Early-onset diffuse gastric cancer associated with a de novo large genomic deletion of CDH1 gene

Sugimoto, Seiichiro; Yamada, Hidetaka; Takahashi, Mutsuo; Morohoshi, Yuichi; Yamaguchi, Naotaka; Tsunoda, Yuya; Hayashi, Hiroyuki; Sugimura, Haruhiko; Komatsu, Hirokazu

doi:10.1007/s10120-013-0278-2

Cited by 36 publications

(27 citation statements)

References 17 publications

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“…Mutation in ARID1A appears to be causal to chains of alterations within the same gene. For example, we observed that ARID1A mutation precedes mutation, downregulation, and deletion within the CDH1 gene [158], [159], [160], [161], [162]. Similarly, we also observed a causal link to upregulation and deletion of TP53 [163], [164].…”

Section: Resultssupporting

confidence: 62%

Progression inference for somatic mutations in cancer

Peterson

Kovyrshina

2017

Heliyon

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Computational methods were employed to determine progression inference of genomic alterations in commonly occurring cancers. Using cross-sectional TCGA data, we computed evolutionary trajectories involving selectivity relationships among pairs of gene-specific genomic alterations such as somatic mutations, deletions, amplifications, downregulation, and upregulation among the top 20 driver genes associated with each cancer. Results indicate that the majority of hierarchies involved TP53, PIK3CA, ERBB2, APC, KRAS, EGFR, IDH1, VHL, etc. Research into the order and accumulation of genomic alterations among cancer driver genes will ever-increase as the costs of nextgen sequencing subside, and personalized/precision medicine incorporates whole-genome scans into the diagnosis and treatment of cancer.

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Section: Resultssupporting

confidence: 62%

Progression inference for somatic mutations in cancer

Peterson

Kovyrshina

2017

Heliyon

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“…Long‐sought changes in CDH1 in the germline of Japanese gastric cancer cases have been discovered using multiplex ligation‐dependent probe amplification (MLPA) in addition to ordinary Sanger sequencing, and some of the germline changes were copy number changes, including de novo types …”

Section: Approaches From the Practice Of Pathology To Investigating Tmentioning

confidence: 99%

Susceptibility to human cancer: From the perspective of a pathologist

Sugimura

2016

Pathology International

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The etiologies of human cancer can only be discerned when the genetic clustering of cancer occurs within a family or when cancer occurs endemically in a particular environment. The possible approaches to solving the nature/nurture problem, especially for human carcinogenesis, posit a fascinating challenge for pathologists. This perspective review presents some examples of how clues to human cancer etiologies and/or susceptibilities reside in the realm of pathology practice. These examples using various omics techniques including adductomics, which I would like to highlight in this article, show that the currently available concepts and methods in human pathology can open a path toward the brave new world of a post-genomic era of medicine for young pathologists, whether their original intention was toward the pursuit of diagnostic or investigative knowledge.

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“…. However, CDH1 may partially explain EOGC , and more studies would suggest p53 as a candidate mutated gene in EOGC.…”

Section: Introductionmentioning

confidence: 97%

Expression profile of E‐cadherin, estrogen receptors, and P53 in early‐onset gastric cancers

Zhang

Shi

et al. 2016

Cancer Medicine

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Early‐onset gastric cancer (EOGC) is predominant in females, diffuse histology, and hereditary pattern. Germline mutation of CDH1 and p53 has been reported previously and female dominance was speculated to be associated with estrogen and its receptors. Expression of E‐cadherin, estrogen receptor α (ER α), estrogen receptor β (ER β), and p53 in EOGC remains unclear, which was the focus of this study, to assess clinical significance of their expression in EOGC. The expression of E‐cadherin, ER α, ER β, and p53 in tumors and normal tissues from surgically resected EOGCs was assessed by immunohistochemistry (n = 139) and Western blot (n = 7) methods, respectively. The expression in tumor tissues was significantly higher for ER α, ER β, and p53, but lower for E‐cadherin, compared to uninvolved mucosa. Positive staining of ER β and p53 was more frequently observed in younger patients with advanced TNM stages. For E‐cadherin, significant correlation was observed between the immunopositivity and TNM stages IA+IB. P53‐negative patients had significantly better outcomes than p53‐positive patients. Significant association between expression of E‐cadherin and histologic types was found in familial, but not in sporadic, EOGC. In conclusion, our results demonstrated E‐cadherin may have a role in initiation of EOGC and positive ER β and p53 expression may partially explained early‐onset and tumor progression of EOGC.

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Early-onset diffuse gastric cancer associated with a de novo large genomic deletion of CDH1 gene

Cited by 36 publications

References 17 publications

Progression inference for somatic mutations in cancer

Progression inference for somatic mutations in cancer

Susceptibility to human cancer: From the perspective of a pathologist

Expression profile of E‐cadherin, estrogen receptors, and P53 in early‐onset gastric cancers

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