ReviewFamilial cancer2026
Routes to colorectal cancer in Lynch syndrome: a decade of molecular and clinical insights converging on Schrödinger's cat.
Review in Familial cancer, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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0 citing papers in PubMed.
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Authors and funding
5 authors.
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Abstract
Colorectal cancer (CRC) development in Lynch syndrome (LS) has long been regarded to follow an adenoma-carcinoma sequence accelerated in comparison to microsatellite-stable (MSS) CRC development. Yet, several clinical observations challenged this hypothesis, most notably the persistently high CRC incidence under colonoscopy surveillance, a non-measurable benefit from shorter screening intervals, and substantial differences in cancer risk between carriers of the different mismatch repair (MMR) genes. Advances in the last decade have produced new hypotheses, highlighting the distinct biology of LS CRC and unravelling several co-existing pathways to cancer. Alongside the genomic heterogeneity, the immunogenic load created by the accumulation of frameshift mutations imposing selective pressure and leading to immune evasion, appears to be a critical step for cancer manifestation. We discuss potential clinical implications of these advances in understanding CRC pathogenesis for cancer prevention in LS and outline open questions that remain.
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