Difference between revisions of "Colorectal tumours"

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'''Colorectal tumours''' are very common.  They are the bread and butter of GI pathology.  Non-tumour colon is dealt with in the ''[[colon]]'' article.
'''Colorectal tumours''', especially '''colorectal carcinomas''', are very common.  They are the bread and butter of GI pathology.  Non-tumour colon is dealt with in the ''[[colon]]'' article.


An introduction to gastrointestinal pathology is in the ''[[gastrointestinal pathology]]'' article.  The precursor lesion of colorectal carcinoma (CRC) is, typical, an adenomatous polyp.  Polyps are discussed in the ''[[intestinal polyps]]'' article.  
''Colonic tumours'' and ''rectal tumours'' redirect here.


==Classification==
An introduction to gastrointestinal pathology is in the ''[[gastrointestinal pathology]]'' article. The precursor lesion of colorectal carcinoma (CRC) is, typically, an [[adenomatous polyps|adenomatous polyp]].  Polyps are discussed in the ''[[intestinal polyps]]'' article.
*Colon & rectum, most common --by far-- is [[adenocarcinoma]].<ref>{{Ref PBoD|864}}</ref>


Other tumours - many (incomplete list):<ref>{{Ref WMSP|198}}</ref>
=Classification=
*Mucinous carcinoma.
===Most common===
*Adenosquamous carcinoma.
*Colon & rectum - most common = [[colorectal adenocarcinoma|adenocarinoma]].<ref name=Ref_PBoD864>{{Ref PBoD|864}}</ref>
 
===Others===
Other tumours - many (incomplete list):<ref name=Ref_WMSP198>{{Ref WMSP|198}}</ref>
*[[Mucinous carcinoma]].
**Need > 50% mucinous component.<ref name=pmid17679024 >{{cite journal |author=Tozawa E, Ajioka Y, Watanabe H, ''et al.'' |title=Mucin expression, p53 overexpression, and peritumoral lymphocytic infiltration of advanced colorectal carcinoma with mucus component: is mucinous carcinoma a distinct histological entity? |journal=Pathol. Res. Pract. |volume=203 |issue=8 |pages=567–74 |year=2007 |pmid=17679024 |doi=10.1016/j.prp.2007.04.013 |url=}}</ref>
*[[Adenosquamous carcinoma]].
*Signet-ring carcinoma.
*Signet-ring carcinoma.
*Squamous carcinoma.
*Squamous carcinoma.
*Neuroendocrine neoplasms (carcinoid tumours).
*[[Neuroendocrine neoplasm]]s (carcinoid tumours).
*Lipoma.
*[[Lipoma]].
*Leiomyoma.
*[[Leiomyoma]].
*[[Gastrointestinal stromal tumour]] (GIST) - dealt with in a separate article.
*[[Gastrointestinal stromal tumour]] (GIST) - dealt with in a separate article.
*Angiosarcoma.
*[[Angiosarcoma]].
*Lymphoma (Non-Hodgkin's lymphoma).
*Lymphoma (Non-Hodgkin's lymphoma).


==Grading==
Notes:
*"Adenocarcinoma in situ" and "high-grade dysplasia" is used interchangeably by many in the colon and rectum.
*[[Mucinous carcinoma]] - percentage required to call varies by site:
**Splitting hairs - ''adenocarcinoma in situ'' is ''invasion into the lamina propria'', high-grade dysplasia does not have lamina propria invasion. Ergo, the difference (in my opinion) amounts to seeing a [[desmoplastic stroma]] (adenocarcinoma) or not seeing one (dysplasia).
 
====Squamous carcinoma====
{{Main|Squamous carcinoma}}
*Rare.
**In the context of a rectal tumour, retrograde growth from the [[anus]] should be considered.
 
==Staging of colorectal cancer==
{{Main|Colorectal cancer staging}}
 
==Pathogenesis of colorectal carcinoma==
===Overview===
Colorectal carcinoma is thought to arise from one of two pathways:<ref name=pmid16483003>{{cite journal |author=Goldstein NS |title=Serrated pathway and APC (conventional)-type colorectal polyps: molecular-morphologic correlations, genetic pathways, and implications for classification |journal=Am. J. Clin. Pathol. |volume=125 |issue=1 |pages=146–53 |year=2006 |month=January |pmid=16483003 |doi= |url=}}</ref><ref name=pmid18314605>{{cite journal |author=Rüschoff J, Aust D, Hartmann A |title=[Colorectal serrated adenoma: diagnostic criteria and clinical implications] |language=German |journal=Verh Dtsch Ges Pathol |volume=91 |issue= |pages=119–25 |year=2007 |pmid=18314605 |doi= |url=}}</ref>
#APC (adenomatous polyposis coli) gene mutation pathway, [[AKA]] classic adenoma-carcinoma pathway.
#Serrated pathway, AKA mutator pathway, mismatch repair pathway.
 
====Syndromes====
Both of the above described pathways are associated with syndromes:
#''[[Familial adenomatous polyposis]]'' (FAP) or ''familial polyposis coli'' (FPC).
#''Lynch syndrome'' ([[AKA]] ''[[hereditary non-polyposis colorectal cancer syndrome]]'' (HNPCC)).
 
===Pathways===
====APC gene mutation pathway====
Microscopic:
*[[Adenomatous polyps]].
 
====Mismatch repair pathway====
*Associated with [[microsatellite instability]] (MSI).
 
===Other ancillary studies===
*BRAF ''V600E'' missense mutation found in ~10% CRC.<ref name=pmid20635392>{{cite journal |author=Tie J, Gibbs P, Lipton L, ''et al.'' |title=Optimizing targeted therapeutic development: Analysis of a colorectal cancer patient population with the BRAF(V600E) mutation |journal=Int J Cancer |volume= |issue= |pages= |year=2010 |month=July |pmid=20635392 |doi=10.1002/ijc.25555 |url=}}</ref>
*[[KRAS mutation]] status.
 
====BRAF V600E mutation====
{{Main|BRAF V600E mutation}}
Features:<ref name=pmid20635392/>
*Independently associated with BRAF V600E:
**Usually older (>70 years old).
**Female gender.
**Right-sided tumour location.
*Worse prognosis - in the context of metastatic disease.


Grading of tumours:
====KRAS mutation====
*Tis - in situ (intramucosal),
{{Main|KRAS mutation}}
*T1 - into submucosa (through mucularis mucosae),
Features:<ref name=pmid20956938>{{cite journal |author=Dunn EF, Iida M, Myers RA, ''et al.'' |title=Dasatinib sensitizes KRAS mutant colorectal tumors to cetuximab |journal=Oncogene |volume= |issue= |pages= |year=2010 |month=October |pmid=20956938 |doi=10.1038/onc.2010.430 |url=}}</ref><ref name=pmid19001320>{{cite journal |author=Di Nicolantonio F, Martini M, Molinari F, ''et al.'' |title=Wild-type BRAF is required for response to panitumumab or cetuximab in metastatic colorectal cancer |journal=J. Clin. Oncol. |volume=26 |issue=35 |pages=5705–12 |year=2008 |month=December |pmid=19001320 |doi=10.1200/JCO.2008.18.0786 |url=}}</ref>
**This is different than elsewhere, e.g. in the ''small bowel'' tumour cells in the ''lamina propria'' is defined as T1. The rationale for the ''T1'' definition in CRC is that no lymphatics are present in the mucosa, ergo no risk of distant spread.
*Patient must have ''wild type'' KRAS to get drugs; KRAS mutation predicts resistance to [[cetuximab]] (Erbitux) and [[panitumumab]] (Vectibix).
*T2 - into muscularis propria,
**Cetuximab and panitumumab are [[EGFR inhibitors]].
*T3 - into fat beyond musclaris propria,
*T4 - into something else.


Nodes:
==Microsatellite instability cancers==
*N0 - no positive nodes.
*Abbreviated ''MSI cancers''.
*N1 - 1-3 positive nodes.
{{Main|Microsatellite instability in colorectal cancer}}
*N2 - 4+ positive nodes.


