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Year 2: EMS > Cancer > Flashcards

Cancer Flashcards

1
Q

Cancer

A

uncontrolled cells that can grow and spread to different parts of the body

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2
Q

Tumour

A 
Abnormal swells (not necessarily cancer) 
same as neoplasm
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3
Q

Neoplasm

A

Lesion = autonomous growth or relative abnormal growth of cells that then persists in absence of stimulus

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4
Q

Histogenesis

A

The differentiation of cells into specialist tissues and organs

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5
Q

Histogenic Classification of Tumours (definition)

A

The cell, tissue or organ of origin - NOT the organ/ tissue it is now in (mets)

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6
Q

Most common cancers (4) in order

A

Breast/Prostate
Lung
colorectal

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7
Q

Most fatal (4) in order

A

Lung
Prostate/ breast
Colorectal

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8
Q

Classification of tumours - rate of growth (3 ways)

A

Doubling time (number of cells double)
% cells in replicating pool
Rate at which cells die/ shed

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9
Q

Differentiation

A

the extent that neoplasmic cells represent normal parenchymal cells
BOTH morphologically and functionally

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10
Q

Grade? = how differentiated?

A

Grade 1 = well differentiated
Grade 2 = moderate differentiated
Grade 3 = poorly differentiated
Grade 4 = anaplastic (not differentiated)

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11
Q

Pleomorphic

A

cells the vary in shape and size (from normal cells)

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12
Q

Abnormal nuclei

A

Can be too large

Vary in shape

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13
Q

Chromatin distribution variation (3)

A

Coarsely clumped
Along cell membranes
Hyperchromatism = stain darkly

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14
Q

Abnormal Mitosis? Mitosis = indicator of proliferation and turn over rate

1) asymmetrical bikaryokineses
2) Trikaryokineses
3) tetrapolar division
4) Multipolar

A

1) asymmetrical separation of condensed chromosomes
2) organisation of chromosomes into 3 groups
3) organisation of chromosomes into 4 groups
4) Multiply spindle fibres

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15
Q

Loss of polarization?

A

orientation of cells disturbed

disorganized growth

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16
Q

Classification of tumours by invasion? (stage)
Benign
Malignant

A

Benign = encapsulated expansible mass, no infiltration or mets

Malignant = local invasion into adjacent structures, no boundaries, mets

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17
Q

Metastasis? (staging)

A

Spread of tumour to site NOT physically attached to site of origin

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18
Q

Mets are associated with? (5)

A 
Poorer prognosis
Less differentiation
increased size
local invasion
rapid growth
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19
Q

Met pathways (3)

A

Direct seeding
Lymphatic drainage
Venous pathway

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20
Q

Direct seeding met process?
Transcoelomic
eg. Colonic cancers

A

Penetration natural open field (eg. Open cavity) and remain adhere to surface with in it - eg. peritoneal mets

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21
Q

Lymphatic spread mets process?

A

Follow lymph node drainage

Senital nodes –> distant nodes

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22
Q

Stroma ?

A

connective tissue framework the solid tumours are embedded in
Contains blood vessel, lymphatics, fibro and myofibroblasts

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23
Q

Desmoplasmic reaction?

A

stroma formation due to fibroblast proliferation by growth factors from tumours

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24
Q

Complications - local?

A

Compression eg. pituitary on CN2 = visual defects

Destruction eg. ulceration on mucosal surfaces

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25
Q

Complications - metabolic?
General (4)
Specific

A

General = cachexia (weaknes), Neuropathies and loss of endocrine function, myopathies (muscle fibers)

Specific examples for neurological and endocrine

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26
Q

Histological classification of tumours

A

Make up the names include reference to:

Cell type - tissue type - benign or malignant

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27
Q

Pampilloma

A

Bengin non glandular surface epithelial tumour (cell type before)

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28
Q

Adenoma

A

Benign tumour of the Glandular endothelial (Tissue type before)

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29
Q

Carcinomas

A

Malignant non glandular surface epithelial tumour (add cell type before)

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30
Q

Adenocarcinomas

A

Malignant glandular epithelial tumour

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31
Q

Urothelial carcinoma

A

Malignant epithelial bladder cancer

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32
Q

Benign mesenchymal (connective tissue) tumour

A

__ oma (proceeded by tissue of origin)

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33
Q

Sarcomas

A

Malignant mesenchymal (connective tissue) tumour - proceeded by tissue of origin

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34
Q

Liposarcoma

A

Malignant tumour of adipose

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35
Q

osteoma

A

benign tumour of bone

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36
Q

Melanocytic lesions

A

pigment tumour of the epidermis

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37
Q

Benign Melanocytic lesion

A

Melanocytic naevi - freckles or patchy pigments of skin

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38
Q

Melanoma - Malignancy measured by ABC?

