Autosomal dominant inheritance pattern seen for syndrome cancers in the family pedigree. |
Earlier average age of CRC onset than in the general population: |
average age of 45 years in Lynch syndrome vs. 63 years in the general population |
Proximal (right-sided) colonic cancer predilection: |
70-85% of Lynch syndrome CRCs are proximal to the splenic flexure. |
Accelerated carcinogenesis: (tiny adenomas can develop into carcinomas more quickly): |
within 2-3 years in Lynch syndrome vs. 8-10 years in the general population |
High risk of additional CRCs: |
25-30% of patients having surgery for a Lynch syndrome-associated CRC will have a second primary CRC within 10 years of surgical resection if the surgery was less than a subtotal colectomy |
Increased risk for malignancy at certain extracolonic sites: |
endometrium (40-60% lifetime risk for female mutation carriers) |
ovary (12-15% lifetime risk for female mutation carriers) |
stomach (higher risk in families indigenous to the Orient, reason unknown at this time) |
small bowel |
hepatobiliary tract |
pancreas |
upper uro-epithelial tract (transitional cell carcinoma of the ureter and renal pelvis) |
prostate cancer |
breast cancer |
adrenal cortical carcinomas |
brain (glioblastomas in the Turcot’s syndrome variant of the Lynch syndrome) |
sebaceous adenomas, sebaceous carcinomas, and multiple keratoacanthomas in the Muir-Torre syndrome variant of Lynch syndrome |
Pathology of CRCs is more often poorly differentiated, with an excess of mucoid and signet-cell features, a Crohn’s-like reaction, and a significant excess of infiltrating lymphocytes within the tumor. |
Increased survival from CRC. |
The sine qua non for diagnosis of LS is the identification of a germline mutation in a mismatch repair gene (most commonly MLH1, MSH2, or MSH6) that segregates in the family: i.e., members who carry the mutation show a much higher rate of syndrome-related cancers than those who do not carry the mutation. |