins
  • substrates of these proteins regulate events in the next cycle phase
45
Q

what does INK4A do in cell cycle

A
  • is it a CDK inhibitor
  • binds to CDK
  • includes p16, p14
  • p16INK4A arrests the cell cycle in G1
  • p14 prevents p53 degradation
46
Q

what is CIP/KIP

A
  • CDK inhibitor
  • includes p21, p27 and p57
  • halt cell cycle in G1
  • deactivate CDK/cyclin by binding
47
Q

what does the retinoblastoma gene do

A

enodes a 110 kDa phosphoprotein (pRb) expressed in almost every human cell

48
Q

what does pRb do

A

in the hypo-(non)-phosphorylated (active) state, pRb is active and carries out its role as tumour suppressor by binding to E2F (a signal for cell cycle activation) and therefore this inhibits the cell cycle
- when pRb is phosphorylated it loses affinity to E2F

49
Q

what does p53 do

A
  • in G1 if there is DNA damage p53 arrests cell cycle and induces repair and if that doesn’t work then apoptosis
50
Q

what does mutated p53 do

A

does not arrest G1 or repair damaged DNA

51
Q

what is intra-epithelial neoplasia

A

A condition in which abnormal cells are found on the surface of or in the tissue that lines an organ, such as the prostate, breast, or cervix.

52
Q

what environmental agents can cause carcinogenesis

A
  • chemicals
  • radiation
  • oncogenic viruses
53
Q

what are genotoxins and what do they do

A
  • chemical agents such as alkylating or oxidising agents or non-chemical agents such as UV light and ionising radiation
  • they cause irreversible genetic damage or mutations by binding to DNA
54
Q

what are tumour suppressor genes (anti-oncogenes)

A
  • genes that protect a cell from forming cancers
  • mutation causes loss of function
  • follows ‘two hit hypothesis’ = tumour suppressor alleles are usually recessive, loss of both normal allelic copies gives rise to cancer
55
Q

what type of genes are affected by inherited cancer syndromes

A
  1. tumour suppressor genes
  2. proto-oncogenes (help cells grow but mutation can cause it to be permanately turned on)
  3. mismatch repair genes (correct mismatched nucleotides
56
Q

what are oncogenes activated by

A
  • alteration of port-oncogene structure

- can be due to point mutation or chromosome re-arrangements and translocations

57
Q

what do chemical carcinogens do

A
  • react with DNA forming covalently bound products (DNA adducts)
  • adduct formation can lead to activation of oncogenes and loss of anti-oncogenes
58
Q

what are oncoviruses and what do they do

A
  • viruses known to cause cancer in humans e.g. HPV, hep B
    Either:
  • virus genome inserts near port-oncogene causing over expression
  • virus directly inserts an oncogene into host DNA causing cell division

principles of disease (19 decks)

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