A

asymmetrical shape, irregular Boarders and inconstant Colour

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39
Q

Leukaemias

A

cancers of blood cells or in the bone marrow

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40
Q

Lymphomas

A

lymph nodes and solid organs BUT also lymphocytes in blood (cross over with leukaemias)

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41
Q

Myeloma

A

plasma cells tumour

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42
Q

Special features of brain tumours (3)

A

Can not break through basement membrane
Can’t metastasise BUT can have mets in it (from elsewhere)
Benign tumours are very harmful due to increase ICP

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43
Q

Examples of Brain and CNS tumours (4)

A

Meningiomas
astrocytomas
oligodrendroglioma
Pituitary tumours

44
Q

Where do germ cell tumours normally arise

A

Gonades

Midline - due to germ cell migration

45
Q

Ovarian Germ cell tumours

A

dysgerminoma

46
Q

Sperm germ cell tumours

A

seminoma

47
Q

Embryonal tumours - resembled? named after?

A

pediatric tumors of not fully differentiated cells

Resemble to embryonic cells of the organ it is destined to be BUT named after organ of origin

48
Q

_blastomas

A 
Emryonal tumours (due to not being fully differentiated) 
Preceeded with tissue of origin
49
Q

Harmatomas

A

non neoplastic tissue overgrowth = benign
Confused with tumours
Insidious and idiopathic

50
Q

Choristoma

A

heterotopic - tissue types in the wrong site.

Non neoplastic and benign

51
Q

Primary

A

tumour is at site of origin

52
Q

Secondary (met)

A

not at site of origin BUT still named after primary tissue type/ organ

53
Q

Cancers of unknown primary source (3 reasons)

A

Occult primary - unknown or too small to see
Migrating pre malignant stem cells
Regressed primary tumour

54
Q

Malignant tumours with benign names (4)

A

Melanoma (skin cancer)
Mesothelioma (mesothelium)
Myeloma (plasma)
lymphoma (lymphocytes)

55
Q

Exposure to carcinogens (3)

A

Geographic - environmental (UV light)
Occupational - eg. silica dusts
Accidental - lab tests or radiations

56
Q

Types of carcinogens (6)

A 
Chemicals
infectious agents
Radiation
Minerals
Physiological - hormones
Chronic inflammation
57
Q

Carcinogens

A

any agents the significantly increase the risk of developing cancer

58
Q

Initiator carcinogens

A

Genotoxic

Damage/ modify the DNA = exasperating tendency for polymerases to make mistakes

59
Q

Promotors carcinogens

A

non-genotoxic
Induce proliferating and DNA replication = clonal expansion of mutated cells
(after 2 rounds of replication = mutation is fixed)

60
Q

Complete carcinogens

A

both promote and initiated

61
Q

Result of mutations (2) - which genes altered

A

Gain of function - activation of proto-oncogenes

Loss of function - inactivation of tumor suppressor gene

62
Q

CpG islands are associated with?

A

promotor regions that are methylation –> turns off the gene

63
Q

Tumor suppress genes are associated with?

A

Famillia cancers

64
Q

Procarginogens - how taken in?

example

A

carcinogens (usually ingested) that require enzymatic activation
Benzopryene - found in meat, tobacco and fuel

65
Q

3 examples of DNA repair - which carcinogen they repair

A

Nucleotide-excision repair (NER) = UV light, hydrocarbons
Recombinantional repair = X-rays
Mismatch repair = replication agent

66
Q

Proto-oncogene - what do they do

A

promote cell cycle Proliferation, growth, survival and angiogenesis

67
Q

How does mutation affect Proto-oncogenes?

A

activates them to oncogenes

68
Q

Oncogenes - what do they do? (2)

Dominant - one mutated allele and one mutational ‘hit’ to be expressed

A

Increase expression of oncogenes = controlled growth and protein development
Aberrent (diversion for normal cell type) proliferation

69
Q

Mechanism of proto-oncogene activation (4)

A

Translocation = low to high transcriptional state
Point mutation = hyperactive
Amplification = more oncogenes –> increased expression
Insertion - of a promoter sequence

70
Q

Oncoproteins - coded for by oncogenes = functions (3)

A

Growth factor receptors
Bind to DNA to stimulate transcription
Secondary messenger that activates the cells cycle

71
Q

Tumor suppressor genes (2 types + what they do)

A

‘gatekeepers’ - negative regulator of cell proliferation
OR
‘caretakers’ - repair DNA so defect DNA doesn’t replicate

72
Q

Mechanism of Tumor suppressor deactivation? (3)

Recessive - two mutation ‘hits’ for mutated tumor supressor to be expressed

A

point mutations
deletions
epigenetic silencing - by methylation on CpG promoter regions

