case 4 - cancer Flashcards

1
Q

what are the two classifications for cancer

A

familial cancers
sporadic cancers

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2
Q

what are the features of familial cancers

A

1% of all cancers
Single gene mutations (Mendelian disorders)
Most are inherited as autosomal dominant traits
Most due to inherited mutations of tumour suppressor genes
Further genetic events are necessary if the mutation is in somatic cells. Even though the mutated gene is inherited, it isn’t sufficient for malignancy

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3
Q

what are the features of sporadic cancers

A

99% of all cancers
Result of exposure to carcinogenic agents and unprepared DNA replication errors
Results in somatic activation/inactivation of cancer genes

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4
Q

what type of onset is familial cancer

A

early onset

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5
Q

what are the features of the cells in familial cancers

A

tumour cells - both copies of TSG inactivated

all other cells - one copy of TSG inactivated

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6
Q

what is the onset of sporadic cancers

A

late onset

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7
Q

what are the features of the cells in sproadic cancer

A

Tumour cells: both copies of tumour suppressor genes inactivated
All other cells: normal

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8
Q

what is an adenoma

A

cancer of the glands

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9
Q

what is a carcinoma

A

epithelial cells - 90% of all cancers

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10
Q

what is a lymphoma

A

lymphocytes or lymphatic tissue

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11
Q

what is a sarcoma

A

connective tissue

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12
Q

what is a blastoma

A

immature / pre-cursor cells - dendrites - WBCs

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13
Q

what is a papilloma

A

surface epthelial

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14
Q

what are the two types of cancer genomic instability

A

Either chromosomal instability - result of many numerical and structural abnormalities

Or microsatellite instability - result of impaired DNA mismatch repair (MMR)

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15
Q

what is telomerase

A

an enzyme that prevents the shortening of the telomere, thus preventing senescence

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16
Q

what happens in normal cells

A

telomerase is switched off

17
Q

what happens in malignant cells

A

telomerase is switched on, thus inhibiting senescence

18
Q

what is sensence

A

specific number of cell divisions

19
Q

what does successful carcinogenesis require

A

either mutations that increase the rate of cell proliferation, so as to provide an expanded target for further mutations (clonal evolution)
or
mutations that destabilise the genome, so as to increase the rate of further mutations

20
Q

to be successful, what must a malignant cancer cell have

A

Become independent of external growth signals
Become insensitive to external anti growth signals
Become able to avoid apoptosis
Become capable of indefinite replication
Become capable of sustained angiogenesis
Become capable of tissue invasion and metastasis

21
Q

what is cancer mediated by

A

oncogenes and TSGs
telomeres
Wnt and Ras
CIN/MMR
p53 and apoptosis
cyclin,CDK, CDi

22
Q

features of (proto) oncogenes

A

gain of function
dominant - only need one mutated allele to be activated

23
Q

features of tumour suppressor genes

A

loss of function
recessive - need two mutated alleles to be inactivated

24
Q

what is a proto oncogene

A

is a normal gene that may be activated into an oncogene due to mutations or increased expression

25
Q

what do proto oncogenes promote

A

cell division, survival and growth

26
Q

what are the four ways in which proto oncogenes can be activated into oncogenes

A

Point mutations that increase protein function

Gene amplification that causes over expression

Chromosomal translocation e.g MYC

Viral stimulation that may lead to addition/deletion of genes when viral DNA is integrated with human DNA

27
Q

what is MYC

A

it is a regulator gene that codes for a transcription factor. if translocated, MYC will continually be expressed, causing unregulated expression of many genes, some of which are involved in cell prolideration e.g cyclin D1 and result in the formation of cancer

28
Q

what is an oncogene

A

a gene that has the potential to cause cancer

29
Q

what are two examples of oncogenes

A

b catenin and KRAS

30
Q

what happens when one allele of oncogenes is mutated

A

there is a gain in protein function

31
Q

what do oncogenes usually code for

A
  • Secreted growth factors (EGF, Wnt, Ras)
  • Cell surface receptors (HER)
  • Signal transduction system components (ABL)
  • Nuclear proteins transcription factors (MYC)
  • Cyclins/cyclin dependent kinases (Cyclin D1, CDK4)
32
Q

what are tumour supressor genes

A

body’s natural defence mechanism against malignancy

33
Q

what happens when both alleles of TSGs are mutated

A

there is a loss of protein function

34
Q

what is inactivation of TSGs caused by

A

Mutations
Chromosomal abnormalities
Methylation of promoters
Interaction with viral proteins

35
Q

what is worse, loss of TSG or activation of oncogenes

A

loss of TSG

36
Q

what is the function of tumour suppressor genes

A

inhibit progress through the cell cycle -CKi’s - p21

promote apoptosis

inhibit cell growth

DNA repair

cell adhesion to prevent metastasis

37
Q

all cancers metastisise except

A

glial cells of the CNS, these usually form benign tumours

basal cell carcinomas of the skin

38
Q

what are the three pathways via which cancer spreads

A

direct seeing of body cavities or surfaces
Lymphatic spread
Hematogenous spread - blood