neoplasia Flashcards
1
Q
neoplasia aka
A
new growth
2
Q
tumour aka
A
neoplasm
3
Q
neoplasm definition
A
a disorder of cell growth that is triggered by a series or acquired mutations affecting a single cell and its clonal progeny
4
Q
The causative mutations give the neoplastic cells a …
A
survival and growth advantage, which then results in excessive proliferation that is independent of physiologic growth signals
5
Q
parenchyma
A
a collection of neoplastic cells. Allows us to classify the tumor and its biologic behaviour
6
Q
reactive stroma
A
comprised of CT, blood vessels, and cells of the immune system. Allows us to determine the rate of growth and its willingness to form metastases
7
Q
if a tumour has a large proportion of parenchyma cells
A
the tumour will be soft and fleshy
8
Q
if a tumour is abundant in collagenous stroma
A
the tumour will be stony and hard
9
Q
benign tumour characteristics
A
- relatively hard to distinguish between healthy tissue and tumour tissue from a microscopic level
- the remain localised and do not metastasise
- are often enclosed in a capsule
- mostly harmless (but still have potential to be lethal)
10
Q
benign tumours nomenclature
A
benign tumours are designated by attaching the suffix ‘-oma’ to the name of the cell type from which the tumour originates
11
Q
chondroma
A
a benign tumour made of hyaline cartilage
12
Q
osteoma
A
a benign tumour made of bone
13
Q
lipoma
A
a bengin tumour made of adipose tissue
14
Q
fibroma
A
a benign tumour originating from fibrous tissues
15
Q
adenoma
A
a benign epithelial tumour derived from glands
16
Q
papilloma
A
a benign epithelial tumour producing microscopically or macroscopically visible fingerlike projections
17
Q
polyps
A
a neoplasm that produces a macroscopically visible projection above a mucosal surface and projects into the lumen of a hollow organ
18
Q
malignant tumours
A
- microscopic appearances are not innocent
- invade and destroy adjacent structures and spread to distant sites (can metastasise)
- have no capsule
- if not treated, cause death
19
Q
malignant tumours nomenclature
A
malignant tumours arising in solid mesenchymal tissues are usually called sarcomas
20
Q
fibrosarcoma
A
a malignant tumour originating from fibrous tissues
21
Q
chondrosarcoma
A
a malignant tumour originating from chondrocytes
22
Q
rhabdomyosarcoma
A
a malignant tumour with mesenchymal origin and showing skeletal muscle differentiation
23
Q
lymphoma
A
a malignant tumour of lymphocytes or their precursors (in the blood)
24
Q
carcinomas
A
malignant tumours of epitheial cell origin
25
squamous cell carcinoma
the tumour cells resemble stratified squamous epithelium
26
adenocaarcinoma
the neoplastic epithelial cells grow in a glandular pattern
27
malignant tumours with term '-oma'
lymphoma, mesothelioma, melanoma
28
cell differentiation
the extent to which neoplastic parenchymal cells resemble the corresponding normal parenchymal cells, both morphologically and functionally
29
anaplasia
lack of differentiation
30
pleomorhpism
variation of cell size and shape
31
the likelihood of a primary tumour metastasising correlates with..
lack of differentiation, aggressive local invasion, rapid growth, large size
32
pathways for malignant cells to spread
- direct seeding of body cavities or surfaces
- lymphatic spread
- haematogenous spread
33
sentinel lymph node
the first node in a regional lymphatic basin that receives lymph flow from the primary tumour
34
displasia
a disordered growth of cells, often considered a doorstep towards developing cancer.
35
carcinoma in situ
when dysplastic changes are marked and involve the full thickness of the epithelium, but the lesion does not penetrate the basement membrane
36
proto-onco genes
genes encode proteins that stimulate cell proliferation
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tumour supressor genes
thes genes encode proteins that inhibit cell division and/or repair dna errors
38
clonal evolution of tumour cells
an accumulation of complementary mutations in a stepwise fashion over time
39
driver mutations
mutations that contribute to the development of the malignant phenotype
40
passenger mutations
mutations that have no phenotype consequence
41
the initiating mutation
the first driver mutation that starts a cell on the path to malignancy
42
genomic instability
loss-of-function mutations in genes that maintain genomic integrity. leads to driver and passenger mutations
43
self-sufficiency in growth signals
a hallmark of cancer. capacity to proliferate without external stimuli
44
autocrine loop
some cancer cells acquire the ability to synthesize the same growth factors to which they are responsive
45
oncoproteins
promote cell growth in the abscence of normal growth-promoting signals
46
insensitivity to growth-inhibitory signals
tumours may not respond to molecules that inhibit the proliferation of healthy cells
47
tumour suppressor proteins
form a network of checkpoints that prevent uncontrolled growth and may force cells to lose their replicative ability
47
Retinoblastoma (RB)
inhibits cell proliferation and controls cellular differentiation
48
familial form retinoblastoma
frequent and bilateral blastoma, as it is quit easy for the second hit to occur when born with an already unfunctional allele
48
TP53 protein
Considered the 'Guardian of the genome' it regulates many cell functions such as:
- cell cycle progression
- DNA repair
- Cellular senescence
- Apoptosis
This gene is only induced in response to cell stress or DNA damage etc.
