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Principles of Disease > PoD - Tumour Pathology > Flashcards

PoD - Tumour Pathology Flashcards

1
Q

what is a tumour?

A
  • an abnormal growing mass of tissue
  • it’s growth is uncoordinated with that of surrounding normal tissue
  • it’s growth continues after the removal of any stimulus which may have caused the tumour - capable of autonomous growth
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2
Q

what types of tumours are there?

A
  • benign (don’t cause any significant or pathological problems - mostly pressure)
  • malignant (cancer)
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3
Q

what is the definition of cancer?

A
  • a fundamental property of cancer is its ability to invade into adjacent tissue and to metastasise and grow at other sites within the body
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4
Q

what are metastases?

A
  • secondary tumours
  • will resemble the primary tumour
  • it is harder to treat patients’ cancers that have metastasised - not feasible to surgically remove all of them
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5
Q

what are the most common cancers in the UK?

A
  • male = prostate
  • female = breast
  • overall = breast
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6
Q

how are tumours classified?

A
  • based on tissue of origin (epithelium, connective tissue, blood cells, lymphoid tissues, melanocytes, neural tissue, germ cells)
  • benign or malignant
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7
Q

how are epithelial tumours named?

A
  • 2 broad types of epithelium which tumours can originate from
  • any type of malignant epithelium is a CARCINOMA
  • glandular
    benign = adenoma
    malignant = adenocarcinoma
  • squamous
    benign = squamous papilloma
    malignant = squamous carcinoma
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8
Q

how are connective tissue tumours named?

A
  • bone, fat or fibrous tissue
  • any type of malignant connective tissue is called a SARCOMA
  • bone
    benign = osteoma
    malignant = osteo-sarcoma
  • fat
    benign = lipoma
    malignant = lipo-sarcoma
  • fibrous tissue
    benign = fibroma
    malignant = fibro-sarcoma
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9
Q

how are blood cell tumours named?

A
  • only WBCs can develop a tumour
  • there are no benign tumours

malignant
= leukaemia

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10
Q

how are tumours of lymphoid tissue named?

A
  • there are no benign tumours

malignant
= lymphoma

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11
Q

how are tumours of melanocytes named?

A
  • benign tumours = naevus

- malignant tumour = melanoma

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12
Q

how are neural tissue tumours named?

A
  • central nervous system = astrocytoma

peripheral nervous system
= schwannoma

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13
Q

what are germ cell tumours called?

A 
- tumour composed of various tissues - indicates the pluripotent capability of germ cells 
= teratomas 
- develop in ovary/testis 
- ovarian teratomas = benign 
- testicular teratomas = malignant
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14
Q

list features of malignant tumours

A
  • invasive growth pattern
  • no capsule/capsule breached by tumour
  • cells look abnormal
  • cancers poorly differentiated - lack of normal tissue left
  • loss of normal function
  • metastases
  • frequently cause death
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15
Q

what is a tumour suppressor gene?

A
  • keep cells under regulatory control
  • loss of these = tumour formation (normally need to lose both to cause cancer)
  • examples = retinoblastoma (RB1), breast cancer (BRCA1)
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16
Q

what is an oncogene?

A
  • oncogene activates abnormal cell division

e. g B-raf, cyclin D1, erbB2, k-ras

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17
Q

what happens to tumour cell links?

A
  • loss of cell-cell adhesion (normal cells stick together, but this fails in cancer cells which allows them to invade and spread)
  • altered cell-matrix adhesion
  • production of tumour biomarkers
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18
Q

what are tumour biomarkers useful for?

A
  • screening - detecting cancers while still asymptomatic
  • diagnosis
  • prognostic - identifying a patient’s outcome
  • predictive - identifying how patients will respond to a particular therapy
19
Q

list the tumour biomarkers currently used clinically

A
  • alpha-fetoprotein
    = teratoma of testis
    = hepatocellular carcinoma
  • carcinoma-embryonic antigen (CEA)
    = colorectal cancer
  • oestrogen receptor
    = breast cancer
  • prostate specific antigen
    = prostate cancer
20
Q

what are clinically useful predictive tumour markers?

A
  • Kras = colorectal c
  • Braf = melanoma
  • EFGR = lung c
  • PD-L1 = lung c
  • Her2 = breast/gastric x
21
Q

how do tumours grow?

A
  • balance between angiogenesis and apoptosis
  • angiogenesis = new blood vessel formation, required to sustain growth via nutrients, O2, also provides a route for metastases
  • apoptosis = mechanism of programmed cell death, regulates tumour growth
22
Q

how do tumours spread?

A
  • invasion and metastasis
  • need to create a track to move through = increased matrix degradation by proteolytic enzymes
  • need to be able to move = altered cell-cell/cell-matrix adhesion
23
Q

what happens in tumour invasion?

A
  • tumour invasion occurs when adhesion has broken down, allowing invasion into connective tissue the into the lymph/blood vessels
24
Q

what happens in tumour metastasis?

A
  • lymphatic metastasis occurs when there is adhesion of tumour cells to lymph vessels, they invade into the lymph node, form metastasis in lymph node
  • metastasis via blood = adherence of tumour cells to blood cells, invasion from BVs, invasion into tissue and formation of metastasis
25
Q

where are common sites of metastasis?

A
  • liver, lung, brain, bone (axial), adrenal gland
  • uncommon = spleen, kidney, skeletal muscle, heart
    breast c = bone metastases
    prostate c = bone mets
    CRC = liver mets
    ovary = omentum/peritoneum mets
26
Q

what are the effects of benign and malignant tumours?

A
  • benign tumours = pressure and obstruction

- malignant = tissue destruction, bleeding, pain, side effects from tumour

27
Q

can tumours produce hormones?

A
  • yes
  • they can produce normal hormones for that tissue but abnormal amounts
  • they can also have abnormal hormone secretion where the tumour produces hormones not normally produced in that organ i.e ACTH in lung cancer
28
Q

what are paraneoplastic syndromes?

A
  • can’t be explained by local or metastatic effects of tumours
    i. e neuropathy, myopathy
29
Q

what is dysplasia?

A
  • an early sign of cancer
  • pre-malignant change
  • earliest change in process of malignancy
  • characterised by disorganisation of cells
    (increased nuclear size, increased mitotic activity, abnormal mitoses)
  • there is no invasion
30
Q

describe normal cell division

A
  • mitosis
  • Interphase - cell grows and accumulates nutrients needed for mitosis, RNA is synthesised, produce proteins (irreversible)
  • Mitosis - cell splits itself into two distinct cells
  • cytokinesis - new cell is completely divided
31
Q

describe the need for cell checkpoints and list key checkpoints

A
  • to detect and repair genetic damage and prevent uncontrolled cell division
  • checkpoints prevent abnormal cells progressing further in the cycle
  • G1/S checkpoint it the KEY restriction point
  • cells that progress through this point are committed to S phase and progression is autonomous
  • there is also a G2/M checkpoint which stops cells with damaged/incomplete DNA continuing
32
Q

describe cell mutations and where they would arrest in the cycle

A
  • inadequate nutrient supply = G1
  • external stimuli lacking = G1
  • abnormal cell size = G1/S
  • DNA not replicated = S
  • DNA damage detected = G1/2
  • chromosome misalignment = M
33
Q

what are cell cycle checkpoint activators?

A
  • system of cyclically in-/active enzyme switches
  • Cyclins and cyclin-dependant kinases (CDKs) - determine cells progress through cell cycle
  • CDKs are the catalytic subunits but cannot function w/o cyclin
  • the active enzyme = CDK/cyclin complex
  • active complex phosphorylates target proteins = activates/inactivates target proteins

example
- a pro-mitotic signal induces G1 cyclin-CDK complexes, becomes active and prepare the cell for S phase

34
Q

what are cell cycle inhibitors?

A
  • molecules that bind to cyclin-CDK complexes, inhibiting next phase of cell cycle
  • INK4a - p16 binds to CDK4 and arrests the cycle in G1 phase
  • CIP/KIP genes p21/27/57 halt cell cycle in G1 by inactivating CDK-cyclin complexes
35
Q

how does the retinoblastoma gene regulate the cell cycle?

A
  • the Rb gene is ACTIVE when NOT phosphorylated, phosphorylation inactivates enzyme
  • in the hypophosphorylated state, pRb carries out it’s role as a tumour suppressor by inhibiting cell-cycle progression
  • Active cyclin D-CDK complexes phosphorylate Rb as the cell cycle progresses
  • inactive Rb loses affinity for E2F transcription factor which is vital for cells to pass the restriction point (G1/S)
36
Q

what is carcinogenesis?

A
  • failure of cell cycle control which results in uncontrolled proliferation of cells - tumour
  • the cyclin D-pRb-E2F pathway and p53 pathway are the two most frequently disrupted cell-cycle regulators
37
Q

what does p53 do?

A
  • p53 is activated when exposed to DNA-damaging agents
  • activation leads to cell cycle arrest in G1 and attempts to repair DNA
  • triggers up regulation of the CDK inhibitor p21 and the GADD45 gens (growth arrest & dna damage)
  • successful repair of DNA allows cells to continue with cycle
  • however, if DNA repair fails - p53 induces apoptosis genes
  • in cells with loss/mutated p53, DNA damage doesn’t induce cell-cycle arrest or DNA repair = tumours
38
Q

how can carcinogenesis be induced?

A
  • chemical damage
  • radiation
  • oncogenic viruses
  • genetic predisposition
39
Q

describe two-hit hypothesis

A
  • suggests that in order to get the cancer, two mutations have to occur
  • some individuals may have inherited the first DNA insult, meaning any second insult would rapidly lead to cancer
  • in non-inherited (sporadic cases), two mutations would have to occur before a tumour can develop
  • explains why individuals with inherited cancers are likely to experience it at a younger age
40
Q

what are tumour suppressor genes?

A
  • protect cell from forming cancers
  • generally follow the two-hit hypothesis ideal
  • loss of both normal alleles gives rise to cancer
  • mutation gives rise to loss of function, means cells are able to grow & proliferate without control
    examples
    = p53, Rb, INK4a
41
Q

list examples of inherited cancer syndromes

A
  • familial retinoblastoma
    (mutation of RB1 gene)
  • familial adenomatous polyposis of colon
  • hereditary breast & ovarian cancer (mutated BRCA1/2 genes)
  • hereditary non-polyposis CRC (mutations in DNA mismatch repair genes)
42
Q

what are oncogenes?

A
  • increased function of growth regulating hormones (GFs, signal transducers, cell cycle regulators)
  • caused by alteration of porto-oncogene structure (point mutation/translocation) or dysregulation of proto-oncogene expression (gene amplification/over-expression)
43
Q

what are the targets for chemical and radiation carcinogenesis?

A
  • purine and pyrimidine bases in DNA

- chemicals oxidise and alkylate the bases = damaging them

44
Q

what occurs in viral carcinogenesis?

A
  • virus genome inserts near a host proto-oncogene
  • viral promoter causes proto-oncogene over-expression
  • virus directly inserts an oncogene into host DNA causing cell division
    (HPV - genital cancers)

Principles of Disease (15 decks)

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