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.
Table 1: Cardinal features of HNPCC/Lynch syndrome.