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TNM staging of colorectal carcinoma

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Christopher Hills

on 23 June 2014

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Transcript of TNM staging of colorectal carcinoma

TNM staging of
colorectal carcinoma
Dr Christopher Hills
Anatomical Pathology
History of staging
Established by Cuthbert Dukes

A – Within bowel wall
B – Beyond wall but not nodes
C – Lymph nodes involved
D – Metastases

No longer used in Pathology
Dukes Classification 1932

A – Limited to mucosa
B1 – invades muscularis propria, no nodes
B2 – beyond muscularis propria, no nodes
C1 – invades muscularis propria, nodes positive
C2 – beyond muscularis propria, nodes positive
D – metastases
Modified Dukes (Astler & Coller) 1954
Separated staging into three parts
T – tumour
N – regional nodes
M – distant metastases

Prefixes include
p - pathological stage
c - clinical stage

Adopted by American Joint Committee of Cancer
TNM system - Denoix 1952
1st edition released in 1977

7th edition released in 2009 - came into effect 2010

Covers all organ systems and cancers

Each edition has small changes and new prognostic factors
Cancer staging manual
In Feb 2010 our pathology college released a colorectal cancer protocol for reporting

Covers minimum requirements for prognostic information in five areas
clinical details
specimen handling
macroscopic findings
microscopic findings
ancillary studies

Incorporates AJCC 7th Edition TNM staging

This is what we use to report colorectal carcinoma
RCPA Proforma
Clinical information is vitally important to us
Often all we get on the form is ‘sigmoid colon’

Important prognostic information that should be provided (and can change our handling)
Site of tumour
Operation type
Surgeon’s opinion of completeness of resection
Any known metastases
Neoadjuvant treatment – especially if can’t find tumour
Clinical details
Important prognostic features
Site of tumour
Size of tumour
Margin status
Perforation present
Invasion into adjacent tissue
Macroscopic findings
Not all parts of the colorectal system are created equal

Rectal specimens requires special care
Has non-peritonealised resection margin
Need to know if tumour is above, astride or below anterior peritoneal reflection
Also intactness of mesorectal tissue - complete, nearly complete or incomplete
more chance of residual disease if not all of perirectal fat removed
Tumours below anterior peritoneal reflection have highest rates of local recurrence
Bigger not necessarily worse - not a reliable prognostic factor
Distance to margins
End margins – rarely involved
Circumferential resection margin (CRM)
Size & margin
If perforation of colon at site of tumour
poor prognosis as tumour likely to be in peritoneal space
becomes pT4
If perforation of proximal bowel due to obstructing tumour, not classed as perforation
Important prognostic factors
Type of tumour
Grade of tumour
Depth of invasion (T)
Lymph node status (N)
Vascular and perineural invasion
Margin status and completeness of resection
Response to neoadjuvant treatment
Microscopic features
Not all tumours are the same
Most cancers are adenocarcinoma, NOS
Other types are mucinous, signet ring, small cell, medullary, adenosquamous and undifferentiated
Small cell, signet ring and undifferentiated have worse prognosis
Tumour type
Mucinous carcinoma
Small cell
Signet ring
Poor prognosis
Depends on proportion of gland formation
Well differentiated = >95% glands
Moderately differentiated = 50 – 95% glands
Poorly differentiated = 5-50% glands
Undifferentiated = <5% glands

