14.5 Pathology: Dysplasia carcinoma sequence

Question 1

What are the ‘on/go’ genes?

Answer 1

Oncogenes

Question 2

What mutations can occur to alter proto-onco genes?

Answer 2

One hit: single mutation

Question 3

How do tumour supressor genes lose function?

Answer 3

Two hits (2 mutations have to occur)

Question 4

What are 2 types of pre-malignant lesions?

Answer 4

Dysplasia (intraepithelial neoplasis)

Carcinoma in situ

Question 5

What types of cancers are:
Carcinoma
Sarcoma
Lymphoma/leukaemia

Answer 5

Malignant:
Carcinoma (epithelium)
Sarcoma (stroma)
Lymphoma (haematopoeitc)

Question 6

What is the definition of a malignant lesion?

Answer 6

Cells that breach the basement membrane to invade underlying stroma

Question 7

What can occur as a result of:
Chronic reflux oesophagitis
Chronic atrophic gastritis
Chronic inflammation/smoking

Answer 7

Barrett’s oesophagus
Intestinal metaplasia
Squamous metaplasia (lung bronchial epithelium)

Question 8

What types of HPV are involved in high risk types?

Answer 8

Types 16 and 18 (severe squamous dysplasia–>carcinoma)

Question 9

What is diagnostic confirmation of severe dysplasia?

Answer 9

P16 Upregulation

Ki67 (cell proliferation marker)

Question 10

What is a cellular feature of displasia (e.g. on a pap smear)?

Answer 10

Increased nuclear:cytoplasmic ratio

Question 11

How do we distinguish mild/moderate/severe cervical dysplasia?

Answer 11

Mild: 1/3rd
Moderate: 2/3rds
Severe: all the way through

Question 12

What is Barrett’s oesophagus caused by? (what is the increased relative risk)?

Answer 12

Chronic reflux oesophagitis (30-60x relative risk)

Question 13

What is special about breast ductal carcinoma in situ (DCIS)?

Answer 13

No metaplastic precursor