Colorectal Cancer (Colon Carcinoma): Classification

When carcinoma is detected, the histologic findings (fine-tissue findings) should include the following features, according to the S3 guideline:

  • The extent of deep infiltration (pT category), and for sessile polyps (firmly grown polyps), the sm invasion measurement in μm,
  • The histological degree of differentiation (grading),
  • Presence or absence of lymphatic vessel invasion (L classification),
  • And assessment of resection margins (R classification) with respect to local removal in healthy individuals (to depth and to the side).

The following staging classifications are distinguished in colon carcinoma (colorectal cancer): The TNM classification is a prognosis-oriented classification system of the UICC (Union internationale contre le cancer).

TNM system – tumor size / nodus (lymph node involvement) / metastases (daughter tumor) 0 = not present ; 1 = present.

Stage Tumor size Nodus Metastasis
0 Tis – tumor in situ N0 M0
I T1 N0 M0
T2 N0 M0
II T3 N0 M0
T4 N0 M0
III each T N1 M0
each T N2, N3 M0
IV each T each N M1

Dukes classification

Dukes UICC Findings 5-year survival rate
A I Tumor growth confined to intestinal wall, infiltration maximal to muscularis propria, no lymph nodes affected 95-100 %
B1 II Tumor growth beyond muscularis propria, no lymph nodes involved 85-95 %
B2 II Invasion of serosa or pericolic adipose tissue, no lymph nodes involved
C III Lymph node involvement (for tumor spread A or B). 55-65 %
D IV Distant metastases 5 %

Consensus Molecular Subtypes (CMS).

Approximately 87 percent of all colorectal cancers are distributed among four molecular subtypes:

Subtype Description
CMS 1 (“MSI Immune”, share 14 %)
  • Characterized by microsatellite instabilities and hypermethylation in DNA segments with increased CpG dinucleotide density.
  • BRAF mutations are often present and strong activation of the immune system. [possibly immunotherapy useful?]
CMS 2 (“canonical”, share: 40%)
  • Shows highest chromosomal instability of all four groups.
  • Cancer genes WNT, MYC, and EGFR are frequently active. [These can be blocked by drugs].
CMS 3 “metabolic”, share 15%)
  • Characterized by deregulation of metabolic pathways and mutations in the KRAS gene[Currently no targets for therapy].
CMS 4 (“mesenchymal”, proportion 30%)
  • Conspicuous by the high number of somatic copy number variations.
  • Tumor grows in a highly infiltrative manner, activating TGF-beta and stimulating the formation of its own blood vessels. [Responds poorly to standard treatment.]
  • Recurrence-free and overall survival are lower than for the other three subtypes.