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Biology subjects

Kamatani, T.

Publications and source records attributed to Kamatani, T..

4 recordsLinked to original sources

MARiO: predicting cancer variant pathogenicity by integrating in silico evaluation and patient-level mutational contexts

Comprehensive genomic profiling (CGP) supports precision medicine in cancer care, but accurate assessment of missense variant pathogenicity, especially for variants without established consensus, remains challenging. Various computational tools have been developed for variant functional prediction, but most current tools rely solely on variant-level features and do not capture the clinical context of individual patients. To address this limitation, we developed MARiO (Missense Alteration Risk for Oncogenicity), a machine-learning model that integrates variant-level features and patient-level clinical and genomic contexts to effectively predict the pathogenicity of missense variants in cancer. We collected a total of 10,642 missense variants from 1271 patients, and evaluated candidate features for their association with variant pathogenicity, identifying informative features including in silico functional predictions, population allele frequency, variant allele frequency, and tumor mutational burden. Using these selected features, MARiO was developed with extreme gradient boosting. The model integrates multiple in silico prediction tools and patient-specific genomic contexts while accommodating missing values frequently observed in real-world CGP datasets. MARiO outperformed existing tools, achieving an area under the receiver operating characteristic curve of 0.942. The model demonstrated strong generalizability across multiple external datasets and showed consistency with real-world molecular treatment proposals. MARiO offers a robust and clinically relevant approach for missense variant pathogenicity assessment by integrating variant- and patient-level features and serves as a valuable tool to support clinical decision-making.

bioinformatics↗

Quantitative live-cell imaging of secretion activity reveals dynamic immune responses

The measurement of cytokine secretions has contributed to the development of immunology; however, new methods that enable highly sensitive and efficient analysis are required for the precise characterisation of dynamic secretion activity when using rare cells or limited human specimens. Here, we report a new technology for quantitative live-cell imaging of secretion activity (qLCI-S), that enables high-throughput and dual-colour detection of prolonged secretion activity at the single-cell level, followed by transcriptome analysis for individual cells based on their phenotype. The power of the qLCI-S was demonstrated by visualising the individual and longitudinal cytokine secretion patterns of group 2 innate lymphoid cells, which comprised <0.01% human peripheral blood mononuclear cells, and identifying their minor subpopulations. This new technology will provide new insights into the spatiotemporal dynamic nature of various secretory functions and the development of fundamental tools for phenotypic drug discovery and regenerative and precision medicine.

biophysics↗

Systematic detection of Mendelian and non-Mendelian variants associated with retinitis pigmentosa by genome-wide association study

To uncover genetic basis of autosomal recessive retinitis pigmentosa (ARRP), we applied 2-step genome-wide association study (GWAS) in 640 Japanese patients prescreened with targeted re-sequencing. Meta-GWAS identified three independent peaks at P < 5.0x10-8, all within the major ARRP gene EYS. Two were each tagged by a low frequency variant (allele frequency < 0.05); a known founder Mendelian mutation (c.4957dupA, p.S1653Kfs*2) and a presumably hypomorphic non-synonymous variant (c.2528G>A, p.G843E). c.2528G>A newly solved 7.0% of Japanese ARRP cases, improving genetic diagnosis by 26.8% and simultaneously serving as a new attractive target for genome editing gene therapy. The third peak was tagged by an intronic common variant, representing a novel disease-susceptibility signal. GWAS successfully unraveled genetic causes of a rare "monogenic" disorder for the first time, which provided unexpected insights into significant contribution of non-Mendelian genetic factors and identified a novel high frequency variant directly linked to development of local genome therapeutics.

genetics↗

Quantification of multicellular colonization in tumor metastasis using exome sequencing data

Metastasis is a major cause of cancer-related mortality, and it is essential to understand how metastasis occurs in order to overcome it. One relevant question is the origin of a metastatic tumor cell population. Although the hypothesis of a single-cell origin for metastasis from a primary tumor has long been prevalent, several recent studies using mouse models have supported a multi-cellular origin of metastasis. Human bulk whole-exome sequencing (WES) studies also have demonstrated a multiple clonal origin of metastasis, with different mutational compositions. Specifically, there has not yet been strong research to determine how many founder cells colonize a metastatic tumor. To address this question, we developed a method to quantify the founder cell population size in a metastasis using paired WES data from primary and metachronous metastatic tumors. Simulation studies demonstrated the proposed method gives unbiased results with sufficient accuracy in the range of realistic settings. Applying the proposed method to real WES data from four colorectal cancer patients, all samples supported a multi-cellular origin of metastasis and the founder size was quantified, ranging from 3 to 15 cells. Such a wide-ranging founder sizes estimated by the proposed method suggests that there are large variations in genetic similarity between primary and metastatic tumors in the same subjects, which might be involved in (dis)similarity of drug responses between tumors.

cancer biology↗