Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

zFoM by me > Neoplasia 1-5 🗸 > Flashcards

Neoplasia 1-5 🗸 Flashcards

1
Q

Cancer

A

uncontrolled cell proliferation and growth that can invade other tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Tumour

A

swelling, can be benign or malignant (possibly inflammation or a foreign body)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

neoplasia

A

new growth that is not in response to a stimulus
can be benign, premalignant or malignant
can occur in any cell in any organ

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Malignancy

A

in the epithelium, malignancy goes beyond the basal membrane -invasion
it gains access to the blood or lymph vessels and can travel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

is malignancy binary?

A

no, there are some precursor stages (dysplasia, metaplasia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

metastatic potential

A

malignancy that can spread to other sites (metastases)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Dysplasia

A

abnormal cells growing without a stimulus
no invasion
often graded (higher grade = higher risk of malignancy)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Carcinoma in-situ CIS

A

dysplasia affecting the whole of epithelium
last stage before malignant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Metaplasia

A

reversible change from one mature cell type to another mature cell type due to a change in the demand placed on the tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

common cause of metaplasia

A

noxious stimulus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

two examples of metaplasia

A

thermal/chemical injury (ie smoking) to bronchial epithelium in the lung = squamous epithelium
catheter creates inflammation of the bladder = transitional epithelium changes to squamous

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

metaplastic tissue risk?

A

higher risk of developing cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what do metaplastic tissues look like

A

they dont change appearance, they change signals to the stem cells causing differentiation down a different line

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Double hit hypothesis

A

one working gene is enough and one faulty gene puts a person at increased risk
two faulty mutated genes will result in functional problem

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

two types of chemical carcinogens

A

initiators and promoters

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

initiators

A

long lasting genetic damage, not sufficient to cause cancer, must be followed by a promter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

promoters

A

require initiators to have caused damage time period can vary after initiation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

smoking

A

> 40 carcinogens (ie polycyclic aromatic hydrocarbons)
can be present in animal fat, smoked meat and fish
causes lung, head, neck and cervical cancers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Aflatoxin (fungus on peanuts)

A

associated with p35 mutations
common in china
liver cancers
(note that most liver cancers in the west wont have p35 abnormality until later stages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

beta-naphthylamine (chemical dyes)

A

conjugated in the liver with glucuronic acid, not too toxic for too long
causes bladder cancers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Nitrosamines

A

food preservatives

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Arsenic

A

skin cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Weinbergs 5 hallmarks of cancer

A

resisting apoptosis
sustained proliferation signalling
evading growth supressors
activation invasion and metastases
inducing angiogenesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Non-chemical carcinogens

