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Aberrant DNA methylation plays a critical role in the development and progression of colorectal cancer (CRC), which has high incidence and mortality rates in Korea. Various CRC-associated methylation markers for cancer diagnosis and prognosis have been developed; however, they have not been validated for Korean patients owing to the lack of comprehensive clinical and methylome data. Here, we obtained reliable methylation profiles for 228 tumor, 103 adjacent normal, and two unmatched normal colon tissues from Korean patients with CRC using an Illumina Infinium EPIC array; the data were corrected for biological and experiment biases. A comparative methylome analysis confirmed the previous findings that hypermethylated positions in the tumor were highly enriched in CpG island and promoter, 5' untranslated, and first exon regions. However, hypomethylated positions were enriched in the open-sea regions considerably distant from CpG islands. After applying a CpG island methylator phenotype (CIMP) to the methylome data of tumor samples to stratify the CRC patients, we consolidated the previously established clinicopathological findings that the tumors with high CIMP signatures were significantly enriched in the right colon. The results showed a higher prevalence of microsatellite instability status and MLH1 methylation in tumors with high CMP signatures than in those with low or non-CIMP signatures. Therefore, our methylome analysis and dataset provide insights into applying CRC-associated methylation markers for Korean patients regarding cancer diagnosis and prognosis. [BMB Reports 2024; 57(3): 161-166].

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Copyright of Journal of Information Processing & Management / Joho Kanri is the property of Japan Science & Technology Agency and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Flipping genetic on-off switches can treat diseases in mice.

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Researchers from Duke and the University of California at Irvine screened a library of more than 1,000 compounds and discovered that an old, experimental cancer drug called kenpaullone enhances the expression of the gene KCC2, which is essential for silencing pain signals. The drug was effective in treating mouse models of pain from nerve injury and bone cancer, they reported. [ABSTRACT FROM AUTHOR]

A team led by the Princess Margaret Cancer Centre in Toronto discovered that chemotherapy drugs known as DNA hypomethylating agents directly affected the anti-tumor response of a specific type of T cell in several tumor types, including melanoma and breast cancer. They believe their findings could inspire new immuno-oncology combination treatments. [ABSTRACT FROM AUTHOR]

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While studying how cancer cells evolve, researchers from MIT and Harvard discovered that the protein RUNX2 plays a key role in promoting the spread of aggressive lung cancer. The finding could guide new diagnostic and treatment strategies in lung cancer, they suggested. [ABSTRACT FROM AUTHOR]