Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

omgmbd > L21: Mechanisms Of Oncogenesis > Flashcards

L21: Mechanisms Of Oncogenesis Flashcards

1
Q

What is cancer characterised by?

A

→Abnormal cell proliferation
→ Tumour formation
→Invasion of neighbouring normal tissue
→Metastasis to form new tumours at distant sites

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

What are the two enabling characteristics of cancer?

A

→genome instability

→tumour inflammation

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

What are the two emerging hallmarks of cancer?

A

→avoiding immune destruction

→ reprogramming energy metabolism

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

What are the hallmarks of cancer?

A 
→sustaining proliferative signalling
→resisting cell death
→genome instability
→enabling replicative immortality 
→evading growth suppressors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How has long life span increased risk of cancers?

A

→longer we live the more time there is for DNA to accumulate
mutations that may lead to cancer

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

What type of developmental is cancer?

A

→clonal

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

How does heterogeneity arise in tumour cells?

A

→Tumour cells can ‘evolve’- sub clonal selection allowing a growth advantage

→Dependent on interaction with other tumour cells and the tumour microenvironment

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

What are proto-oncogenes?

A

→Normal genes that can be activated to be oncogenic

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

What is an oncogene?

A

→a proto-oncogene that has been mutated in a way that leads to signals that cause uncontrolled growth

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

What are tumour suppressor genes?

A

→inhibit both growth and tumour formation

→braking signals during phase G1 of the cell cycle, to stop
or slow the cell cycle before S phase.

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

What are the 3 assumptions in multistage carcinogenesis?

A

→Malignant transformation of a single cell is sufficient to give rise to a tumour

→Any cell in a tissue is as likely to be transformed as any other of the same type

→Once a malignant cell is generated the mean time to tumour detection is generally constant

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

What are the five models of carcinogenesis?

A 
→mutational
→genome instability
→non-genotoxic
→Darwinian
→tissue organisation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What supports that cancer arises through the accumulation of irreversible DNA damage?

A

→presence of multiple mutations in critical genes is a distinctive feature of cancer cells

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

What are the 4 classes of carcinogens?

A

→chemical
→physical
→heritable
→viral

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

What are the two types of physical carcinogens?

A

→radiation eg ionisation or ultraviolet

→asbestos

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

What are two examples of viral carcinogens?

A

→Hepatitis B

→Epstein Barr

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

How do chemical carcinogens exert their effects?

A

→effects by adding functional groups to DNA bases called DNA adducts

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

Give an example of a chemical carcinogens

A

→coal tar, which contains benzo[a]pyrene, a polycyclic hydrocarbon

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

What chemical carcinogen is easiest to enter cells?

A

→Benzo[a]pyrene

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

Which enzymes in the body activate benzopyrene?

A

→cytochrome p450

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

What is the function of Ames test?

A

→determine the mutagenic activity of chemicals by observing whether they cause mutations in sample bacteria

22
Q

How does the Ames test work?

A

Point mutations are made in the histidine (Salmonella typhimurium) or the tryptophan (Escherichia coli) operon,

→the bacteria incapable of producing the corresponding amino acid

→organisms that cannot grow unless histidine or tryptophan is supplied.

→culturing His-Salmonellais in a media containing certain chemicals, causes mutation in histidine encoding gene, such that they regain the ability to synthesize histidine

23
Q

how do physical carcinogens exert their effects?

A

→imparting energy into the biological material
→DNA breaks Pyrimidine dimers
→Translocations
Mutations as a result of failed repair

24
Q

What type of mutations are found in hereditary malignant syndromes?

A

→mutation of a single gene

25
Q

What are some DNA repair defects syndromes predisposing to cancer?→

A 
→ataxia telangiectasia
→Bloom’s syndrome
→Fanconi’s anaemia
→Li-Fraumeni syndrome
→Lynch type II
→xeroderma pigmentosum
26
Q

What are some chromosomal abnormalities predisposing to cancer?

A

→Down’s syndrome

→Klinefelter’s syndrome

27
Q

What is ataxia telangiectasia?

