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Neoplasia Flashcards

1
Q

What are the two basic components of a neolplasia

A
  • Transformed neoplastic cells
  • Supporting stroma (connective tissue and blood vessels)
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2
Q

What are adenomas

A

benign epithelial tumors from glands or
forming glandular patterns

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3
Q

What are cystadenomas

A

adenomas producing large cystic masses,
seen typically in ovary

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4
Q

What are papillomas

A

epithelial tumors forming microscopic or
macro finger-like projections

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5
Q

What is a polyp

A

a tumor projecting from mucosa into lumen of
hollow viscus (e.g. stomach or colon)

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6
Q

What are adenocarcinomas

A

Epithelial tumours with glandular growth

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7
Q

What is a sarcoma derived from

A

Mesenchymal tissue

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8
Q

What are the 4 phases of neoplasia

A
  1. Transformation
    - Differentiation and anaplasia
  2. Growth
    - Of the transformed cells, some tumours grow faster than others, possibly reflected by hormone sensitivity and growth factor
  3. Invasion
    - Locally, involves breaching of the ECM
  4. Metastasis
    - Systemic invasion via blood, lymphatics or body cavitites
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9
Q

What is anaplasia characterised by

A
  • Nuclear and cellular pleomorphism. Wide variation in the shape & size of cells and nuclei
  • Hyperchromatism
  • Increased nuclear-cytoplasmic ratio . approaching 1:1
  • Abundant mitoses ,lots of proliferative activities
  • Tumor giant cells, contain a single large polyploidy nucleus or multiple nuclei; sometimes seen
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10
Q

What processes does a cell have to avoid before becoming cancerous

A
  • proto-oncogenes ,oncogenes
  • tumour suppressor genes
  • mismatch repair genes
  • apoptosis regulators
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11
Q

What does a clonal expansion have to do before becoming canceorus

A
  • evade immunological response
  • Produce angiogenesis for tumour growth
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12
Q

7 fundamental changes to carcinogenesis

A
  • self sufficiency to growth signals, from oncogene activation
  • insensitivity to growth inhibiting signals
  • evade apoptosis
  • defects in DNA repair
  • limitless replicative potential, maintenance of telomere length
  • sustained angiogenesis
  • ability to invade and metastasise
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13
Q

What does DNA viral carcinogenesis involve

A
  1. is a multistep process, multiple hits, tumour progression
  2. may act by neutralizing the influence of growth-inhibiting genes
  3. may involve incorporation of viral oncogene into host DNA
  4. may activate growth promoting genes
  5. may cause stimulation of function of growth-promoting proteins
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14
Q

Is DNA damage by chemicals always carcinogenic

A

No, because DNA damage can be repaired by cellular enzyme systems

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15
Q

What are proto-oncogenes

A

are normal cellular genes that affect growth and differentiation, thus in normal cell, are active and regulate physiological
actions

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16
Q

How are proto-oncogenes converted into onco-genes

A
  • transduction into retroviruses (v-onc)
  • changes in situ that affect their expression, function, or both, thereby converting them into c-onc, e.g. point mutations, chromosomal rearrangements, gene amplification
  • May be activated by translocation
  • May be activated by destruction of adjacent controller genes, which normally suppress their action
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17
Q

Why does oncogeneis involve multiple DNA mutations before neoplastic behaviour develops

A

All human cancers have been found to have mutations which involve both activation of promoter genes and loss of cancer- suppressor genes

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18
Q

What abnormality is thought to be a primary event in the development of many human neoplasms and why

A
  • Karyotype/ chromosomal abnormalities
  • Because in certain types of human neoplasia, karyotype abnormality is non-random and common in that tumour type.
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19
Q

What is the physiological role of tumour suppressor genes

A

Supress growth/ act as a regulator

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20
Q

Give exmamples of tumour suppressor genes

A

Rb gene, p53, HNPCC, BRCA I and II

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21
Q

Why is p53 important in controlling growth of potential cancer cells

A

Apoptosis genes arrest the mitotic process of cells with DNA damaged by mutagenic agents which allows time for DNA repair or, if repair does not occur, induces cell autodestruction