49
what is the most frequently mutated gene in human cancers?
the TP53 gene
50
Malignant transformation
an increased likelihood of the emergence of numerous cancer cell clones
51
if a cancer patient is negative in TP53
the are relatively resistant to chemotherapy and irradiation
52
altered cellular metabolism
a metabolic switch to aerobic glycolysis
53
cancer cell metabolism differs to healthy cells as they
have a high glucose uptake, which can be identified in a PET scan
54
warburg effect
cancer cells convert glucose to lactose following the fermentation pathway despite the availability of oxygen
55
why do cancer cells undergo an aerobic glycolysis?
proliferative cells need both energy and lots of metabolic intermediates due to rapid cell division. thus aerobic glycolysis seems to be the sweet spot that is optimal for growth
56
aerobic glycolysis
heavily biased toward aerobic fermentation with a bit of oxidative phosphorylation chucked in
57
evasion of apoptosis
tumours are resistant to programmed cell death. cancer cells have found a limitless replicative potential
58
angiogenesis
controlled by a balance between angiogenesis promoters and inhibitors
59
sustained angiogenesis in tumours
the angiogenic balance in tumours is skewed in favour of the promoters, this allows a blood vessel growth within and around the tumour, supplying blood and therefore nutrients to the cancer cells, enabling the tumour to rapidly proliferate
60
neoangiogenesis
when growing cancers stimulate vessels to sprout from previously existing capillaries
61
1. invasion of the extracellular matrix
A carcinoma must breach the underlying basement membrane, transverse the interstitial CT and gain access to the circulation by penetrating the vascular basement membrane
62
2. Vascular dissemination and homing
cancer cells may die in the circulatory system, as the consequence of mechanical shear stress, apoptosis stimulated by loss of adhesion, and innate and adaptive immune defences.
63
How can cancer cells increase their survival whilst in the circulatory system?
- formation of platelet-tumour aggregates
- tumour cells may bind and activate coagulation factors
- fibrin coating helps block immune response
64
Immune evasion
Cancer cells can 'hide' their abnormal (onco-) proteins
65
immune surveillance
the immune system constantly 'scans' the body for emerging malignant cells and destroys them (via cell-mediated immunity)
66
Genomic instability
cancer cells are more prone to mutations
67
cancer-promoting inflammation
infiltrating cancers are 'wounds that do not heal' and they provoke and maintain a chronic inflammatory reaction
68
Inflammatory cells
can modify the local tumour microenvironment and enable many of the cancer hallmarks
69
initiated cell
a cell is permanently altered, making it potentially capable of giving rise to a tumour, however it alone is not sufficient for tumour formation
70
promoters
chemical agents that can induce tumours to arise from initiated cells and stimulate cellular proliferation, but they are nontumorigenic by themselves
71
direct acting initiators
require no metabolic conversion to become carcinogenic
72
indirect acting initiators
require metabolic conversion to become active carcinogens. certain metabolic pathways me inactivate the procarcinogen or it derivatives
73
human oncogenic viruses
HPV and Hepatitis B Virus
74
How can HPV lead to more genomic instability?
some HPV viral proteins interfere with the functions of TP53 and increase telomerase activity
75
Hepatitis B virus
the dominant effect seems to be immunologically mediated chronic inflammation and hepatocyte death leading to regeneration and, over time, genomic damage.
76
Helicobacter pylori
a bacterium which my induce cancer formation via increased increased epithelial cell proliferation in a background of chronic inflammation
77
cachexia
progressive loss of body fat and lean body mass accompanied by profound weakness, anorexia, and anaemia
78
cancer cachexia is associated with
- equal loss of both fat and lean muscle
- elevated basal metabolic rate
- evidence of systemic inflammation
79
TNF-α
a chemical leading suspect amoung several mediators released from immune cells that may contribute to cachexia
80
malignancy
the presence of cancerous cells that have the ability to metastasize or to invade locally and destroy tissues
81
atherosclerosis
a chronic inflammatory and healing response of the arterial wall to endothelial injury.
- causes more morbidity and mortality in the western world than any other disease
82
