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1Principles of Biomedicine - MD1 > 125 - Dysplasia and Carcinoma Sequence > Flashcards

125 - Dysplasia and Carcinoma Sequence Flashcards

1
Q

Biological factors that define malignancy
1
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3

A

– Cells with dysregulated growth (loss of cell cycle control)
– Invasive and metastatic potential
– Morbidity and mortality

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2
Q

Morphological features that define malignancy
1
2

A

– Demonstration of invasion or metastasis

– Aberrant cytomorphology and disordered architecture

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3
Q 
Molecular/genetic features that define malignancy 
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4
A

– Inherited or acquired mutations
– Oncogenes, tumour suppressor genes, DNA repair genes
– Chromosomal gains/losses, translocations and aneuploidy
– Epigenetic changes (hyper/hypomethylation, miRNA) and altered gene expression

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4
Q

Example of a tumour suppressor gene involved in some breast cancers

A

BRCA1

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5
Q

Example of an anti-cancer therapy targeted to cells avoiding immune destruction

A

Immune-activating anti-CTLA4 mAb

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6
Q

Threat of pre-malignancies

A

Could become invasive

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7
Q

Intraepithelial neoplasia

A

Pre-malignant epithelium that hasn’t become invasive

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8
Q

Transformation

A

Change from a pre-malignant neoplasm into an invasive cancer

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9
Q

Cancer of epithelium

A

Carcinoma

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10
Q

Cancer of connective tissue

A

Sarcoma

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11
Q

When is a dysplasia classed as a carcinoma?

A

When it breaches basement membrane to invade underlying stroma

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12
Q

A cellular response to microenvironment

A

Metaplasia

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13
Q

Normal metaplasia

A

Cervical epithelial mucosa changes with hormonal cycle

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14
Q

Examples of pathological metaplasias
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A

1) Barret oesophagus
2) Chronic atrophic gastritis leads to intestinal metaplasia
3) Chronic inflammation or smoking leads to squamous
metaplasia in lung bronchial epithelium

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15
Q

HPV viral oncogenes

A

E6, E7

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16
Q

Low-risk HPVs

A

– Low risk types (e.g. types 6 and 11)
• major cause of genital warts
• mild squamous dysplasia (CIN1)

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17
Q

High-risk HPVs

A

– High risk types (e.g. types 16 and 18)
• moderate to severe squamous dysplasia (CIN 2-3)
• major cause of squamous cell carcinoma

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18
Q

Aspect of HPV that can lead to invasive tumour

A

Genome integration into host genome

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19
Q 
HPV genome integration
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A

1) E2 gene disruption during viral genome integration
2) Overexpression of E6 and E7 oncoproteins
3) Loss of p53 and Rb tumour suppressor function
4) Cell cycle can proceed despite DNA damage
5) Loss of p53 apoptosis function

20
Q

Name for characteristic appearance of HPV-infected histology

A

Koilocytosis

21
Q

Way to differentiate dysplasia in cervix

A

Can have low-level replication with inflammation.

Without inflammation, replication could be dysplasia.

22
Q

CIN grading

A

Used for squamous epithelial lines (CIN1, 2, 3 -> squamous cell carcinoma)

23
Q

CIN 2

A

Cell proliferaiton, mild dysplasia (squamous)

24
Q

CIN 3

A

Severe dysplasia.

25
Q

E6 effect

A

Binds p53.
Confers resistance to apoptosis.
Loss of G1/S, G2.M phase cel cycle check points.
Genome instabolity

26
Q

E7 effect

A
  • E7 binds Rb
  • Disrupts G1/S phase cell cycle checkpoint
  • Compensatory upregulation of P16 expression (G1/S function) due to loss of Rb function
27
Q 
Cytological features of dysplasia on a pap smear 
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5
A

1) Increased nuclear:cytoplasmic ratio
2) More marked nuclear hyperchromasia
3) Enlargement and irregularity
4) Mitoses
5) Loss of cytoplasmic differentiation

28
Q

CIN, AIN, VAIN

A

Cervical intraepithelial neoplasia, anal intraepithelial neoplasia, vaginal intraepithelial neoplasia, etc

29
Q

What do CIN, AIN, VAIN measure?

A

Classifications of dysplasias (1 is least severe, 3 is close to becoming a carcinoma)

30
Q

Proportion of those with longstanding reflux oesophagitis that develop Barrett’s oesophagus

A

5-8%

31
Q

How is Barrett’s oesophagus diagnosed (American College of Gastroenterology)?
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A

– Endoscopic evidence of columnar lining in oesophagus
above gastroeosophageal junction, AND
– Histological evidence of intestinal metaplasia (goblet
cells) in biopsies from the columnar epithelium
– N.B. Presence of goblet cells not required for
diagnosis of Barrett’s oesophagus in Japan or UK

32
Q

Metaplasia in Barrett’s oesophagus

A

Re-epithelialisation of simple squamous epithelium with columnar epithelium

33
Q

What can Barrett’s oesophagus lead to?

A

Adenocarcinoma

34
Q

Increase in adenocarcinoma risk with Barrett’s oesophagus

A

30-60x increase

35
Q

Annual rate of malignant transformation of Barrett’s oesophagus

A

0.5% progress to adenocarcinoma

36
Q

Most reliable way to ID cancers

A

Microscopically. Molecular techniques can be unreliable

37
Q

Aspect of low-grade dysplasia in Barrett’s oesophagus versus Barrett’s oesophagus without dysplasia

A

Dysplasic epithelium becomes pseudostratified

38
Q

Carcinoma in situ

A

Pre-invasive term for severe dysplasia at certain sites

39
Q

Name for carcinoma in situ of skin

A

Bowen’s disease

40
Q

Names of carcinoma in situ of breast

A

Ductal carcinoma in situ

Lobular carcinoma in situ

41
Q

Are there metaplastic precursors to breast cancers?

A

Not really

42
Q

Ductal carcinoma in situ

A

Carcinoma in situ of breast, with ducts present under microscope

43
Q

Features of progression from carcinoma in situ to invasive carcinoma
1 a

A

1) Breach of mucosal/anatomical boundary

a) Access to lymphatics, blood vessels, now has metastatic potential

44
Q 
Modes of carcinoma spread
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A

1) Direct invasion
2) Lymphatic invasion
3) Vascular invasion
4) Perineural invasion

45
Q

Direct invasion
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A

– Transcoelomic spread in body cavities

– Pleura (lung), peritoneum (ovary, GI tract)

46
Q 
Lymphatic invasion
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A

– Nodal metastases
– Sentinel lymph nodes
– Regional and distal lymph nodes
– Virchow’s node / Troisier’s sign: Left supraclavicular node

47
Q

Vascular invasion
1
2

A

– Direct invasion of blood vessels (renal cell carcinoma)

– Lymphatic drainage -> thoracic duct -> L subclavian vein

1Principles of Biomedicine - MD1 (157 decks)

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