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22
Q

Is p53 gene expression necessary for normal cell division

A

no

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23
Q

Explain how p53 works

A
  • once cells are exposed to mutagenic agenst, e.g. chemicals or radiation, the p53 protein (normally with very short half-life) is
    stabilized and accumulates in the nucleus where it binds to DNA, causing cells to arrest in the G1 phase
  • this allows time for DNA repair mechanisms to work
  • if this does not occur, the cell undergoes apoptotic death
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24
Q

Name 2 tumour angiogenic factors and what do they stimulte

A
  • vascular endothelial growth factor (VEGF)
  • basic fibroblast growth factor (bFGF)

Fibroblast growth

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25
Q

What are tumour angiogenic factors dervied from

A

Tumour cells or inflammatory cells e.g macrophages
(i.e they aren’t uniquely tumour dervived)

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26
Q

What family do tumour aniogenic factors belong to

A

Heparin binding growth factors

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27
Q

What do tumour angiogenic factors bind to

A

Cell surface receptors (not steroid receptors)

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28
Q

What 3 variables influence tumour cell growth

A
  • Doubling time of tumour cells
  • Growth fraction
  • Cell production and loss
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29
Q

Examples of carcinoegens

A
  • Alkylating drugs (cyclophosphamide, chlorambucil, busulphan) -cause leukaemia/lymphoma
  • Arsenic -cause skin cancers
  • Aromatic amines (dye and rubber industries) - bladder cancers
  • Asbestos - causes mesotheliomas, lung cancer (much more common)
  • Lung cancer factors ! tobacco (polycylic hydrocarbons), asbestos, ionizing radiation, arsenic, nickel
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30
Q

What 5 things are true with regards to carcinogenic initiation

A
  1. effects are rapid
  2. effects are irreversible
  3. induces DNA alteration
  4. has ‘memory’
  5. can be active when given in divided doses
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31
Q

How do carcinogenic initiating agents produce their actions by mutagenic effects

A

Carcinogenic initiation produces irreversible alterations in DNA chemistry in target cells

32
Q

Why are carcinogenic promoters thought to be potentially reversible

A

Tumors do not eventuate if the ‘promoter-effective’ dose is applied prior to the application of the appropriate initiator

33
Q

4 key facts about promoters

A
  1. not electrophilic compounds
  2. do not damage DNA
  3. they induce clonal proliferation of initiated cells and influence their differentiation programes
  4. they bring about these changes by the use of existing normal growth-promoting physiologic transduction pathways, not by inducing new ones
34
Q

4 properties of chemical carcinogens

A
  • intrinsically electrophilic
  • usually produce characteristic molecular fingerprints
  • metabolism may not be correlated with genetically determined enzyme levels
  • cause more cell necrosis than proliferation
35
Q

Describe the mechanism of of initiation and promotion

A
  1. Initiation - dose dependent, rapid, irreversible, has memory (i.e. divided doses are as effective as one), causes permanent
    DNA changes
  2. Promoters - by themselves are non-mutagenic and non-oncogenic; act on initiated cells, are inactive (reversible effect) before action of the initiator, actions are time dependent

Complete carcinogens bring about both steps of oncogenesis with one chemical

36
Q

Examples of DNA viruses that cause cancer

A
  • HPV - skin cancer (HPV5) and cervical cancer (HPV16 and 18)
  • EBV - Burkitt’s lymphoma (very strong); nasopharyngeal carcinoma (100%)
  • HBV - heptocellular carcinoma
37
Q

RNA virus that causes caner

A

HTLV-1
- T4 (CD4) lymphoma/leukemia

38
Q

5 cancers associated with viruses

A
  1. carcinoma of the nasopharynx
  2. carcinoma of the liver
  3. Burkitt’s lymphoma
  4. skin cancer
  5. cervical cancer
39
Q

What is the doubling time of tumour cells

A

Amount of time it takes for a cancer to double in size

40
Q

Describe the 5 steps of the cell cycle

A

G0 - quiescent phase
G1 - Growth - organelles are made
S - Syntehsis, DNA is duplicated
G2 - Preparation for mitosis, check point occurs here
M - mitosis

