Cancers exhibit a four-fold higher mutation burden than normal tissues across five organs, driven by individual baseline mutation rate differences.
Genetic factors in colorectal cancer
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Latest in Genetic factors in colorectal cancer
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AI-assisted colonoscopy in Lynch syndrome surveillance did not significantly increase adenoma detection rates, with a 33.8% rate compared to 30.9% in standard procedures.
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Mismatch repair-proficient Colorectal Cancer evades immune attack through intrinsic secretome-driven suppression, despite identical antigen presentation in 25 words.
- Open access
Having 5 to 10 nonadvanced adenomas significantly increases the risk of advanced colorectal neoplasm, with a 10.1% 5-year incidence, highlighting the need for tailored surveillance.
RO7589831, a WRN inhibitor, shows manageable safety and a 74.2% disease control rate in MSI solid tumors at doses of 150 mg and 600 mg BID.
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Cooperative action of two conserved Glu/Asp residues is essential for early ATP hydrolysis in GHKL ATPases, with mutations impairing activity in human disease variants.
- Open access
DNA double-strand break repair pathway choice is governed by complex mechanisms involving chromatin modifications and key repair factors, with BRCA1-BARD1 and 53BP1 playing antagonistic roles.
Disruption of the BRCA1 coiled-coil domain does not impair suppression of tandem duplications in mouse cells and tumor models, indicating a non-essential role in this process.
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Circulating tumor DNA-guided therapy in high-risk colon cancer achieved a 2-year relapse-free rate of 88% in ctDNA-negative patients, but did not meet the predefined threshold.
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Exposure-driven processes may cause accelerated colorectal carcinogenesis, accounting for up to 20% of early-onset and post-colonoscopy CRC cases, challenging current prevention models.
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Genomic factors influencing mutation susceptibility are largely consistent across 25 human tissues, with chromatin structure and sequence context playing key roles.
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SPOP mutations cause cancer by shifting a structural equilibrium from autoinhibited to active filament states, leading to abnormal substrate turnover.
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