A

→neuromotor dysfunction, dilation of blood vessels,

telangiectasia = spider veins

28
Q

How does ataxia tenlangiectasia?

A

→Mutation in ATM gene

29
Q

What is the function of the ATM gene activation?

A

→cell cycle arrest(p53), DNA repair and apoptosis -cell cycle arrest

30
Q

What is the ATM gene activated by?

A

→dsDNA breaks leading to cell cycle arrest

31
Q

What are the cancer predispositions of ATM mutation?

A

→lymphoma,
→leukaemia
→breast cancer

32
Q

What causes Bloom’s syndrome?

A

→Mutation in BLM gene

33
Q

What is the function of the BLM gene?

A

→that provides instructions for coding a member of the RecQ helicase family
that help maintain the structure and integrity of DNA

34
Q

What are the signs of Bloom’s syndrome?

A

→short stature
→rarely exceed 5 feet tall,
→skin rash that develops after exposure to the sun

35
Q

What are the cancer dispositions of Bloom’s syndrome?

A

→skin cancer
→basal cell carcinoma
→squamous cell carcinoma

36
Q

What mutations cause Lynch type?

A

→Mutations in DNA mismatch repair (MMR) genes, notably MLH1, MSH2, MSH6 and PMS2

37
Q

What are the symptoms of Lynch type?

A

→doesn’t cause any symptoms

38
Q

What are the caner predispositions of Lynch type?

A

→colorectal cancer

39
Q

At what stage of a virus does it have restricted gene expression?

A

→latent phase

40
Q

What are the properties required of tumorigenic viruses?

A

→stable association with cells
→must not kill cells
→must evade immune surveillance of infected cells

41
Q

What does the latent phase of viruses express?

A

→express non immunogenic to allow virus to survive within the host

42
Q

What are some RNA retroviruses associated with cancer?

A

→HTLV-I = Adult T-cell leukaemia, lymphoma

43
Q

What is genome instability of the cancer model?

A

→At least two events are necessary for carcinogenesis and that the cell with the first event must survive in the tissue long enough to sustain a second event.

44
Q

What is the non-genotoxic model of cancer?

A

→do not seem to act through a structural change in DNA but rather through functional changes including epigenetic events

45
Q

What are the group of carcinogens that induce cancer via non-genotoxic mechanis?

A

→tumour promoters (1,4-dichlorobenzene),
→endocrine-modifiers (17β-estradiol),
→receptor-mediators (2,3,7,8tetrachlorodibenzo-p-dioxin),
→immunosuppressants (cyclosporine) or
→inducers of tissue-specific toxicity and inflammatory responses (metals such as arsenic and beryllium), also in model 1

46
Q

What is the Darwinian model of cancer?

A

→Sequential accumulation of mutations due to exposure to carcinogens

→Tumour cells will be selected for ability to grow and invade

→Selection will include resistance to therapy

→Some mutations may be deleterious for tumour

47
Q

What are the two forces driving carcinogens?

A

→somatic mutation theory (SMT)

→the tissue organization field theory (TOFT

48
Q

What is the SMT approach to cancer?

A

→cancer is derived from a single somatic cell that has successively accumulated multiple DNA mutations

→those mutations damage the genes which control cell proliferation and cell cycle

49
Q

What is the TOFT approach to cancer?

A

→Carcinogenesis is primarily a problem of tissue organization

→carcinogenic agents destroy the normal tissue architecture thus disrupting cell-to-cell signaling and compromising genomic integrity

50
Q

What is the difference between the SMT and TOFT approach to cancer?

A

→SMT= single catastrophic event triggering carcinogenesis

→TOFT=carcinogenesis as general deterioration of the tissue microenvironment due to extracellular causes

51
Q

What are the three Es of cancer immnunoediting?

A

→elimination
→equilibrium
→escape-expanding tumour populations becomes
clinically detectable

52
Q

What can happen during the equilibrium of cancer immunoediting?

A

→some of the tumour may mutate
or give rise to genetic variants that
survive, grow and enter the next phase

omgmbd (29 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions