Between February 1999 and September 2002, researchers at the Hereditary Cancer Institute of Riga Stradins University collected cancer family histories from 865 colorectal cancer (CRC) patients (~30% of all new Latvian CRC cases) using a structured questionnaire covering first- and second-degree relatives. Families were classified against Amsterdam II, late-onset HNPCC, suspected HNPCC, familial colorectal cancer (FCC), and cancer familial aggregation (CFA) criteria, then underwent DHPLC screening plus sequencing of MLH1, MSH2, and MSH6 heteroduplexes, with MSH2/MSH6 immunohistochemistry (IHC) on 27 available tumor samples .
Reported results: 463 patients (53.53%) reported at least one malignancy in a blood relative; only 3 pedigrees (0.35%) fulfilled Amsterdam II criteria (without histopathologic confirmation); 14 (1.62%) met suspected HNPCC criteria; 41 (4.74%) matched FCC; and 69 (8%) showed CFA. Molecular testing yielded four germline mutations: MLH1 c.1409+1G/A (exon 12), MSH2 c.508C>T (Gln170Stop, exon 3), MSH2 c.1786delAAT (596delAsn, exon 12), and MSH6 c.1815-1816delTA (exon 4) .
The most actionable finding is the mutation-detection gradient by age: 2 of 11 probands aged 30β39 (18.2%) carried a germline mutation, versus 0.3β0.4% in older age bands and zero below age 30. The authors accordingly propose targeted screening of all CRC patients aged 30β39 . However, this is built on just 2 mutations in 11 patientsβan extremely small denominatorβand the 0-mutation finding in the <30 group rests on only 2 cases, so the "age 30β39 priority" is hypothesis-generating, not established.
Strengths: A genuinely first-of-its-kind national effort for Latvia, ethically approved, with written informed consent, an international collaboration (Pomeranian Medical University, Poland), and consistent with the Finnish prospective estimate of 0.7β2.4% HNPCC frequency .
Blind spots the authors partially acknowledge: pedigree reliability is explicitly flagged as poorβmany families had few relatives and sparse medical documentation, and none of the three Amsterdam II pedigrees could be histopathologically verified, which formally disqualifies them by their own criteria. The cohort is hospital-based and non-consecutive (patient refusals, limited research capacity), so representativeness is asserted by demographic comparability rather than demonstrated. Sequencing was restricted to DHPLC heteroduplexes, missing variants DHPLC is known to miss; large rearrangements in MSH2/MLH1 were not testedβa documented cause of under-detection. Only 27 IHC analyses were performed out of ~865 cases. The claim of "one of the lowest reported HNPCC incidences" may therefore reflect detection-method limitations as much as biology. No data-availability statement or public deposit exists, and no confounder-adjusted analysis was performed.
Missing information: microsatellite instability status, PMS2 testing, tumor sequencing of IHC-negative cases beyond one MSH6 mutation, follow-up outcomes of counseled relatives, and per-patient consent/uptake rates.
Confidence: Moderate. The descriptive counts are clearly reported, but the ~2% incidence estimate carries wide, unquantified uncertainty (authors themselves state 0.5β2%), and the age-stratification recommendation rests on n=2 mutations. The conclusion would change if a modern, comprehensively sequenced, randomly sampled Latvian CRC cohort (with MMR rearrangement testing and verified pathology) found a substantially different incidence or mutation spectrum.
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