Oncology Flashcards

1
Q

What is cancer?

A

When abnormal cells divide in an uncontrolled way

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2
Q

Why can cancer be called a clonal disease?

A

It can arise from a single cell

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3
Q

What makes a cell divide?

A

Specific positive signals, e.g. growth factors and hormones

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4
Q

What is contact inhibition?

A

When in contact with neighbouring cells, cells initiate cell cycle arrest and down regulate proliferation so they stop dividing so as not to grow over neighbouring cells

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5
Q

What is DNA damage response?

A

If there’s something wrong with the DNA of a cell, it won’t divide until that DNA is repaired

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6
Q

What are somatic mutations?

A

Mutations in a single cell

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7
Q

Define oncogene

A

A gene which, in certain circumstances, can transform a cell into a tumour cell

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8
Q

Define proto-oncogene

A

A normal gene which, when altered by mutation, becomes an oncogene that can contribute to cancer

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9
Q

What are all known photo-oncogenes involved in?

A

Positive control of cell growth and division

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10
Q

What are the 5 main classes of photo-oncogene?

A

Class I- Growth factors
Class II- Receptors for growth factors and hormones
Class III- Intracellular signal transducers
Class IV- Nuclear transcription factors
Class V- Cell-cycle control proteins

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11
Q

What happens when an oncogene is mutated?

A

Control of growth is relaxed, allowing unregulated proliferation

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12
Q

At the cellular level, are mutations of oncogenes dominant or recessive?

A

Dominant

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13
Q

Are mutations of tumour suppressor genes dominant or recessive?

A

Recessive

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14
Q

In most inherited cancer syndromes due to tumour suppressor gene mutations, are the 2 mutations inherited or somatic?

A

1 mutation is inherited and the other is somatic

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15
Q

What is the significance of TP53 gene?

A

TP53 codes for p53 protein, which inhibits cell replication if DNA damage is detected or virus replication is detected in the cell. If the damage is not repaired, p53 signals apoptosis. In many tumours, TP53 is inactivated due to mutation, gene deletion or both

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16
Q

How does HPV increase the risk of cervical cancer?

A

HPV infects cervical epithelium and inhibits p53, so there’s no apoptosis of cells with damaged DNA

17
Q

How do mutations in DNA repair genes increase risk of cancer?

A

Mutations in DNA repair genes increases the risk of mutations in oncogenes/ tumour suppressor genes

18
Q

What is epigenetics?

A

The study of changes in gene expression caused by mechanisms other than changes in the underlying DNA sequence (DNA methylation and histone modification

19
Q

Name the 3 types of cancer treatment

A

Surgery
Radiotherapy
Drug therapy

20
Q

Name the 4 types of drug therapy

A

Chemotherapy
Targeted therapy
Immunotherapy
Endocrine therapy

21
Q

What is combination therapy?

A

Therapy in which the patient is given 2 or more drugs for a single disease

22
Q

What is Neo-adjuvant therapy?

A

Administration of a therapeutic agent before the main treatment

23
Q

What is adjuvant therapy?

A

Therapy applied after an initial treatment of cancer, often to suppress secondary tumour formation

24
Q

What is prophylactic therapy?

A

Therapy intended to prevent cancer from occurring before it has

25
Q

What are the 5 stages of cancer?

A
Stage 0- Carcinoma in situ
Stage 1- Localised
Stage 2- Early; locally advanced
Stage 3- Late; locally advanced
Stage 4- Metastasised
26
Q

How does radiotherapy work?

A

High energy X-rays or gamma rays cause breaks in DNA, damaging the DNA in cancer cells, as well as healthy cells, so they undergo apoptosis

27
Q

Why is radiotherapy given in multiple fractions?

A

So there are fewer side effects- healthy cells repair themselves better after radiotherapy than cancer cells, so doing radiotherapy in fractions allows healthy cells to recover

28
Q

Name 5 possible side effects of radiotherapy

A

Oedema, alopecia, pain, fibrosis and secondary cancers caused by DNA damage from X-rays

29
Q

How does chemotherapy work?

A

Cytotoxic drugs are used to treat cancer. The drugs damage the DNA of cancer cells, leading to the breakage of the DNA double strands, inhibiting mitosis and DNA replication, leading to apoptosis.

30
Q

What type of cancers is chemotherapy most effective against?

A

Fast-growing cancers that replicate at the fastest rate, so the cells will be killed faster.

31
Q

Aside from fast-growing cancers, what other type of cancer responds best to chemotherapy?

A

Clonal cancers in which all the cells are the same

32
Q

Name 3 drugs used for chemotherapy

A

Cisplatin, paclitaxel and bleomycin

33
Q

Name 7 possible side effects of chemotherapy

A
Damage to rapidly dividing normal cells
Fatigue
Myelosuppression
Risk of infection
Skin toxicity (rash, alopecia)
GI disturbance (nausea, diarrhoea, mucositis)
Venous thromboembolism
34
Q

What can biopsies determine about cancers?

A

The subtype of tumour, or a specific mutation in the cancer

35
Q

How does immunotherapy work?

A

Imunotherapy switches the immune system back on against cancers that evade the immune system. Monoclonal antibodies can block pathways that cancer has unregulated to evade the immune system.

36
Q

In what types of cancers does immunotherapy work better?

A

Cancers with a lot of mutations and Neo-antigens

37
Q

Name 4 side effects of immunotherapy

A
Inflammatory and auto-immune conditions such as:
Rashes
Colitis
Thyroid dysfunction
Pneumonitis