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Miscellaneous > MCB Lecture 23 Cancer > Flashcards

MCB Lecture 23 Cancer Flashcards

0
Q

What are the Big 5 cancers?

A 
Prostate
Bowel
Breast
Skin melanoma
Lung
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1
Q

What are the cancer trends in Australia currently?

A

For the past 20 years, incidence has increased, but the rate has stayed roughly constant

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2
Q

How many deaths per year do the Big 5 represent collectively?

A

40,000

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3
Q

Has there been any improvement in the cancer incidence rate in Australia?

A

Yes in some cancers there has been some improvement in morbidity

However, in pancreatic and lung, there has been little to no improvement

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4
Q

What does the term cancer refer to?

A

Cancer is a generic term for a collection of generic terms

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5
Q

What are the four general types of cancer?

A
  1. Carcinoma: cancer of epithelial cells
  2. Sarcoma : cancer of connective tissue
  3. Lymphoma: cancer of lymphatic system
  4. Leukaemia: cancer of blood cells
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6
Q

What are sarcomas?

A

Cancers of connective tissue

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7
Q

What are carcinomas?

A

Cancer of epithelial cells

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8
Q

What are leukaemias?

A

Cancers of blood cells

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9
Q

What are lymphomas?

A

Cancer of the lymphatic system

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10
Q

What is the relationship between cancer incidence and age?

A

As age increases, cancer incidence increases

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11
Q

Describe delayed onset

A

Cancer onset will be a number of years after the exposure to the carcinogen

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12
Q

What are the two types of tumours?

A

Benign and malignant

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13
Q

What is a benign tumour?

Give an example

A

Benign tumours do not invade healthy tissues and cause spread of cancerous cells

Cannot create new tumours

Eg. Freckles and moles

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14
Q

What is a malignant tumour?

A

These tumours can invade healthy tissues, metastasise and cause more tumours

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15
Q

What is metastasis?

A

This is when cancerous cells are mobile. They move from one area to another.
This may be from the origin to elsewhere, or not

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16
Q

What is the name for the process where a normal cell becomes cancerous?
How does this occur?

A

Malignant transformation

This occurs when there is a build up of mutations, eventually leading to a cell that has uncontrolled cell division etc.

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17
Q

What is apoptosis?

A

Programmed cell death

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18
Q

What is senescence?

A

When a cell is still alive, but is not still growing

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19
Q

What are the two main pathways to tumourigenesis?

A
  1. Activation of tumour promoting

2. Deactivation of tumour suppressing

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20
Q

Give a general description of the tumour promoting pathway

A

Mutation relating to a proto-oncogene

Proto oncogene becomes an oncogene –> increase is cell proliferation

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21
Q

What is an oncogene?

A

An oncogene is a gene relating to functions such as cell proliferation that has been over expressed somehow, turning a normal cell into a cancerous cell

22
Q

What is a proto-oncogene?

A

This is the normal version of the cancer causing gene.

It has a role in cell proliferation

23
Q

What are the 5 different ways that proto-oncogenes can be turned on?

A
  1. Mutation causing hyperactive protein made in normal amounts
    2 mutation in promoter region causing normal protein to be made in increased amounts
  2. Gene replication: multiple copies of the gene
  3. Chromosome rearrangement:
    a. Gene comes near regulatory sequence
    b. fusion to an actively transcribed gene causing a hyperactive protein
24
Q

What does a deletion/SNP in a proto-oncogene lead to?

A

The gene product may have increased activity

Now, the same amount of the protein has a bigger effect on the cellular processes

25
Q

What does a mutation in the regulatory sequence lead to?

A

Overproduction of a normal gene

26
Q

What does gene amplification of proto-oncogenes lead to?

A

Overproduction of a normal protein

27
Q

What does chromosome rearrangement involve?

What are the two examples of chromosome rearrangement?

A

a. Sequence fused near regulatory sequence –> Burkit’s lymphoma
b. Sequence fused to an actively transcribed gene -> Chronic Myeloid Leukaemia

28
Q

How is Burkitt’s lymphoma caused?

A

Fusion of regions from Cr. 8 to Cr. 14

Myc fused to immunoglobulin regulatory region

29
Q

How is Chronic Myeloid Lymphoma caused?

A

Regions from Cr. 9 and Cr. 22 become spliced
Abl gets spliced to bcr

The Philadelphia chromosome

30
Q

Which two regions are fused in the Philadelphia chromosome?

What does each region do?

A

bcr: break point cluster region

C-Abl: gene for tyrosine kinase receptor

Bcr-c-abl gene for protein with increased tyrosine kinase activity

31
Q

Which two regions are fused on the chimeric chromosome that causes Burkitt’s Lymphoma?
What does each region do?

A

Immunoglobulin regulatory region

Myc: gene for transcription factor involved with cell proliferation, growth, angiogenesis

32
Q

Briefly describe the tumour suppressing pathway

A

When mutations occur in the tumour suppressing pathway, genes that are normally involved with apoptosis and senescence are turned off. Cell don’t die

33
Q

Explain the Knudson Two Hit Model

A

Since we have two copies of each gene, it requires a mutation in both to cause cancer

34
Q

What is it called when the second copy of the gene is mutated?

A

Loss of heterozygosity

35
Q

What are the genetic mechanisms for loss of heterozygosity?

A
  1. Non disjunction
    b. followed by chromosome replication
  2. Mitotic recombination
  3. Deletion
  4. Point mutation
  5. Gene conversion
36
Q

What does non-disjunction lead to?

A

Only one chromosome in the cell, only one copy of the gene

37
Q

What does non-disjunction, then chromosome duplication lead to?

A

Two copies of the mutated gene

38
Q

What does mitotic recombination lead to?

A

The mutated gene replaces the normal gene on the other chromosome

39
Q

What does gene conversion lead to ?

A

Normal gene converted to the mutated one

40
Q

How does deletion lead to L.O.H.?

A

Loss of the normal allele

41
Q

How does point mutation lead to L.O.H.?

A

Loss of the normal allele

42
Q

How can both genetic and epigenetic changes lead to L.O.H.?

A

Genetic: mutation in the normal allele

Epigenetic: silencing of the normal allele, so only the mutated one is active

43
Q

What is p53?

A

This is a tumour suppressor gene

The mutated version is extremely common in cancers

44
Q

What is normal function of p53?

A

It’s a transcription factor -> binds to DNA and alters expression of genes

Normal function is cell cycle control
DNA repair
apoptosis
Genetic stability
Inhibition of angiogenesis
45
Q

Where are most mutations of p53 localised?

A

In the DNA binding region of the transcription factor

46
Q

What happens when p53 mutates?

A

When the gene for p53 mutates, the protein has a different DNA binding site
The transcription factor will bind differently to promoter regions

47
Q

Explain Li-Fraumeni syndrome

A

This is a syndrome where people are born with one copy of a mutant allele of p53

This means they only have to receive one hit and they will develop the cancer

48
Q

Does the p53 product undergo modifications?

A

Yes, post- translational

49
Q

What are the hallmarks of cancer?

A
  1. Uncontrolled cell proliferation
  2. No cell death
  3. Angiogenesis, blood supply to tumour
  4. Avoids signals from growth repressors
  5. Metastasis
  6. Immortality
50
Q

What is Myc?

A

This is a gene coding for a transcription factor that is involved with regulation of cell proliferation and angiogenesis

51
Q

What is the structure of p53?

A

Tetramer

52
Q

Describe the features of the loss of function mutations of p53

A

Some mutations of p53 are dominant negative

This means a single hit it sufficient to lose the tumour suppressor activity

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