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Year One - Principles of Disease > Cancer > Flashcards

Cancer Flashcards

1
Q

What two factors can cause cancer?

A

Environment

Genetics

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2
Q

What are somatic mutations?

A

Mutations in nongermline tissues

Noninheritable

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3
Q

What are germline mutations?

A

Mutation in germline mutations

Heritable

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4
Q

What are proto-oncogenes?

A

Normal genes that code for proteins that regulate cell growth and differentiation

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5
Q

What are oncogenes? When do these genes cause cancer?

A

Proto-oncogenes with a mutation

Accelerate cell division

Cancer arises when the oncogenes are stuck in ‘on’ mode

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6
Q

How many ‘hits’ are needed for oncogenes to cause cancer?

A

One mutation

As they are dominant in effect

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7
Q

What are tumour suppressor genes? When do these genes cause cancer?

A

Genes that regulate a cell during cell division and replication. They regulate cell division by either inhibiting the cell cycle or promoting apoptosis.

Cancer arises when the genes are mutated, as this means cell division and replication won’t be regulated and the cells will grow uncontrollably

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8
Q

How many ‘hits’ are needed for tumour suppressor genes to cause cancer?

A

Two mutations

As they are recessive in effect. Therefore they fit the “two hit” hypothesis

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9
Q

What are DNA damage-response genes? When do these genes cause cancer?

A

DNA damage response genes are the genes that are involved in coding for key enzymes involved in repairing DNA when it is damaged.

Cancer arises when the genes are mutated in a way that results in the proteins not being formed or having no function. This results in there being an accumulation of mutation in other critical genes

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10
Q

What are monoclonal cancers?

A

Cancers that arise from a single cell

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11
Q

What is a carcinoma?

A

Type of cancer that starts off from the disorderly growth of epithelial cells in the skin or tissue lining organs.

These epithelial cells can then invade adjacent tissues and spread by the lymphatic and blood vessels to other parts of the body.

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12
Q

Describe the features of normal cells.

A

Normal cells are spaced out in a uniform manner

A few of the cells are mitoses, which means that few cells are going through the cell cycle

Oncogene expression is rare within normal cells and there is a presence of tumour suppressor genes

Normal cells also secrete growth factors, which is done in a co-ordinated manner.

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13
Q

Describe the features of cancerous cells.

A

Loss of contact inhibitor and are not uniformed

A lot of cells are dividing, which means that there are frequent mitoses and a lot of the cells are in their unstable state

There is also an increase in oncogene expression and a loss of tumour suppressor genes.

They also secrete growth factors at an increased rate

Lots of blood vessels surroundings the cancerous cells as they require a lot of oxygen and nutrients in order to grow and divide as frequently as they do

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14
Q

Describe the multi-step process of tumour formation.

A

Initiation - mutation occurs within a single cell that results in its ability to no longer respond to normal cell signals.

Promotion - the cell divides to form a number of other abnormal cells.

Tumour growth - Which is when the abnormal cells stick together to form mass of abnormal cells

The above stages are pre-clinical stage

Progression - tumour metastasises and spreads to other parts within the Boyd.

The above stage is the mass can now be detected.

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15
Q

What is the diagnostic threshold?

A

The number of cancer cells it takes in order for the cell to be clinically detectable.

Ideally, we want to detect the cancer as close to the diagnostic threshold as possible.

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16
Q

What causes the initiation stage?

A

Chemically, physically or virally caused.

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17
Q

What causes promotion?

A

Growth factor or oncogenes.

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18
Q

What are growth factors?

A

Growth factors are polypeptide molecules that regulate cell growth and function.

They do this binding to cell membranes and receptors and stimulating the activation of intracellular signal transduction pathways.

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19
Q

What two ways are growth factors stimulated?

A

Autocrine

Paracrine

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20
Q

What is autocrine stimulation?

A

When a cell secretes a hormone or chemical messenger that binds to autocrine receptors on that same cell. This leads to the secretion of the growth factor.

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21
Q

What is paracrine stimulation?

A

When a cell produces a signal to induce changes in nearby cells, causing them to secrete growth factor

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22
Q

What is the most common tumour suppressor gene?

A

p53 gene

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23
Q

What two things commonly mutate tumour suppressor genes?

A

DNA damage

Hypoxia

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24
Q

What causes progression? What does this step involve?

