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Mima, Kosuke

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Mima

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Kosuke

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Mima, Kosuke
Author's Publications: search.filters.isAuthorOfPublication.3142a66f-e084-4655-ab0c-9d85003b7ff9

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    Tumor LINE-1 methylation level and colorectal cancer location in relation to patient survival
    (Impact Journals LLC, 2016) Mima, Kosuke; Nowak, Jonathan; Qian, Zhi Rong; Cao, Yin; Song, Mingyang; Masugi, Yohei; Shi, Yan; da Silva, Annacarolina; Gu, Mancang; Li, Wanwan; Hamada, Tsuyoshi; Zhang, Xuehong; Wu, Kana; Meyerhardt, Jeffrey; Baba, Hideo; Giovannucci, Edward; Chan, Andrew; Fuchs, Charles; Ogino, Shuji; Nakashima, Reiko
    Colorectal tumors arise with genomic and epigenomic alterations through interactions between neoplastic cells, immune cells, and microbiota that vary along the proximal to distal axis of colorectum. Long interspersed nucleotide element-1 (LINE-1) hypomethylation in colorectal cancer has been associated with worse clinical outcome. Utilizing 1,317 colon and rectal carcinoma cases in two U.S.-nationwide prospective cohort studies, we examined patient survival according to LINE-1 methylation level stratified by tumor location. Cox proportional hazards model was used to assess a statistical interaction between LINE-1 methylation level and tumor location in colorectal cancer-specific mortality analysis, controlling for potential confounders including microsatellite instability, CpG island methylator phenotype, and KRAS, BRAF, and PIK3CA mutations. A statistically significant interaction was found between LINE-1 methylation level and tumor location in colorectal cancer-specific mortality analysis (Pinteraction = 0.011). The association of LINE-1 hypomethylation with higher colorectal cancer-specific mortality was stronger in proximal colon cancers (multivariable hazard ratio [HR], 1.66; 95% confidence interval [CI], 1.21 to 2.28) than in distal colon cancers (multivariable HR, 1.18; 95% CI, 0.81 to 1.72) or rectal cancers (multivariable HR, 0.87; 95% CI, 0.57 to 1.34). Our data suggest the interactive effect of LINE-1 methylation level and colorectal cancer location on clinical outcome.
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    Genomic Correlates of Immune-Cell Infiltrates in Colorectal Carcinoma
    (Cell Press, 2016) Giannakis, Marios; Mu, Xinmeng Jasmine; Shukla, Sachet A.; Qian, Zhi Rong; Cohen, Ofir; Nakashima, Reiko; Bahl, Samira; Cao, Yin; Amin-Mansour, Ali; Yamauchi, Mai; Sukawa, Yasutaka; Stewart, Chip; Rosenberg, Mara; Mima, Kosuke; Inamura, Kentaro; Nosho, Katsuhiko; Nowak, Jonathan A.; Lawrence, Michael S.; Giovannucci, Edward L.; Chan, Andrew T.; Ng, Kimmie; Meyerhardt, Jeffrey A.; Van Allen, Eliezer M.; Getz, Gad; Gabriel, Stacey B.; Lander, Eric S.; Wu, Catherine J.; Fuchs, Charles S.; Ogino, Shuji; Garraway, Levi A.
    Summary Large-scale genomic characterization of tumors from prospective cohort studies may yield new insights into cancer pathogenesis. We performed whole-exome sequencing of 619 incident colorectal cancers (CRCs) and integrated the results with tumor immunity, pathology, and survival data. We identified recurrently mutated genes in CRC, such as BCL9L, RBM10, CTCF, and KLF5, that were not previously appreciated in this disease. Furthermore, we investigated the genomic correlates of immune-cell infiltration and found that higher neoantigen load was positively associated with overall lymphocytic infiltration, tumor-infiltrating lymphocytes (TILs), memory T cells, and CRC-specific survival. The association with TILs was evident even within microsatellite-stable tumors. We also found positive selection of mutations in HLA genes and other components of the antigen-processing machinery in TIL-rich tumors. These results may inform immunotherapeutic approaches in CRC. More generally, this study demonstrates a framework for future integrative molecular epidemiology research in colorectal and other malignancies.
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    Loss of CDH1 (E-cadherin) expression is associated with infiltrative tumour growth and lymph node metastasis
    (Nature Publishing Group, 2016) Kim, Sun A; Inamura, Kentaro; Yamauchi, Mai; Nakashima, Reiko; Mima, Kosuke; Sukawa, Yasutaka; Li, Tingting; Yasunari, Mika; Morikawa, Teppei; Fitzgerald, Kathryn C; Fuchs, Charles; Wu, Kana; Chan, Andrew; Zhang, Xuehong; Ogino, Shuji; Qian, Zhi Rong
    Background: Loss of CDH1 (E-cadherin) expression in cancer cells may promote cell migration and invasion. Therefore, we hypothesised that loss of CDH1 expression in colorectal carcinoma might be associated with aggressive features and clinical outcome. Methods: Utilising molecular pathological epidemiology database of 689 rectal and colon cancer cases in the Nurses' Health Study and the Health Professionals Follow-up Study, we assessed tumour CDH1 expression by immunohistochemistry. Multivariate logistic regression analysis was conducted to assess association of CDH1 loss with tumour growth pattern (expansile-intermediate vs infiltrative) and lymph node metastasis and distant metastasis, controlling for potential confounders including microsatellite instability, CpG island methylator phenotype, LINE-1 methylation, and PIK3CA, BRAF and KRAS mutations. Mortality according to CDH1 status was assessed using Cox proportional hazards model. Results: Loss of tumour CDH1 expression was observed in 356 cases (52%), and associated with infiltrative tumour growth pattern (odds ratio (OR), 2.02; 95% confidence interval (CI), 1.23–3.34; P=0.006) and higher pN stage (OR, 1.73; 95% CI, 1.23–2.43; P=0.001). Tumour CDH1 expression was not significantly associated with distant metastasis or prognosis. Conclusions: Loss of CDH1 expression in colorectal cancer is associated with infiltrative tumour growth pattern and lymph node metastasis.