41
Q

How many doublings does it take a cancer to reach 1 gram

A

30

42
Q

Does a tumour have a longer or shorter cycle time than a normal cell

A

equal or Longer

43
Q

When is the longest time of cancer growth

A

Pre-detection

44
Q

What is growth fraction

A

proportion of cells within the tumor population that are in the replicative pool (i.e. out of the G0 phase)

45
Q

What is the growth fraction by the time a cancer is detectable

A

<20%

46
Q

How can cells leave the replicative pool

A

a. Shedding
b. Apoptosis
c. differentiating
d. by reverting to G0

47
Q

What are the treatment implications for GF

A

a. If low GF, cancer is slow growing, not good for chemo
b. If high GF, although fast growing, are susceptible to chemo

48
Q

Give examples of cancers with low GF

A

Breast and colon cancer

49
Q

Give examples of cancer with high GF

A

Oat cell cancer
Leukemia
Lymphoma

50
Q

In general what 4 things do cancer cells have compared to normal cells

A
  1. an equal to longer cell cycle time
  2. less percentage of terminally maturing cells compared to normal cells
  3. less percentage of cells in the replication cycle esp. by the time they are detected
  4. more production compared to loss hence overgrowth
51
Q

What does the degree of cell mutation from radiation depend on

A
  • type of radiation
  • dose and rate of delivery
  • DNA repair (multistep enzyme function)
52
Q

What cancers are linked to ionsing radtion (in order)

A

Most: Leukemia (Not CLL), thyroid (childhood radiation)
Then: Breast, lung, salivary gland
Less so: Skin, bone, GI tract

53
Q

List 8 recognised sequelae of exposure to ionising radiation

A
  1. breast cancer
  2. pericarditis
  3. endarteritis obliterans (subintimal fibrosis)
  4. peritubular fibrosis and glomerular hyalinization
  5. carcinoma of the lung
  6. osteosarcoma
  7. carcinoma of thyroid
  8. carcinoma of the breast
54
Q

What are 3 things that make cancer more sensitive to radiotherapy

A
  1. oxygen - hyperbaric oxygen is better - ?enhanced radical killing
  2. rapidly dividing cells (esp. if they’re in G2)
  3. if the cells are not specialized - i.e. decreased level of specialization
55
Q

What metastatic cancers classically cause hypercalcemia

A
  1. lung
  2. breast
  3. kidney
  4. T cell leukemia/lymphomas
56
Q

What paraneoplastic syndrome is carcinoma of the bronchus associated with

A

Cushings syndrome
Hyponatremia

57
Q

What paraneoplastic syndrome can renal cancer cause

A
  1. polycythemia
  2. hypercalcemia
58
Q

What cancers secrete ACTH

A
  1. oat cell carcinoma of the bronchus
  2. carcinoid tumour of the bronchus
  3. prituitary basophil adenoma
  4. medullary carcinoma of the thyroid
59
Q

What is paraneoplastic syndrome

A
  • Production of chemical signalling molecules (hormones or cytokines) in response to a tumour. I.e abnormal immune response.
  • Symptoms do not directly relate to spread of tumour
  • Hormones released are not indigenous to the tissue from which the tumour arises
  • Can be the earliest clinical manifestation of a neoplasm
  • May occur in the absence of demonstrable primary neoplasm
60
Q

6 most common paraneoplastic syndromes

A
  1. Cushing’s syndrome > ACTH - from ‘oat cell’ Ca of lung/thyroid medullary, Ca/Pancreatic islet, Ca/carcinoid tumors
  2. Hypercalcemia > PTHrH ! Lung SCC/breast Ca/renal Ca/T cell leukemias/lymphomas
  3. ADH/hyponatremia > Lung Ca
  4. Polycythemia > renal Ca, cerebellar haemangioblastoma, hepatoma
  5. Carcinoid syndrome > carcinoid tumour (GIT, bronchus, pancreas, thymus)
  6. Hypoglycemia > sarcomas, hepatoma
60
Q

Give examples of non-hormonal para-neoplastic syndrome (5)

