Inflammation and Carcinogenesis Flashcards

1
Q

What are the hallmarks of cancer-related inflammation?

A

➢ Inflammatory cells and inflammatory mediators (e.g,
chemokines, cytokines and prostaglandins) present in
tumour tissues.
➢ Tissue remodelling is similar to that seen in chronic
inflammatory responses.
➢ Angiogenesis is similar to that seen in tissue repair
(required for the survival of cells within tumours of a
certain size & tumour metastasis).
➢ Inflammatory cells and mediators are present in the
microenvironment.

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2
Q

How does inflammation lead to cancer?

A
  1. When the cancer cells are struggling to gather nutrients and O2 they release cytokines which stimulate immune cells to infiltrate the tumour.
  2. Release of these cytokines stimulates angiogenesis - providing nutrients and O2.
  3. Incoming inflammatory cells also hit the developing tumour with free radicals that further damage cellular DNA.
    4.
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3
Q

How can inflammation encourage metastasis?

A

Inflammation can also initiate tumour spread (metastasis) by stimulating enzyme production that help tumour cells eat through the molecules tethering them to their surroundings.

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4
Q

What is the main infectious agent that causes cancer of the nasopharynx?

A

Epstein-Barr virus

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5
Q

What is the main infectious agent that causes cancer of the bladder?

A

Schistosoma haematobium

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6
Q

What is the normal gastric carcinogenesis pathway?

A
Normal gastric epithelium
Superficial gastritis
Atrophic gastritis
Intestinal metaplasia
Dysplasia
Gastric adenocarcinoma
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7
Q

What does gastric intestinal neoplasia precede and what usually triggers it?

A

GIM considered to be a pre-neoplastic gastric lesion.

Usually triggered by chronic helicobacter pylori infection.

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8
Q

What is the main virulence factor produced by H.pylori?

A

CagA (cytotoxin associated gene A)

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9
Q

Bacterial epithelial interaction may be crucial in the development of cancer for what reasons?

A
  1. Stimulation of epithelial (Toll-Like) receptors and consequent inhibition of apoptosis.
  2. DNA-damaging (genotoxic) effects.
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