Dysplasia Carcinoma Sequence General Principles Flashcards

1
Q

What features define malignancy?

A

dysregulated cell growth, invasive and metastatic potential, aberrant cytomorphology, disordered architecture, and molecular changes in oncogenes, tumour suppressor genes and DNA repair genes

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2
Q

What do oncogenes do?

A

Switch on the cell cycle leading to more proliferation than normal

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3
Q

What to tumour supressor genes do?

A

Regulate the cell cycle at checkpoints

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4
Q

What do DNA repair genes do?

A

Perform checks in DNA at checkpoints

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5
Q

What are some examples of proto-oncogenes?

A

growth factor receptors, kinases, transcription factors

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6
Q

What are some different types of mutations which can occur?

A

translocation, gene amplification, simple mutations

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7
Q

Why do tumour supressor genes need a double hit mutation?

A

Because there needs to be a loss of function in both proteins

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8
Q

What is carcinoma?

A

Cancer of the epithelium

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9
Q

What is sarcoma?

A

Cancer of mesenchymal cells

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10
Q

What is dysplasia?

A

A premalignant lesion

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11
Q

What is metaplasia?

A

An adaptive change in mature cell differentiation in response to the environment which can be a precursor to dysplasia

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12
Q

What is the cervical transformation zone?

A

The are of the cervix where squamous epithelium becomes glandular epithelium - this area shifts and is the area most likely to be infected by HPV

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13
Q

What are the high risk types of HPV?

A

type 16 and 18

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14
Q

How does HPV cause cervical cancer?

A

plasmid may integrate with host DNA and lead to over expression of oncoproteins E6 and E7, lose inhibitor feedback on p53 and Rb and leads to compensatory up regulation of P16

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15
Q

What is used as a biomarker for high risk HPV?

A

P16 upregulation

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16
Q

Why are pap smears important?

A

To screen for cervical cancer

17
Q

How is intraepithelial neoplasia graded?

A

Whether the dysplasia is mild, moderate or severe

18
Q

What is Barrett’s oesophagus?

A

A consequence of oesophageal reflux - columnar lining in oesophagus above gastroesophageal junction

19
Q

What is Barrett’s oesophagus a precursor for?

A

oesophageal adenocarcinoma

20
Q

How can you determine if a breast ductal carcinoma in situ has become invasive?

A

absence of myoepithelial layer on staining

21
Q

What is the boundary that defines whether dysplasia has become an invasive carcinoma?

A

Different depending on the site - basement membrane in the cervix and oesophagus, muscularis mucosae in the colon, myoepithelial cell layer in the breast, basal cell layer in the prostate

22
Q

What are the different modes of carcinoma spread?

A

direct invasion, lymphatic invasion, vascular invasion, perineural invasion