9. Multistep theoryof carcinogens, dysplasia, screening Flashcards

1
Q

Explain the multistep theory of carcinogenesis

A

Several mutations required
Each mutation drives a wave of cellular multiplication associated with gradual increase in tumour size, disorganisation and malignancy.
3-6 mutations appear to be required to complete this process

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2
Q

What are the different stages of morphological appearance for development of a carcinoma? Molecular changes during this time

A
Normal epithelium
Hyperproliferative epithelium 
Early adenoma 
Intermediate adenoma
Late adenoma 
Carcinoma
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3
Q

What are the two types of cancer critical genes?

A

Oncogenes

Tumour Suppressor Genes

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4
Q

What do onogenes do and what effect do they have?

A

Stimulate cell division or inhibit cell death and therefore increasing the number of cells

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5
Q

What do tumour suppressor genes do and what effect to they have?

A

Inhibit cell division or stimulate cell death and decrease cell number

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6
Q

What is meant by dysplasia and carcinoma in situ?

A

Represent stages in the cellular journey to invasive malignancy

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7
Q

How does dysplasia differ from carcinoma in situ ?

A

Dysplasia does not present any symptoms and posses so of the abnormalities associated with cancer however there is no invasion of cells into the surrounding tisssue

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8
Q

What does dysplasia look like microscopically?

A

Many features of cancer present sich as haphazard arrangement of cells, crowding of nucleiand increased number of mitotic figures but there is no evidence of invasion

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9
Q

If dysplasia is asymptomatic how do we find these patients?

A

If the lesion involves the skin then it is visible and patients will present to their GP or through screening programmes

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10
Q

If dysplasia is asymptomatic how do we find these patients?

A

If the lesion involves the skin then it is visible and patients will present to their GP or through screening programmes

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11
Q

What are some the risks associated with cancer screening programs?

A

Anxiety and unnecessary investigation in completely healthy patients
Overtreatment of patients with mild dysplasia
Very early treatment of some small very slow growing cancers which may not be of clinical benefit
Missing some cancer causes

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