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Cancer Flashcards

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Biology 101 flashcards
1
Q

What are cancer cells?

A

Cells that have escaped from cell cycle control - they divide excessively without control and are ‘immortal’ is a continued supply of nutrients is given

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2
Q

Do normal cells and cancer cells require growth factors?

A

Normal cells : require external growth factors to divide, inhibition of synthesis of growth factor by normal cell regulation = cells stop diving

Cancer cells : lost the need for growth factor so they divide whether or not they are present - they do not behave as a part of the tissue, they have become independent cells

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3
Q

Do normal cells and cancer cells show contact inhibition?

A

Normal cells : yes, cells can divide to full in a gap but they stop dividing as soon as there are enough cells to fill the gap

Cancer cells : no, there is a loss of contact inhibition as they continue to grow after they touch other cells causing a large mass of cells to be formed

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4
Q

Do normal cells and cancer cells have a limit on the number of cell divisions?

A

Normal cells : yes, they age and die via apoptosis and are replaced in a controlled and orderly manner by new cells

Cancer cells: telomerase is activated in cancer cells - cells can undergo unlimited number of cell divisions without triggering apoptosis

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5
Q

Do normal cells and cancer cells divide when DNA is damaged?

A

Normal cells : cease to divide and will undergo apoptosis when there is DNA damage or when cell division is abnormal

Cancer cells : continue to divide even when there is a large amount of damage to DNA or when cells are abnormal - these progeny cancer cells contain abnormal DNA and as the cell continues to divide, they accumulate even more damaged DNA

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6
Q

What is contact inhibition?

A

Cells respond to contact with other cells by ceasing cell division

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7
Q

What is cancer ?

A

Unrestrained cell proliferation caused by mutation in genes regulating the cell division cycle
It is a disease of cell division and is characterised by uncontrollable cell growth and cell division

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8
Q

What are protocol-oncogenes?

A

Genes that normally trigger cell division when appropriate

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9
Q

What do proto-oncogenes do in normal cells (function) ?

A

They code for proteins that send signal to the nucleus to stimulate cell division

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10
Q

What are oncogenes?

A

Proto-oncogenes which are turned on at the wrong time or place - “onco” means cancer

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11
Q

What do oncogenes code for (function)?

A

Code for protein that lead to overstimulation of cell growth and division

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12
Q

What is an example of G-protein that is coded by proto-oncogenes?

A

Ras protein coded by ras gene
- associated with the cytoplasmic surface of a membrane receptor, plays important roles in cell signalling pathways
- its activity is regulated by GTP and GDP : GDP bound = ras gene inactive GTP bound = rase gene active

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13
Q

What happens when a point mutation occurs in the ras oncogene?

A

It may cause a change in 3D conformation of the ras protein
The altered ras protein loses its ability to hydrolyse GTP to GDP thus is constitutively active (becomes a hyperactive ras protein)
- it will continuously deliver signals for cell growth and division resulting in uncontrolled cell division

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14
Q

What is a gain-of-function mutation?

A

A dominant mutation - a single copy of the oncogene is sufficient for expression of the trait
Cells with the mutant form of the protein have gained a new function not present in cells with normal gene

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15
Q

What is the result of the presence of an oncogene in the germ line cell ?

A

An inherited predisposition for tumours in the offspring

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16
Q

What are the four genetic changes associated with the conversion of a proto-oncogene into an oncogene that leads towards cancer?

A
  1. Point mutation
  2. Chromosomal rearrangement
  3. Gene amplification
  4. Insertional mutagenesis
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17
Q

What happens when there is a point mutation in coding regions?

A

May result in a change of 3D conformation of the protein and causing the altered protein to become hyperactive

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18
Q

What is a point mutation?

A

A small change in the base sequence - substitution, deletion

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19
Q

What happens when there is a point mutation in the regulatory region (eg promoter) ?

A

May lead to over expression of the gene causing overproduction of the normal functional protein

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20
Q

How does the ras gene function under normal conditions?

A

Binding of appropriate growth factors to a receptor will trigger the activation of the ras protein, a GTP molecule will replace a GDP molecule in the ras protein (inactive to active)

The active ras protein then passes on the signal to a series of cytoplasmic kinases which in turn activate transcription factors that turn on genes for proteins that stimulate the cell cycle

To turn the pathway off, ras protein hydrolyses tus bound GTP to GDP and becomes inactive again

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21
Q

What is chromosomal rearrangement?

A

It involves the breakage and re-joining of DNA (translocation)

It may change the protein-coding region resulting in hyperactive fusion protein or alter the control regions for a gene so that the normal protein is over-produced

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22
Q

What is gene amplification?

A

Errors in DNA replication which may produce extra gene copies which are all transcribed to produce the normal protein which is then translated leading to overproduction of the normal protein

23
Q

How does gene amplification occur?

A

This process may be due to selective replication of a region of chromosome
The process can be repeated many times, making many copies of that particular region

24
Q

What is insertional mutagenesis?

A

Insertion of a retrovirus into the DNA causing overexpression of a proto-oncogene to become an onco-gene

25
Q

How does insertional mutagenesis occur?

A

During infection cycle, a retrovirus may integrate into the host DNA at a region near a proto-oncogene which will then come under the control of active retroviral promoter sequences

Over expression of proto-oncogenes occurs as these retroviral sequences do not respond to the environmental signals that normally regulate protocol-oncogene expression = cell transforms to tumorous state

26
Q

What do tumour suppressor genes do?

