ArticleOncotarget2015
'Cut from the same cloth': Shared microsatellite variants among cancers link to ectodermal tissues-neural tube and crest cells.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- Opposing Effects of Cannabidiol in Patient-derived Neuroendocrine Tumor, Pheochromocytoma/Paraganglioma Primary Cultures.The Journal of clinical endocrinology and metabolism · 2024Article
- Germline microsatellite genotypes differentiate children with medulloblastoma.Neuro-oncology · 2020Article
- Reconstruction of the Global Neural Crest Gene Regulatory Network In Vivo.Developmental cell · 2019Article
- High-depth, high-accuracy microsatellite genotyping enables precision lung cancer risk classification.Oncogene · 2017Article
- MYCN induces neuroblastoma in primary neural crest cells.Oncogene · 2017Article
- Nicotinic acid inhibits glioma invasion by facilitating Snail1 degradation.Scientific reports · 2017Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The pluripotent cells of the embryonic ectodermal tissues are known to be a precursor for multiple tumor types. The adaptability of these cells is a trait exploited by cancer. We previously described cancer-associated microsatellite loci (CAML) shared between glioblastoma (GBM) and lower-grade gliomas. Therefore, we hypothesized that these variants, identified from germline DNA, are shared by cancers from tissues originating from ectodermal tissues: neural tube cells (NTC) and crest cells (NCC). Using exome sequencing data from four cancers with origins to NTC and NCC, a 'signature' of loci significant to each cancer (p-value ≤ 0.01) was created and compared with previously identified CAML from breast cancer. The results of this analysis show that variant loci among the cancers with tissue origins from NTC/NCC were closely linked. Signaling pathways linked to genes with non-coding CAML genotypes revealed enriched connections to hereditary, neurological, and developmental disease or disorders. Thus, variants in genes from tissues initiating from NTC/NCC, if recurrently detected, may indicate a common etiology. Additionally, CAML genotypes from non-tumor DNA may predict cancer phenotypes and are common to shared embryonic tissues of origin.
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Registered trials
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