A

Metastasis

When the cancerous cells spread from the blood vessels to a tissue and start to divide, forming a secondary tumour

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25
Q

What step occurs before metastasis? What does this step involve?

A

Invasion

When the cancerous cells invade through the basement membrane, which allows them to move into the surrounding tissue. They then invade blood vessels

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26
Q

What three enzymes are involved in the invasion of cancerous cells?

A

Matrix metalloproteinases

Plasmin

Cathespin

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27
Q

What are the role of the enzymes involved in the invasion of cancerous cells?

A

Destroying cell adhesions in the extracellular matrix so that the cancerous cells can move between them

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28
Q

What three enzymes are involved in the cells adhering onto another organ?

A

Cadherins

Integrins

CD44

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29
Q

What is angiogenesis? How does it occur?

A

The formation of new blood vessels

The degradation of the extracellular matrix, which means that there is space for the blood vessels to grow

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30
Q

When does angiogenesis occur? Why?

A

After progression

Supplies the cancerous cells with the nutrients it needs to grow

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31
Q

What is VEGF? What is its role?

A

Vascular endothelial growth factor

Massive role in the promotion of cancer cells

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32
Q

What effect does the anti-VEGF have on VEGF?

A

This antibody binds to VEGF and prevents any interaction with receptors and therefore the activation of intracellular signalling pathways. Therefore, the tumour remains dormant and doesn’t metastasise

33
Q

How do cancerous cells hide within the body?

A

They have self antigens, known as PDL-1

T-cells have PD1 antigens on their cell surface which are programmed cell death receptors.

Ligands on tumour cells, known as PDL-1 are able to interact with PD1 and prevent them from being detected as foreign by T-cells.

34
Q

What does screening allow?

A

Early detection of cancer and thus increase the survival rate of those affected by it

35
Q

What are the disadvantages of screening?

A

Give patients false reassurance, as the tests are not perfect and can lead to patients believing that they are cancer free when this is not the case.

Make health inequalities more prominent as lower socioeconomic individuals are less likely to turn up to the screening clinics compared to wealthier individuals.

36
Q

What three cancers are there screening programmes set up for within the NHS?

A

Cervical

Colorectal

Breast

37
Q

What cancer is common in individuals who have the BRCA1 and BRCA2 genes?

A

Breast

38
Q

What cancer is common in individuals who have the FAP gene?

A

Colorectal

39
Q

What do we use to identify where a cancer is?

A

Radiological imaging

40
Q

What do we use to determine the type of cancer?

A

Pathology

Cytology

41
Q

What are the two local treatments of cancer?

A

Surgery

Radiotherapy

42
Q

How can we use surgery to treat cancer?

A

Physically remove the tumour from the tissue.

Surgeons always remove some of the healthy tissues around the tumour, known as the ‘holy plane’ to ensure that they have removed all of the tumour

43
Q

What does surgery require?

A

Anatomical clearance

44
Q

What does radiotherapy require?

A

Anatomical coverage

45
Q

Why can radiotherapy be useful in treating cancer?

A

Treat inoperable lesions and make surgery become possible

Maintain function and appearance of tissue

46
Q

What are the 5R’s when it comes to radiobiology?

A

Radiosensitivity

Repair

Re-population

Re-oxygenation

Re-assortment

47
Q

How does radiosensitivity effect radiotherapy?

A

It is the relative of susceptibility of cell to the harmful effects of radiation

48
Q

How does repair and re-population effect radiotherapy?

A

Most effective when we don’t give cancer a chance to grow in between treatments.

The problem with doing this is that it can affect normal tissue and induce more side effects

49
Q

How does re-oxygenation effect radiotherapy?

A

A low oxygen supply means that the tumours are more resistant to treatment

50
Q

How does radiosensitivity effect radiotherapy?

A

Cells are more or less affected depending on the stage they are in on the cell cycle

Most sensitive - G2
Least sensitive - S

51
Q

What is systemic therapy? What is the disadvantage?

A

Therapy used to treat widespread diseases

Widespread toxicity

52
Q

Name four common systemic therapies?

A

Chemotherapy

Immunotherapy

Hormonal therapy

CAR T-cell therapy

53
Q

What is adjuvant treatment?

A

Additional treatment designed to help reach the ultimate goal

With cancer, it refers to surgery followed by chemotherapy or radiotherapy to decrease the risk of the cancer coming back

54
Q

What is neoadjuvant treatment?