A
  • Neuromyopathic -> myasthenia, degenerative encephalo-neuropathies
  • Dermatopathic -> dermatomyositis, acanthosis nigricans
  • Bone/joint/soft tissue > hypertrophic osteoarthropathy and clubbing
  • Blood & vascular > thrombophlebitis migrans, marantic endocarditis, anaemia, leukaemoid reaction, DIC
  • Immune complex > nephritic syndrome
61
Q

What are the 2 malignant cancers that do not metastasise

A

Glioma and BCC

62
Q

3 routes that cancers use to metastasise

A

Lymph
Blood
Direct extension into cavity

63
Q

List the 2 phases of the metastatic cascade

A
  • Invasion of the ECM
  • Vascular dissemination of homing of tumour cells
64
Q

What cancers have a significant reduction in disease free survival and which doesnt

A
  1. adenocarcinoma of the colon
  2. adenocarcinoma of the breast
    but not thyroid
65
Q

What things increase the metastatic potential of a cancer

A
  1. Down regulation of E-cadherins
  2. Increased binding to laminin and fibronectin via cell surface receptors
  3. Elaboration of plasminogen activator
  4. Secretion of type IV collagenase, or Cathepsin D
  5. Density of laminin receptors
66
Q

What neoplasms have thrombophlebitis margins as a recognised complication

A
  1. stomach
  2. pancreas
  3. kidney
  4. lung
67
Q

Outline the steps involved in invasion of the ECM

A
  1. Detachment. Primary tumour undergoes cloncal expansion, growth diversification angiogenesis. Metastatic subclone down regulates E cadherins which reduces cohesiveness of tumour cells.
  2. Attachment to matrix components. Tumour cells bind to laminin and fibronectin via cell surface receptors. The receptor density determines the degree of invasion and metastasis.
  3. Degradation of the ECM. Cancer cells secrete proteolytic enzymes that degrade matrix components creating a pathway for migration.
  4. Migration of tumour cells
68
Q

3 proteolytic enzymes important in degradation of ECM

A
  • Type IV collagenases, cleaves BM collagen
  • Cathepsin D - a cysteine proteinase
  • Urokinase-type plasminogen activator - important in ECM lysis
69
Q

What 2 categories of molecules mediate migration of tumour cells

A
  • Tumor cell-derived motility factors
  • Cleavage products of matrix components (e.g. collagen, laminin)
70
Q

Describe how vascular dissemination works

A
  1. In circulation, tumor cells form emboli by adhering to circulating leukocytes and particularly platelets - seems to protect it
    from being attacked by immune system
  2. Adhesion to BM at a distant site.
  3. Metastatic deposit will require angiogenesis and growth
71
Q

Outline the 12 key concepts of the metastatic cascade.

A
  1. clonal expansion, growth, diversification, angiogenesis
  2. metastatic subclone
  3. adhesion to and invasion of basement membrane
  4. passage through the extracellular matrix
  5. intravasation
  6. interaction with host lymphoid cells and platelets
  7. Tumour cell embolus
  8. adhesion to basement membrane
  9. extravasation
  10. metastatic deposit
  11. angiogenesis at the new site
  12. growth
72
Q

ECM break down products + breakdown of the ECM itself gives rise to what

A
  1. angiogenesis factors
  2. chemotaxis factors
  3. growth factors
  4. a physical passage for tumour cell migration
73
Q

What increases tumour invasion/ metastatic potential

A
  1. any increase in matrix/tumour cl binding
  2. anything which increases matrix destruction
  3. any factor which makes space or growth factors or chemotactic factors
74
Q

What does adhesion to the distant metastatic site depend on

A
  • Vascular & lymphatic drainage from site of the primary tumor
  • Interaction of tumor cells with organ-specific receptors
  • Microenvironment of organ or site (e.g. a tissue rich in protease inhibitors might be resistant to penetrance by tumor cells)
75
Q

What RNA virus causes adult T cell leukaemia/ lymphoma

A

Human T ell leukemia virus type 1

76
Q

How is Human T cell leukemia virus type 1 spread and what cells does it show tropism for

A

Sexual intercourse, blood products, breast feeding
CD4

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