Colorectal Cancer

Colorectal Cancer (CRC), more frequently detected in western countries, is caused by mutations in target oncogenes, tumor suppressor genes and genes related to DNA repair mechanisms. CRC is classified into 3 types depending on the origin of the mutation: Sporadic (70%), inherited (5%) and familial (25%)[1].

Sporadic cancer: These cancers are derived from point mutations and account for 70% of CRC. The occurrence of mutations follow a specific sequence which is followed by a morphological sequence.

colorectal-cancer img

Adenomatous polyposis coli (APC), a tumor suppressor gene, is the first gene to be mutated leading to the formation of a non-malignant adenomas called polyps. 15% of all adenomas progress to full blown carcinomas over 10 years.

Key genes mutated in Sporadic CRC

APC KRAS TP53 DCC SMAD4 BRAF

Mutant ORF clones Ultra-Specific Antibodies
& other monoclonals 		OEL Controls
(controls for western blot) 		CytoSections
(controls for IHC, ICC)
APC - Antibodies APC – Overexpression lysates APC - CytoSections
KRAS Mutants
(G12C, G12V, G13D & more) 		KRAS - Antibodies KRAS – Overexpression lysates KRAS - CytoSections
TP53 mutants TP53 Ultra-specific antibodies TP53 OEL controls TP53- CytoSections
DCC - Antibodies DCC – Overexpression lysates DCC - CytoSections

Inherited cancer: In the inherited form of CRC, one of the mutation is inherited. The 2nd mutation triggers the apparition of the tumor cell and finally resulting in carcinoma. Inherited CRC is classified into two groups: polyposis and non-polyposis forms. Polyposis mainly involved familial adenomatous polyposis (FAP) which is characterized by the formation of multiple polyps in the colon. Hereditary non-polyposis colorectal cancer (HNPCC) is related to mutation in DNA repair mechanisms. Lynch syndrome is the main cause of hereditary non-polyposis colorectal cancer.

Key genes mutation in Lynch syndrome

MLH1 MSH2 MSH6 PMS1

Mutant ORF clones Monoclonal Antibodies
(Mouse , Rabbit) 		OEL Controls
(controls for western blot) 		CytoSections
(controls for IHC, ICC)
MLH1- Mutants MLH1 Antibodies MLH1 OEL controls MLH1 CytoSections
MSH2 Mutants MSH2 Antibodies MSH2 OEL controls MSH2-CytoSections
MSH6 Mutants MSH6 Antibodies MSH6 CytoSections
PMS1 Antibodies PMS1 OEL Controls PMS1 CytoSections

Tissue samples for Colorectal Cancer

Frozen Sections Tissue Protein Lysates Total RNA FFPE Sections Tissue Genomic DNA

References:

  1. Mármol I, Sánchez-de-Diego C, Pradilla Dieste A, Cerrada E, Rodriguez Yoldi MJ. Colorectal Carcinoma: A General Overview and Future Perspectives in Colorectal Cancer. Int J Mol Sci. 2017 Jan 19;18(1):197.