A

Refers to medicines that are administered before surgery in order to decrease the size of the tumour and make the success of cancer more likely

55
Q

What are targeted therapies?

A

Specific and based on molecular science

It works by targeting the cancer’s specific genes, proteins or the tissue environment that contributes to cancer growth and survival

56
Q

What are non-specific immunotherapies?

A

Involve the recruitment of non-specific cells, such as macrophages and NK cells.

These cells result in apoptosis, which is also known as the PD-1 pathway.

57
Q

What are specific immunotherapies?

A

Involve monoclonal antibodies and CAR T-cells

58
Q

What are monoclonal antibodies?

A

Antibodies produced in the lab and genetically engineered to save as antibodies that can restore, enhance or mimic the immune system’s attack on cancer cells.

59
Q

What are CAR T-cells?

A

T-cells collected from the patient’s blood, which are then modified to produce antigens that are specific to the antigens on cancerous cells

60
Q

Why are hormonal therapies useful when treating cancer?

A

Block what we want, nothing else, which means that the drugs are more tolerable. These drugs also result in a rapid response.

61
Q

What is the usual mechanism of immunotherapies?

A

Inhibit the PDL1 interactions with PD1

62
Q

What is systemic anti-cancer treatment?

A

Chemotherapy

63
Q

How can we administer chemotherapy? What method is preferred why?

A

Intravenously or orally

Oral - doesn’t need to be administered within the hospital and medication can be taken at home.

64
Q

What effects the timing of chemotherapy cycles to patients?

A

The half-life and excretion of the drugs

65
Q

Where do toxicities relating to chemotherapy usually occur?

A

Bone marrow

66
Q

What is the function of ALL cytotoxic agents?

A

To halt the cell cycle

67
Q

How can we maximise the effectivity of cytotoxic agents?

A

Find out the stage that the cancerous cell are in and select the treatment that targets. that stage.

68
Q

Name the four groups of cytotoxic agents

A

Alkylating agents

Antimetabolites

Vinca alkaloids and taxanes

Antimitotic antibodies

69
Q

What are alkylating agents? How do they affect cancer?

A

Contain an alkyl group

This alkyl group covalently binds to free G’s on separated DNA strands. This results in the DNA strand no longer being able to take part in DNA replication, resulting in DNA replication halting and the cell cycle stopping.

70
Q

What are the three mechanisms that cells can develop resistance to alkylating agents?

A

Decreased entry or increased exit of the agent

Cause inactivation of the agent within the cell

Enhance the repair of DNA lesions that are produced by the agents

71
Q

What do we do if cells develop resistance?

A

We switch agents

72
Q

What are antimetabolites?

A

Have a similar chemical structure to essential metabolites required by cells prior to cell division.

They may incorporated into new nuclear material or they may bind irreversibly with vital enzymes to inhibit cell division. In other words, they are agents which are added into the cell and inhibit the cell cycle in this way

73
Q

What are vinca alkaloids?

A

Metaphase arrest agents by binding to tubulin and blocking microtubule and spindle formation, which are essential for mitosis.

They inhibit the cell cycle by affecting spindle formation

74
Q

What are taxanes?

A

Promote spindles and freezes cells at that stage of the cell cycle.

They inhibit the cell cycle by affecting spindle formation

75
Q

What are the two types of anti-mitotic antibodies?

A

Anthracyclines

Non-anthracyclines

76
Q

What are anti-mitotic antibodies`?

A

Inhibit DNA and RNA synthesis by binding to the membranes of cells. This increases their permeability to various ions.

Free radicals can then enter the cell and disrupt the DNA chain and prevent mitosis.

Metal ions can also enter the cell and result in the formation of cytotoxic compounds.

77
Q

Why is it important that we get a balance between efficiency and safety?

A

We don’t want to experience intolerable side effects, but we also don’t want them to have to undergo the treatment longer they should do due to the fact that aren’t delivering the strongest medication

78
Q

Why do we combine agents with different mechanisms of action?

A

Synergistic effect - produce a combined effect greater than the sum of their separate effects

Additive effect - effects of the two chemicals is equal to the sum of the effect of the two chemicals taken separately

79
Q

Why do we combine agents with dissimilar toxicity profiles?

A

Allows us to give the maximum tolerated dose

Year One - Principles of Disease (15 decks)

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