==Staging of colorectal cancer==
=Specific entities=
===Simple version===
==Colorectal adenocarcinoma==
Tumour/node grade for stage:<ref>TN 2006 GS27.</ref>
*[[AKA]] ''colorectal adenocarcinoma not otherwise specified''.
*Stage I - '''T1 or T2''' N0 M0.
*[[AKA]] ''colorectal carcinoma'', abbreviated ''CRC''.
*Stage II - '''T3 or T4''' N0 M0.
{{Main|Colorectal adenocarcinoma}}
*Stage III - Tx '''N1 or N2''' M0.
 
*Stage IV - Tx Nx '''M1'''.
==Secondary colorectal cancer==
===General===
*Uncommon.
*May be suspected.
 
===Microscopic===
Features:
*Normal colorectal mucosa.
*Atypical cells in the lamina propria or submucosa.
 
DDx:
*Colorectal neuroendocrine tumour.


===Complex version===
===Images===
Detailed tumour/node grade for stage:<ref>[http://www.cancer.org/docroot/CRI/content/CRI_2_4_3X_How_is_colon_and_rectum_cancer_staged.asp http://www.cancer.org/docroot/CRI/content/CRI_2_4_3X_How_is_colon_and_rectum_cancer_staged.asp]</ref>
<gallery>
*Stage I - T1 or T2.
Image:Prostate carcinoma in rectum -- very low mag.jpg | Pca in rectum - very low mag. (WC)
*Stage IIA - T3.  
Image:Prostate carcinoma in rectum -- low mag.jpg | Pca in rectum - low mag. (WC)
*Stage IIB - T4.  
Image:Prostate carcinoma in rectum -- intermed mag.jpg | Pca in rectum - intermed. mag. (WC)
*Stage IIIA - T1 N1 or T2 N1.
Image:Prostate carcinoma in rectum -- high mag.jpg | Pca in rectum - high mag. (WC)
*Stage IIIB - T3 N1 or T4 N1.
</gallery>
*Stage IIIC - Tx N2.  
<gallery>
*Stage IV - Tx Nx M1.
Image:Prostate carcinoma in rectum - PSAP -- intermed mag.jpg | Pca in rectum - PSAP - intermed. mag. (WC)
Image:Prostate carcinoma in rectum - PSA -- intermed mag.jpg | Pca in rectum - PSA - intermed. mag. (WC)
Image:Prostate carcinoma in rectum - CK20 -- intermed mag.jpg | Pca in rectum - CK20 - intermed. mag. (WC)
</gallery>


==See also==
=See also=
*[[Anus]] - covers anal cancer and anal intraepithelial neoplasia.
*[[Colon]].
*[[Colon]].
*[[Gastrointestinal pathology]].
*[[Gastrointestinal pathology]].
*[[Tumour budding]].
*[[Tumour perforation in colorectal cancer]].
*[[Transanal minimally invasive surgery]].


==References==
=References=
{{reflist|2}}
{{reflist|2}}


[[Category:Gastrointestinal pathology]]
[[Category:Gastrointestinal pathology]]

Latest revision as of 16:50, 29 August 2018

Colorectal tumours, especially colorectal carcinomas, are very common. They are the bread and butter of GI pathology. Non-tumour colon is dealt with in the colon article.

Colonic tumours and rectal tumours redirect here.

An introduction to gastrointestinal pathology is in the gastrointestinal pathology article. The precursor lesion of colorectal carcinoma (CRC) is, typically, an adenomatous polyp. Polyps are discussed in the intestinal polyps article.

Classification

Most common

Others

Other tumours - many (incomplete list):[2]

Notes:

Squamous carcinoma

Main article: Squamous carcinoma
  • Rare.
    • In the context of a rectal tumour, retrograde growth from the anus should be considered.

Staging of colorectal cancer

Main article: Colorectal cancer staging

Pathogenesis of colorectal carcinoma

Overview

Colorectal carcinoma is thought to arise from one of two pathways:[4][5]

  1. APC (adenomatous polyposis coli) gene mutation pathway, AKA classic adenoma-carcinoma pathway.
  2. Serrated pathway, AKA mutator pathway, mismatch repair pathway.

Syndromes

Both of the above described pathways are associated with syndromes:

  1. Familial adenomatous polyposis (FAP) or familial polyposis coli (FPC).
  2. Lynch syndrome (AKA hereditary non-polyposis colorectal cancer syndrome (HNPCC)).

