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Dysfunction > MO > Flashcards

MO 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

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2
Q

What are the two enabling characteristics of cancer?

A

→genome instability

→tumour inflammation

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3
Q

What are the two emerging hallmarks of cancer?

A

→avoiding immune destruction

→ reprogramming energy metabolism

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4
Q

What are the hallmarks of cancer?

A 
→sustaining proliferative signalling
→resisting cell death
→genome instability
→enabling replicative immortality 
→evading growth suppressors
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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

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6
Q

What type of developmental is cancer?

A

→clonal

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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

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8
Q

What are proto-oncogenes?

A

→Normal genes that can be activated to be oncogenic

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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

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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.

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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

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12
Q

What are the five models of carcinogenesis?

A 
→mutational
→genome instability
→non-genotoxic
→Darwinian
→tissue organisation
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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

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14
Q

What are the 4 classes of carcinogens?

A

→chemical
→physical
→heritable
→viral

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15
Q

What are the two types of physical carcinogens?

A

→radiation eg ionisation or ultraviolet

→asbestos

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16
Q

What are two examples of viral carcinogens?

A

→Hepatitis B

→Epstein Barr

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17
Q

How do chemical carcinogens exert their effects?

A

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

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18
Q

Give an example of a chemical carcinogens

A

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

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19
Q

What chemical carcinogen is easiest to enter cells?

A

→Benzo[a]pyrene

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20
Q

Which enzymes in the body activate benzopyrene?

A

→cytochrome p450

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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

Dysfunction (29 decks)

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