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Year 1 Medicine > Cancer > Flashcards

Cancer Flashcards

1
Q

What is a carcinoma?

A

Disorderly growth of epithelial cells that invade adjacent tissues and spread vis the lymphatics and bloodstream to other parts of the body.

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2
Q

What does it mean that most cancers are monoclonal?

A

They are derived from a single cell mutation.

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3
Q

How to cancer cells grow and divide?

A

Mitosis

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4
Q

How do some cancer cells escape chemotherapy treatment?

A

They hide within the non proliferating stage of mitosis and then recover and re-cycle in the body later on.

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5
Q

Give some properties of cancer cells?

A 
Increased growth factor secretion
Increased oncogene expression
Loss of contact inhibition
Loss of tumour suppressor genes. 
Frequent mitoses
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6
Q

What are oncogenes?

A

Genes that programme for cancer. Accelerate cell division.

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7
Q

Which type of cancer normally causes the death in a patient?

A

Cancer that has metastases rather than the primary cancer.

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8
Q

What are some causes of cancer

A 
Chemical carcinogens
Physical carcinogens
Viral carcinogens
Growth factors 
Oncogenes
Metastasis
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9
Q

Give some examples of a chemical carcinogen?

A

Polycyclic hydrocarbons
Nitrogen mustard
Alcohol and smoking

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10
Q

Give some examples of physical carcinogens?

A

Ionising radiation

Mechanism - chromosome translocation, gene amplification, oncogene activation.

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11
Q

Give some examples of viral carcinogens?

A

Herpes virus
Papillomavirus
Retroviruses
Hepatitis B

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12
Q

What do oncogenes do?

A

Involved in the promotion of cancer. They are transformed genes and promote the positive regulators for growth.

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13
Q

Give some examples of growth factors?

A

Polypeptide molecules.

VEGF - vascular endothelial growth factor.

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14
Q

What is the normal function of a tumour suppressor gene?

A

Acts as a transcriptional regulator:
Promotes DNA repair, apoptosis and cell differentiation.
The cell’s brakes for cell growth.

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15
Q

How do cancer cells induce the alteration of tumour suppressor genes?

A

Induced by DNA damage and hypoxia

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16
Q

What are the properties if metastasis?

A

Not random
Cascade of limited sequential steps
Involves humour-host interactions
Survival of the fittest pertains

17
Q

What are the main stages within invasion and metastasis?

A

Tumour invades through the basement membrane.
Moves into extracellular matrix/connective tissue/surrounding cells
Invades blood vessels
Tumour cells ‘arrested’ in distant organ

18
Q

What is angiogenesis?

A

The formation of new blood vessels.

19
Q

What is the role of angiogenesis in cancer.

A

Key factor in the maintenance and progression of malignant tumours.
A new blood vessel must form before a tumour can reach < 2mm in diameter.
It also provides a route for the cancer to spread and enter the circulatory system.

20
Q

What is the role of VEGF?

A

VEGF normally binds to receptors one the surface of vascular endothelial cells. This binding activates the signalling pathways that lead to growth, proliferation and migration of endothelial cells - increasing cancer.

21
Q

What is the function of Avastin?

A

Avastin is an anti-VEGF drug that prevents VEGF from interacting with its receptors. ultimately leads to a reduction in microvascular growth, inhibits progression of metastatic disease and reduces intratumoral pressure, which may improve the delivery of cytotoxic agents.

22
Q

What percentage of cancer patients have metastases?

A

65%

23
Q

How does the immune system not recognise foreign cancer cells?

A

Cancer cells can hide from T cells by the PDL-1 ligand on tumour cells binding with PD1 (programmed death receptor) on T lymphocytes. This suppresses the T cells and they become blinded.

24
Q

Where do somatic mutations occur?

A

Occur in nongermline tissues
Are nonheritable
E.g breast

25
Q

Where do germline mutations occur?

A

Present in egg or sperm
Are heritable
Cause cancer family syndromes
(All cells affected in offspring)

26
Q

What is a Proto-oncogene?

A

Normal gene that codes for proteins to regulate cell growth and differentiation.

27
Q

What is the two-hit hypothesis?

A

Cancer arises when both brakes fail

Cancer is the result of accumulated mutations to a cell’s DNA. Both genes need to be affected.

28
Q

What is the role of MisMatch Repair (MMR)?

A

Corrects errors that spontaneously occur during DNA replication like single base mismatches or short insertions and deletions.

29
Q

What is micro satellite instability?

A

MSI is the phenotypic evidence that MMR is not functioning normally.

30
Q

Define benign?

A

Lacks ability to metastasize.
Rarely or never become cancerous.
Can still cause negative health effects due to pressure on other organs.

31
Q

What is a dysplastic tumour?

A

‘Benign’ but could progress to malignancy.

Cells show abnormalities of appearance & cell maturation. Sometimes referred to as ‘pre-malignant’.

32
Q

Define malignant?

A

Able to metastasize.

33
Q

What are de novo mutations?

A

New mutations that occur within the germ cell of the parent. No family history of hereditary cancer syndrome

34
Q

What are some features of retinoblastoma?

A

Most common eye tumour in children.

Occurs in heritable and nonheritable forms

35
Q

What are the risk factors for breast cancer?

A 
Ageing
Family history
Early menarche
Late menopause
Nulliparity - not had children
Oestrogen use
Dietary factors (eg: alcohol)
Lack of exercise
36
Q

What are the risk factors for colorectal cancer?

A 
Ageing
Personal history of CRC or adenomas
High-fat, low-fibre diet
Inflammatory bowel disease
Family history of CRC

Year 1 Medicine (37 decks)

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