Pathways

APC gene mutation pathway

Microscopic:

Mismatch repair pathway

Other ancillary studies

BRAF V600E mutation

Main article: BRAF V600E mutation

Features:[6]

  • Independently associated with BRAF V600E:
    • Usually older (>70 years old).
    • Female gender.
    • Right-sided tumour location.
  • Worse prognosis - in the context of metastatic disease.

KRAS mutation

Main article: KRAS mutation

Features:[7][8]

  • Patient must have wild type KRAS to get drugs; KRAS mutation predicts resistance to cetuximab (Erbitux) and panitumumab (Vectibix).

Microsatellite instability cancers

  • Abbreviated MSI cancers.
Main article: Microsatellite instability in colorectal cancer

Specific entities

Colorectal adenocarcinoma

  • AKA colorectal adenocarcinoma not otherwise specified.
  • AKA colorectal carcinoma, abbreviated CRC.
Main article: Colorectal adenocarcinoma

Secondary colorectal cancer

General

  • Uncommon.
  • May be suspected.

Microscopic

Features:

  • Normal colorectal mucosa.
  • Atypical cells in the lamina propria or submucosa.

DDx:

  • Colorectal neuroendocrine tumour.

Images

  • Pca in rectum - very low mag. (WC)

  • Pca in rectum - low mag. (WC)

  • Pca in rectum - intermed. mag. (WC)

  • Pca in rectum - high mag. (WC)

  • Pca in rectum - PSAP - intermed. mag. (WC)

  • Pca in rectum - PSA - intermed. mag. (WC)

  • Pca in rectum - CK20 - intermed. mag. (WC)

See also

References

  1. ↑ Cotran, Ramzi S.; Kumar, Vinay; Fausto, Nelson; Nelso Fausto; Robbins, Stanley L.; Abbas, Abul K. (2005). Robbins and Cotran pathologic basis of disease (7th ed.). St. Louis, Mo: Elsevier Saunders. pp. 864. ISBN 0-7216-0187-1.
  2. ↑ Humphrey, Peter A; Dehner, Louis P; Pfeifer, John D (2008). The Washington Manual of Surgical Pathology (1st ed.). Lippincott Williams & Wilkins. pp. 198. ISBN 978-0781765275.
  3. ↑ Tozawa E, Ajioka Y, Watanabe H, et al. (2007). "Mucin expression, p53 overexpression, and peritumoral lymphocytic infiltration of advanced colorectal carcinoma with mucus component: is mucinous carcinoma a distinct histological entity?". Pathol. Res. Pract. 203 (8): 567–74. doi:10.1016/j.prp.2007.04.013. PMID 17679024.
  4. ↑ Goldstein NS (January 2006). "Serrated pathway and APC (conventional)-type colorectal polyps: molecular-morphologic correlations, genetic pathways, and implications for classification". Am. J. Clin. Pathol. 125 (1): 146–53. PMID 16483003.
  5. ↑ Rüschoff J, Aust D, Hartmann A (2007). "[Colorectal serrated adenoma: diagnostic criteria and clinical implications]" (in German). Verh Dtsch Ges Pathol 91: 119–25. PMID 18314605.
  6. ↑ 6.0 6.1 Tie J, Gibbs P, Lipton L, et al. (July 2010). "Optimizing targeted therapeutic development: Analysis of a colorectal cancer patient population with the BRAF(V600E) mutation". Int J Cancer. doi:10.1002/ijc.25555. PMID 20635392.
  7. ↑ Dunn EF, Iida M, Myers RA, et al. (October 2010). "Dasatinib sensitizes KRAS mutant colorectal tumors to cetuximab". Oncogene. doi:10.1038/onc.2010.430. PMID 20956938.
  8. ↑ Di Nicolantonio F, Martini M, Molinari F, et al. (December 2008). "Wild-type BRAF is required for response to panitumumab or cetuximab in metastatic colorectal cancer". J. Clin. Oncol. 26 (35): 5705–12. doi:10.1200/JCO.2008.18.0786. PMID 19001320.
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