73
Q

Example of TSG (3)

A

RB1 - retinoblastoma
p53 - Li- Fraumai (Breast sarcomas)
APC - Famillial adenomatous polyposis (colorectal)

74
Q

Examples of Caretaker genes (2)

A

BRACA1 and BRACA2 = familliar breast caner

hMLH1 and hMLH2 = familliar non-polyposis colorectal cancer

75
Q

Minimum number of mutations (germline or somatic) for carcinogenesis

A

3

76
Q

Hallmarks of cancer - acquired functional capabilities (6)

A

Self sufficent growthpathways
Insensitivity to antigrowth factors
Immortality - talomeres on the end of chromosome never diminish in length = can replicate multiple times
Resistant to apoptosis
Sustained angiogenesis
Local invasion (basement membranes) and mets

77
Q

How do tumor cells self stimulate growth? (names of genes that mutate)

A

Over expression of EGFR (growth factor receptor)

RAS and RAF mutations = produces proliferating proteins

78
Q

Mutation that causes resistance to anti-growth factors?

A

Rb (gatekeeper) = inactivated

79
Q

Telomerase ?

A

Is over expressed in tumor cells so chromosomes always have telomere = replicate infinite number of times

80
Q

Mutation that makes tumour cells resistant to apoptosis

A

T53 = normally cause cell cycle arrest followed by DNA repair OR apoptosis of faulty cells

81
Q

Size of tumors that can sustain angiogenesis

A

2 mm

82
Q

How do tumour cells invade and metastasis

A

Mutation in gene = loss of E-cadherin –> motile

Secrete proteases = pass through basement membranes

83
Q

Genetic screening

A

Cancer predisposition

84
Q

Tumor markers for diagnosis? - type of cancer

A

Raised PSA in the blood (prostate specific antigen)

85
Q

Predictive markers for therapeutic response/ targeting drugs?

A

HER2 growth factor receptor over expressed in breast caner and responsive to Herceptin

86
Q

Tumor markers for monitoring response to treatment?

A

CA-125 in ovarian cancer

87
Q

5 clinical applications of tumor markers

A 
screening
diagnosis
prognosis
therapy 
monitoring
88
Q

Dysplasia

A

abnormal differentiation

89
Q

Anaplasia

A

no differentiation

90
Q

Epithelial become _____ cells in tumors

A

Mesenchymal cells (as these are not adhered and able to move even in health)

91
Q

Mutation in
Ecaderhins
Intergrin expression
in epithelial cells Cause?

A 
E-caderhins = loss of cell to cell adhesion
Intergrin = loss of cell to matrix adhesion
92
Q

Matrix Metalloproteinases

eg. gelatinases, stomolysins

A

degrade the basement membrane and collagen in the extra cellular matrix

93
Q

Mechanical pressure and the effect on the behavior of the tumor (6 step process)

A

No contact inhibition

Mass = pressure = occlude vessel = ischemia and death –> tumor then moves along line of weakness

94
Q

Cancer that metastasis via lymphatics firstly

A

carcinomas

95
Q

Cancers that met via blood (firstly) + from where?

A

Sarcomas from liver, lungs, bone and brain

96
Q

Process of Blood spread of Mets? (4 stages)

A

Tumor locally invades a blood vessel –> cells break off –> carried to narrower vessel –> embed and cause secondary tumor

97
Q

Implantation spread of mets?

A

Accidental deposit of cells during resection/ other surgery

98
Q

‘seed and soil’ theory

A

The idea that cancer cells have to find an ideal tissue environment to met is = organ selectivity for mets

99
Q

Angiogenesis

- part of healing process (physiological)

A

New vessel formation (derived from existing vessels)

100
Q

Growth factors released by tumor cells that control angiogenesis
VEGF
PDGF
TGFBeta

A

Vascular endothelial growth factor
platelet derived growth factor
Transforming growth factor beta

101
Q

Staging (3 components)

A

How big the primary tumor is
How far its spread
Any mets?

102
Q

TMN staging? (all 1 - 4)

A 
T = tumor - size of primary and how far spread
M = mets - how many and how far
N = nodes - how many and how far
103
Q

Dukes staging? - what cancer?

A

Colon cancer

104
Q

Ann arbor stages for Lymphoma

LN = lymph nodes

A 
1 = one lymph in isolation
2 = 2 physically unasocciated LN
3 = Multiple unassociated LN - at least one on the oposite side of the diaphragm
4 = multiple unassociated LN
105
Q

Grade

A

How differentiated the cells are = how aggressive

Less differentiated = more aggressive

106
Q

Stage and Grade do what?

A

Diagnose and guide prognosis - surgery? chemo? years left?

Year 2: EMS (1 decks)

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