A

They code for proteins that send appropriate signals to prevent cell division or lead to cell death (apoptosis)

if conditions for growth are not met, the protein products : - halt the cell cycle
- carry out DNA repair
- induce cell death (apoptosis)

27
Q

What is the loss of function mutation?

A

Results from a mutation in the tumour suppressor genes when they are no longer able to inhibit cell growth

Mutation is usually recessive (trait is not expressed unless both copies of the normal alleles are mutated

28
Q

What is the loss of heterozygosity?

A

It is the disruption of the remaining normal allele after a single allele of a tumour suppressor gene has undergone mutation

29
Q

What is an example of a tumour suppressor gene?

A

p53 tumour suppressor gene codes for p53 protein - transcription factor that can bind directly to DAN in nucleus

30
Q

What are the three anti-cancer mechanisms p53 has?

A
  1. It can activate DNA repair proteins when DNA has sustained damage - helps maintain genetic stability
  2. It can hold the cell cycle at G1 checkpoint (cell cycle arrest) on recognition of DNA damage so that the DNA repair proteins will have time to fix the damage before cell is allowed to continue the cell cycle
  3. It can initiate programmed cell death (apoptosis) if DNA damage proves to be irreparable
31
Q

What will mutations in the p53 gene cause?

A

Non-function p53 proteins synthesised which would be unable to carry out DNA repair, halt cell cycle nor induce apoptosis
DNA damage is allowed to accumulate within a cell thus increasing the risk for cancer formation

32
Q

What does the development of cancer involve?

A

Development of cancer is a multi-step process which involves the accumulation of (~4-6) independent mutations in key cell-cycle regulatory genes

33
Q

What is the evidence for the multi step process of cancer development?

A
  • the need to inactive several regulatory genes : most humans develop cancer over many decades (~40 years)
  • analysis of tumours reveal that tumours have different degree of malignancy
  • there is accumulation of genetic alterations as tumour progresses
34
Q

What are the genetic changes a cell must show for it to turn cancerous?

A

(In no specific order)
- gain of function mutation in at least one proto-oncogene leading to activation of onco-gene
- loss of function mutation in several tumour suppressor genes

35
Q

What happens once a cancer promoting mutation occurs in a particular cell?

A

It is passed on to all its descendants

36
Q

What does accumulation of mutations in genes over time lead to ?

A
  • overstimulation of cell growth and division (proto-oncogene to onco-gene)
  • inability of cell to halt cell cycle, carry out DNA repair, initiate apoptosis (tumour suppressor gene)
37
Q

What is cell proliferation?

A

the process of increase in the number of cells which occurs as a result of regulated cell growth and cell division

The process is balanced by cell division and cell differentiation/cell death, which maintains an appropriate number of cells in the body

Cell proliferation is increased in tumours

38
Q

What are malignant tumours?

A

Benign tumours which acquire further mutations over time and the cells in the tumour gain the ability to invade normal tissues and migrate to other parts of the body

Malignant tumours are referred to as cancer

39
Q

What are benign tumours?

A

Formed initially and lack the ability to invade or spread to other tissue

40
Q

What is metastasis?

A

Tumour cells which can penetrate blood or lymphatic vessels, circulate through the circulatory system and then proliferate at another site

41
Q

What is angiogenesis?

A

Induced by other mutations

It is the formation of new blood vessels which play a role in supplying nutrients and oxygen to the growing tumour at the new site

42
Q

How do malignant tumours develop?

A

Benign tumour > mutation > metastasis > angiogenesis > malignant tumour

43
Q

What are causes of cancer (internal factors) ?

A

Loss of immunity

Genetic predisposition

Hormones

44
Q

How does loss of immunity cause cancer?

A

Functional cytotoxic T cells in the body’s immune system help rid the body of cells that have been infected by virus and cells that have been transformed by cancer but not yet adapted to evade the immune detection system

Loss of immunity = increased chance of cancer cells multiplying in the body

45
Q

How does genetic predisposition cause cancer?

A

Individuals who display increased risk of developing cancer often are born with one defective copy of a tumour suppressor gene (germ line mutation) that is inherited from their parents

46
Q

How does hormones cause cancer?

A

Eg. In females, the hormone oestrogen is needed for breast tumours to grow

47
Q

What are the causes of cancer (external factors) ?

A

Chemical carcinogens

UV and ionising radiation

Viruses

Agents that stimulate rate of mitosis

Agents that cause chronic inflammation

48
Q

How does chemical carcinogens cause cancer?

A

They damage or alter DNA
eg. Tobacco smoke

49
Q

How does UV and ionising radiation cause cancer?

A

Cause DNA to become more reactive

Ionising radiation (eg x-rays) can penetrate to the nucleus and form damaging ions inside the cell that can cause breaks or mutate DNA

50
Q

How does viruses cause cancer?

A

Eg. Human papilloma viruses (HPVs) - HPV infection is the main cause of cervical cancer
Human immunodeficiency virus (HIV) - HIV infection is associated with greater risk of cancer like lymphoma and a rare cancer called Kaposi’s sarcoma

51
Q

How does agents that stimulate the rate of mitosis cause cancer?

A

Agent : Chronic tissue injury - increases rate of mitosis in cells needed to repair damage

52
Q

How does agents that cause chronic inflammation cause cancer?

A

They generate DNA-damaging oxidising agents in the cell
eg. Chronic hepatitis B viral infection leads to 100 fold increase in liver cancer

53
Q

(Summary)
Using cars as analogy

A

Oncogene (accelerators) : presence can stimulate development of cancer

Tumour suppressor gene (brakes) : absence leads to cancer

In cancer :
- accelerators are jammed = accelerate cell division
- no brakes working = cannot stop cell division

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