16 GI cancers Flashcards

1
Q

What are the 2 main types of GI cancers

A

Adenocarcinoma (often from Barrett’s M)

Squamous Cell Cancer

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2
Q

How would we test those with Barrett’s to see if they have ADC?

A

sponge on a string mate for a biopsy

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3
Q

What proportion of Barrett’s patients have ADC, and where is the research directed?

A

15%
the research is going into developing a biomarker of cancer risk in those with barrett’s, which owuld save a lot of money on endoscopy

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4
Q

What are the epithelial cell changes occuring from normal cells to ADC?

A

normal stratified squamous
BM - columnar simple
Dysplasia - bigger nucleus, chromosomal gains
ADC - even bigger nucleus, more chromosomal gains

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5
Q

Generally, what might promote the risk of ADC?

A

anything that promotes reflux

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6
Q

What might suppress the risk of oesophageal cancer?

A

H. Pylori

decreased stomach H+, reducing the likelihood of reflux

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7
Q

How does H.Pylori achieve its’ functions?

A

releases exotoxins, like urea, which converts stomach acid into bicarbonate, neutralising its’ local niche
also secretes mucinase, allowing them to attach to the epithelium to mount an inflammatory response (mediated by IL-6) to protect them.

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8
Q

What is E-cadherin?

What might happen if it’s mutated?

A

transmembrane protein in the adherins junctino, forming a zip between 2 cells
in mutation, cell integration is limited, and cells become more motile and invasive during proliferation
Hereditary Diffuse Gastric Cancer (HDGC)
cells that wouldn’t normally produce E-cadherin now begin to produce it, to stick together

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9
Q

What might cause E-Cadherin repression?

A

epigenetic events
promotor hypermethylation
EMT (epithelial mesenchymal transition) regulators

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10
Q

How might we suppress E-Cadherin?

A

slug and snail are EMT regulators, with slug/snail the epithelial cells grown in culture are more spindly, and hence more likely to metastatise

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11
Q

What use might there be to understanding what enduces EMT regulators?

A

potential therapies

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12
Q

What sort of lifestyle is colorectal cancer associated with?

A

western lifestyle, with red and processed meats

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13
Q

What are the 2 main types of colorectal cancer?

A

Sporadic

Familial (people tend to be young)FAP

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14
Q

What is FAP?

A

Familial adenomatous polyposis coli

the polyps can develop into coli

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15
Q

How might FAP be treated?

A

prophylactectomy, reducing their risk of developing FAP elsewhere

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16
Q

What is the difference between cancerous colonic cells and normal colonic cells?

A

non cancerous cells use APC to phosphorylate proteins like beta-catenin, preventing them from switching on oncogenes, this is inhibited in cancerous colonic cells

17
Q

How will nuclear beta-catenin molecules affect matastasis?

A

beta-catenin presence in the nucleus will increase