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PHAM02 > Wk 16: GI cancers > Flashcards

Wk 16: GI cancers Flashcards

1
Q

What is familial adenomatous polyposis (FAP)?

A
  • Inherited mutation in APC gene
  • Diagnosed: colonoscopy + genetic testing
  • Develop age 40
  • Colectomy in early life when detected
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2
Q

What are the variants in FAP?

A

Tumour supressor gene:

  • Attenuated FAP: specific APC mutants, fewer polyps
  • MUTYH: base excision repair
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3
Q

What are the risk factors of CRC?

A
  • Inc red/processed meat
  • Lack physical activity
  • Obesity
  • Alcohol + smoking
  • Genetic predisposition
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4
Q

What could decrease the likelihood of CRC?

A

Fibre, chicken + fish

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5
Q

Where is sporadic CRC most commonly found?

A
  • Descending colon
  • Sigmoid colon (KRAS)
  • Rectum (KRAS)
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6
Q

Where is IBD related CRC most commonly found?

A

Ascending colon (BRAF)

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7
Q

What is the CRC histology?

A
  • Loss of normal architecture
  • Hyperchromatic
  • Invasion through submucosa
  • Nucleus takes up greater proportion of cell
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8
Q

What are the 2 main sites for CRC metastases?

A
  • Liver (most common): venous drainage from colon to liver
  • Lungs: rare to see lungs alone
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9
Q

What is used to screen CRC?

A
  • Faecal occult blood stool test

Endoscopy:

  • Colonoscopy (gold standard)
  • Flexible sigmoidoscopy
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10
Q

What is faecal occult blood stool test?

A
  • Measure blood in stool
  • Card coated w/ guaic resin
  • Sample of stool applied to card
  • Hydrogen peroxide developer sol applied
  • Detects pseudoperoxidase activity of Hb
  • +ve = sigmoidoscopy
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11
Q

What are the limitations of faecal occult blood stool test?

A
  • +ve: red meat, cauliflower, uncooked veg + haemorrhoids
  • -ve: vit C
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12
Q

What happens when a patient undergoes colonoscopy?

A
  • Diet 3 days advance (low fibre + clear liquid)
  • Bowel prep (laxatives)
  • Every 5-10 yrs
  • Detects: polyps, adenomas + tumours
  • Usually for colitis associated CRC
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13
Q

What happens during sigmoidoscopy?

A
  • Removal of polyps + takes biopsies
  • Covers descending colon
  • No sedation
  • Red cost + shorter duration
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14
Q

What is the first treatment for CRC?

A
  • Surgery to remove tumour + adjuvant chemo red metastases
  • Adjuvant begins 6 wks after surgery
  • Radio not usually used
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15
Q

When would you usually use radiotherapy?

A
  • Not clear if tumour completely removed
  • Unable to have surgery
  • Rectal cancer to prevent recurrence
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16
Q

What are the agents used to target CRC?

A
  • EGFR inhibitors
  • VEGFR inhibitors: VEGF promotes neovasculature growth
  • Immunotherapy: targets PD-1, inc immune response - usually when not responding to chemo
17
Q

What can wild type patients receive + what renders this therapy ineffective?

A
  • Cetuximab/panitumumab - EGFR MAb
  • Ras mutant
18
Q

What is the VEGF pathway in CRC?

A
  • Tumour secretes VEGF
  • VEGF inc blood vessel expression + movement to tumour
  • Tumour inc blood supply
19
Q

What are examples of VEGF MAb?

A
  • Bevacizumab
  • Aflibercept
  • Ramucirumab
  • Regorafenib
20
Q

What are the key pathways in CRC?

A
  • Mismatch repair deficiency
  • High microsatellite instability

Mutations = abnormal antigens, targeted by immune cells

21
Q

What agent is used as immunotherapy to target PD-1?

A

Pembrolizumab

22
Q

What is the adjuvant treatment for Duke B + C colorectal cancer?

A

5-FU + folinic acid weekly

23
Q

What is the adjuvant treatment for Duke C?

A
  • FOLFOX (Oxaliplatin + 5 FU)
  • CAPOX (Capecitabine & Oxaliplatin)
  • Capecitabine
24
Q

What is the treatment for advanced disease?

A
  • FOLFIRI (Irinotecan + 5 FU)
  • CAPIRI (Irinotecan & Capecitabine)
25
Q

What is PD-L1?

A

Immune checkpoint that distinguishes self from nonself cells triggering an immune response against the tumour

26
Q

What does the vogelstein model describe in CRC?

A

How accumulation of DNA mutation leads to CRC progression

27
Q

What is the classification used in CRC?

A

Dukes

PHAM02 (35 decks)

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