Summary Research Q7 – Screening as early diagnostics
What is colorectal cancer
What is colorectal cancer? Multiple levels:
- Origin (cells)
- Biological background (precursors, mechanisms and molecules)
- Diagnostic procedure (presence and stage, when do you call something colorectal cancer)
- Treatment options
- Outcomes
Adenocarcinoma risk factors:
- Hereditary cancer syndromes (check precursors and molecules)
- Chronic inflammation (IBD, crohn > damage)
- Ageing > risk factor for all kinds of cancer
Inflammation and ageing: CRC
- Changing of the microenvironment
o Cytokine networks/bioactive molecules
o Cell recruitment and decreased anti-tumor response
- Reactive oxygen and nitrogen
o DNA damage
o Activation of oncogenes
o Inactivation of tumor suppressor genes
o Structural damage
- CpG island methylation
- Telomere shortening
Hallmarks of cancer:
- Resist cell death / telomere
- Sustain proliferative signalling
- Evade growth suppressors
- Induction of angiogenesis (easier in environment with lot of inflammation)
- Activate invasion and metastasis
- Enable replicative immortality
Emerging hallmarks:
- Avoiding immune distruction
- Deregulating cellular energetics
Enabling characteristics:
- Tumor-promoting inflammation
- Genome instability and mutation
Cancer development: histology
Normal mucosa > bump (hyperplastic epithelium) > polyp formation > darker > instability > cancer
Normal mucosa is always of the same thickness
, Histology picture > darker > more cells > mutations
Cancer = invasion of tumor cells outside their original compartment > through muscularis mucosa
Hyperplasia: reaction on damage or inflammation > difficult in the bowel because every cell has his
own place with function on the basal membrane > starshaped lumen // premalignant sign
Dysplasia: loose majority of gobletcells, increase in size but also in number of nuclei (darker) + loose
contact with membrane, large variation, you can’t recognize the crypts
What is colorectal cancer
What is colorectal cancer? Multiple levels:
- Origin (cells)
- Biological background (precursors, mechanisms and molecules)
- Diagnostic procedure (presence and stage, when do you call something colorectal cancer)
- Treatment options
- Outcomes
Adenocarcinoma risk factors:
- Hereditary cancer syndromes (check precursors and molecules)
- Chronic inflammation (IBD, crohn > damage)
- Ageing > risk factor for all kinds of cancer
Inflammation and ageing: CRC
- Changing of the microenvironment
o Cytokine networks/bioactive molecules
o Cell recruitment and decreased anti-tumor response
- Reactive oxygen and nitrogen
o DNA damage
o Activation of oncogenes
o Inactivation of tumor suppressor genes
o Structural damage
- CpG island methylation
- Telomere shortening
Hallmarks of cancer:
- Resist cell death / telomere
- Sustain proliferative signalling
- Evade growth suppressors
- Induction of angiogenesis (easier in environment with lot of inflammation)
- Activate invasion and metastasis
- Enable replicative immortality
Emerging hallmarks:
- Avoiding immune distruction
- Deregulating cellular energetics
Enabling characteristics:
- Tumor-promoting inflammation
- Genome instability and mutation
Cancer development: histology
Normal mucosa > bump (hyperplastic epithelium) > polyp formation > darker > instability > cancer
Normal mucosa is always of the same thickness
, Histology picture > darker > more cells > mutations
Cancer = invasion of tumor cells outside their original compartment > through muscularis mucosa
Hyperplasia: reaction on damage or inflammation > difficult in the bowel because every cell has his
own place with function on the basal membrane > starshaped lumen // premalignant sign
Dysplasia: loose majority of gobletcells, increase in size but also in number of nuclei (darker) + loose
contact with membrane, large variation, you can’t recognize the crypts