Divided into two grades
Low grade = well and moderate differentiation
High grade = poorly differentiated and undifferentiated
Independent prognostic factor
Tumour grade
We have to search for lymph nodes within the mesocolon and mesorectal fat
Current guidelines for minimum number is 12 regional nodes
Apical node is identified
The greater the number of positive nodes the worse prognosis
If positive nodes – adjuvant treatment
Lymph nodes (pN)
Tumour within the lumen of a blood vessel or along nerve bundles
Gives the tumour a path to get to lymph nodes and other organs
If present then worse prognosis
Increased rates of lymph node and distant metastases
Vascular and perineural invasion
Most important is circumferential resection margin (CRM)
Up to 36% of rectal tumours have positive CRMs
Need to measure distance from tumour to inked margin
if less than 1mm then positive margin
The closer the tumour to margin the worse prognosis – increased local recurrence and cancer-related deaths
Three grades
R0 = complete resection, no residual tumour
R1 = Incomplete resection, margins involved or microscopic residual disease
R2 = Incomplete resection, macroscopic residual disease (either primary tumour, nodes or mets)
Completeness of resection (R status)
Neoadjuvant chemoradiation used for rectal cancers – downstages lesion
Amount of regression linked to prognosis
4 grades of response
Grade 0 – complete response
Grade 1 – single or small groups of cancer cells
Grade 2 – residual cancer within fibrosis
Grade 3 – Minimal or no response
TNM staging has y in front to indicate treatment
e.g ypT3 N0 MX
Response to neoadjuvant treatment
Specific genetic mutations seen in colorectal carcinoma can affect prognosis and treatment response
Complicated series of pathways that control cell division and growth involved
Current mutations being requested
Mismatch repair gene mutations
B-raf mutations
K-ras mutations
Ancillary studies
Also known as microsatellite instability
Four genes (MLH1, MSH2, MSH6 and PMS2) that act as proofreaders of DNA
Mutations to these genes causes mistakes in DNA during copying – leads to mutations in other genes – increases chance of cancer
Defects in mismatch repair genes can be familial (20%) or sporadic (random – 80%)
Mismatch repair genes
All four MMR proteins usually expressed in all cells of the body – normal proof-reading
If mutation in gene then loss of staining
Testing done on all patients under 50, multiple tumours or if requested by clinicians
MMRD testing
Tumours tend to be right sided and often are mucinous or medullary type
Tumours have better prognosis than non-MMRD tumours
However less responsive to 5-FU treatment (including Capecitabine)
Mismatch repair defect (MMRD)
Classified as Hereditary Non-Polypoid Colorectal Cancer syndrome (HNPCC)
Due to inherited mutations in mismatch repair genes
Cancers earlier and frequently multiple
Increased risk of other cancers (endometrial, gastric, ovarian etc)
Need to test other family members
Familial MMRD
In sporadic MMRD, MLH1 loses its proofreading ability due to hypermethylation, not inherited mutation
Part of its area of DNA to proof-read is the B-raf gene
B-raf is a promotor of cell growth
Leads to B-raf mutation and permanent activation
B-raf mutation only occurs in sporadic MMRD, not hereditary MMRD
B-raf gene testing performed if MLH1 stain is negative
If B-raf mutation present – sporadic MMRD
If B-raf mutation not present – could be HNPCC
Sporadic MMRD
Another gene involved in cell growth
Mutations in K-ras lead to permanent activation – results in uncontrolled cell growth
K-ras mutations most frequently seen in aggressive cancers with metastases at presentation
Worse progression free and overall survival
Anti-EGFR drugs (Cetuximab) won’t work if K-ras mutation
Vascular invasion
Perineural invasion
T, N and M combined into one line

Combines clinical and pathologic staging

eg. pT3 pN1b cM1a
tumour beyond muscularis, two or three nodes positive, metastases in one organ
Summary of above data into a few lines

Includes TNM, stage, resection status and any other pertinent points
Separates tumours into prognostic groups based on combination of T, N & M scores

Worse prognosis with higher stage

Does not include other prognostic factors apart from TNM
Sometimes deposits of tumour are found in soft tissue away from main tumour with no evidence of residual lymph node
Classed as a tumour deposit (TD)
If only TD present and no true lymph node mets then classed as N1c
Similar prognosis to N1a or N1b
Tumour deposit
Important changes
Reversed T4a and T4b
Added in N1c into node classification
Split M1 into M1a and M1b

Added in important prognostic factors
Tumour deposits
Response to adjuvant treatment
Circumferential resection margin
Perineural invasion
Mismatch repair status
K-ras mutation
new category in 7th edition
Metastasis (M) is usually a clinical diagnosis as usually not seen in specimen
M0 = no metastases
M1a = one site of metastases
M1b = two or more sites
new categories in 7th edition
previously other way round
New prognostic factor in 7th edition
New prognostic factor in 7th edition
New staging and prognostic factor in 7th edition
New prognostic factor in 7th edition
New prognostic factor in 7th edition
New prognostic factor in 7th edition
Invasion into other organs
Sometimes other organs that hang out near the colon get stuck to it around the cancer

The adhesion can be due to tumour invasion or from fibrosis and inflammation

We take plenty of sections from the area as proven invasion by cancer into another organ or structure is T4b - fibrosis is not
Thank you
Colorectal Oncology Nurse Specialist teaching, 10th August 2012
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