A

Radiation
Viruses
Chronic Inflammation
Obseity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Radiation
Causes formation of pyrimidine dimers in the DNA Nucleotide excision repair is eventually overwhelmed Xeroderma pigmentosa can be cause by CT scanners
26
Xeroderma pigmentosa
genetic defect in the NER, suffer from numerous skin cancers
27
Two carcinogenic viruses
HPV EBV
28
HPV
Produces E6 and E7 E6 increases destruction of p53 E7 prevents Rb protein from acting - E2F can promote transcription
29
EBV
glandular fever responsible for a subset of malignancies including: Burkitt lymphoma B-cell lymphoma Hodgkin lymphoma Nasopharyngeal carcinoma
30
Chronic Inflammation
Constant lymphocyte reproduction may lead to errors in production which leads to lymphomas tissues replicates to often causing it to be unstable leads to tumours Schistosomiasis
31
schistosomiasis
squamous cell tumours caused by chronic inflammatory response to parasite
32
Obesity
hyperplastic tissue cholesterol is analogue to oestrogen which leads to renal cell carcinoma
33
Oncogenes
turn up genes that promote growth
34
six examples/types of oncogene
RAS BRAF C-KIT Myc P13K Wnt/APC/beta catenin
35
RAS
linked with many cancers including colon and lung cancer
36
BRAF
50% of melanomas
37
C-KIT
GI and stomach cancers
38
Myc
nuclear transcription factor that promotes growth common in lymphoma, neuroblastoma, small cell carcinoma of the lung
39
P13K
Most commonly mutated kinase in cancer Limited success in trails, targeted at haematologiccal malignancies
40
Wnt/APC/beta catenin
One of the earliest mutations in colorectal cancer can occur as a germline mutation causing inherited condition (familial adenomatous polyposis, Gardner's syndrome)
41
Tumour suppressors
stop growth cells with malignant ambitions must remove them to survive and proliferate lots of proteins inhibit the cell cycle e.g. p53 and VHL
42
6 hallmarks of malignancy
unlimited replicative potential avoid apoptosis angiogenesis repair evasion of the immune system MMPs
43
unlimited replicative potential
in malignancy there is often a mutation that reactivates telomerase (renews length of telomeres)
44
avoids apoptosis
Bcl-2 binds to Bax/Bak to stop holes being punched in mitochondria
45
angiogenesis
formation of new, abnormal blood vessels 'successful' cancers must create their own blood supplies to supply oxygen for growth VEGF is frequently upregulated in some malignancies (useful target in treatment)
46
Repair
three types nucleotide excision repair BRCA Mismatch repair protiens
47
nucleotide excision repair (NER)
can be damaged by radiation
48
BRCA
associated with breast, ovarian and pancreatic tumours have a complex role in ER and AR regulation DNA repair and cell cycle arrest at G1/S phase
49
Mismatch repair proteins
family of proteins responsible for identifying faults in the code lynch syndrome we can also find faulty protein expression
50
lynch syndrome
mutation in mismatch repair proteins associated with colorectal carcinomas
51
how do we find faulty protein expression?
using immunohistochemistry - looking for the frequency of mismatched segments by analysing microsatellites
52
evasion of the immune system
malignant cells may express foreign proteins or expose proteins to the immune system that aren't normally exposed patients with cancers with a pronounced inflammatory response have a better prognosis PD-L1 also helps to evade
53
PD-L1
inhibits T cell proliferation tumours can over express this and avoid the immune system
54
MMPs
malignant cells increase expression od matrix metalloproteinases (MMPs) means that cells can chew their way though surrounding tissues and blood vessels
55
subclones
cancer is not clonal - there is a single parent but they are not identical new mutations each division
56
can all clones be eliminated the same way?
no, chemo and targeted therapies may not work against all clones, some may even have survival advantage
57
five features of a benign tumour
macro (round) symmetrical, organised homogenous - cut surface is uniform encapsulated - means legion is lowly growing, usually benign normal N:C (nucleus : cytoplasm) ratio
58
features of malignant tumours
look unnatural, nasty irregular infiltrative and destructive heterogenous N:C ratio increased pleomorphism hyperchromatia
59
heterogenous
as a tumour progresses it begins to consist of more diverse cells (may denote haemorrhage or necrosis)
60
pleomorphism
cells grow in multiple shapes and sizes
61
hyperchromatia
darkly stained nuclei, usually due to increased DNA content
62
13 classifications of tumours
epithelium (glandular or squamous) bladder mesenchyme (connective tissue) fat bone cartilage skeletal muscle smooth muscle nerves blood vessels CNS melanocytic blood
63
glandular epithelium
carcinoma benign- adenoma malignant- adenocarcinoma
64
squamous epithelium
carcinoma benign- papilloma malignant- SCC
65
Bladder
transitional cell carcinoma (TCC)
66
mesenchyme (connective tissues
malignant- sarcomas
67
fat
benign- lipoma malignant- liposarcoma
68
Bone
benign- osteoma malignant- osteosarcoma
69
cartilage
benign- enchondroma malignant- enchondrosarcoma
70
skeletal muscle
benign- rhabdomyoma malignant- rhabdomyosarcoma
71
smooth muscle
benign- leiomyoma malignant- leiomyosarcoma
72
nerves
benign- neurofibroma, schwannoma malignant- malignant peripheral nerve sheath tumour
73
blood vessels
benign- haemomagnioma malignant- angiosarcoma, kaposi's sarcoma
74
CNS
gliomas, range from being benign to malignant tumours
75
Melanocytic
freckle- ephelis mole- naevus malignant- melanoma
76
blood
all malignant, already systemic leukaemia's, lymphomas
77
cytogenetics
large changes, look at chromosomes (FISH)
78
molecular genetics
small changes, e.g. oncogenes
79
stage of a tumour
how far tumour has spread well differentiated and grown slowly but present for ages = high stage aggressive, rapidly growing caught early on = low stage
80
grade
how bad it is; the degree of cytological atypia (differentiation) well differentiated = low grade (look normal) poorly differentiated = high grade (don't know original cell anymore)
81
mass effect
compression of adjacent structures (blood vessels, airways, bile ducts) anatomically dependant e.g. any mass effect in brain is bad can result in loss of function of an organ
82
energy consumption of tumours
very metabolically active so need lots of energy can also lead to increased metabolism (mainly through TNF) which also increases weight loss
83
infiltration
direct invasion of other structures e.g. other organs, the brain
84
what happens when the nerves are infiltrated?
loss of function motor- swallowing, diaphragm sensory- pain or loss of sensation autonomic functions
85
what happens if blood vessels are infiltrated?
haemorrhage
86
what happens if bone marrow is infiltrated?
cancer cells use up vitamins e.g. folate which are used by bone marrow to produce blood vessels
87
Paraneoplastic syndromes
tumour produces hormones which cause electrolyte disturbances
88
examples of paraneoplastic syndromes
osteoarthropathy - big fingers unusual neurological symptoms skin rash fever - pyrogens (pyrexia of unknown origin- lots of causes but could be cancer)
89
immunosuppression
tumours express proteins that are normally not expressed, this can stimulate an immune response (if the response is strong, there's usually a good prognosis) many tumours have developed mechanisms to evade the immune system cancer patients are at risk of infection and will often get unusual reactions
90
metastases
the development of secondary malignant growths at a distance from the primary site loss of function (liver, lung) can cause pathological fractures in bone
91

zFoM by me (37 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions