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Items: 3

1.

Diverse routes to oral cancer differing in genome instability and risk for cervical node metastasis

(Submitter supplied) Clinically evident oral lesions, oral epithelial dysplasia, precede development of oral squamous cell carcinomas (SCC) and are considered to transform to cancer by acquisition of genetic or epigenetic alterations. Here, we show that, +3q24-qter, -8pter-p23.1, +8q12-q24.2 and +20 are early events identifying two pathways to oral cancers that differ in clinical behavior. One or more of these copy number aberrations is present in the major subgroup (3q8pq20 subtype, 75-80% of lesions) that develops with chromosomal instability and risk for metastasis, while they are absent from the smaller and chromosomally stable non-3q8pq20 subgroup (20-25% of lesions) associated with low risk for metastasis. more...
Organism:
Homo sapiens
Type:
Genome variation profiling by genome tiling array
Platforms:
GPL6359 GPL4421 GPL4999
168 Samples
Download data: TXT
Series
Accession:
GSE28407
ID:
200028407
2.

UCSF Cancer Center HumArray2.0

(Submitter supplied) For a detailed description on how the arrays were made please refer to: Snijders et al. Nat Genet. 2001 Nov;29(3):263-4.
Organism:
Homo sapiens
6 Series
255 Samples
Download data: TXT
Platform
Accession:
GPL4999
ID:
100004999
3.

X6486

Organism:
Homo sapiens
Source name:
Genomic DNA from oral dysplasia (channel 1) Normal human genomic DNA (channel 2)
Platform:
GPL4999
Series:
GSE28407
Download data: TXT
Sample
Accession:
GSM702170
ID:
300702170
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Supplemental Content

db=gds|term=GSM702170[Accession]|query=1|qty=2|blobid=MCID_6750c95451e3a106b4695dd5|ismultiple=true|min_list=5|max_list=20|def_tree=20|def_list=|def_view=|url=/Taxonomy/backend/subset.cgi?|trace_url=/stat?
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