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ELN (Elastin) is a gene whose normal job is to hold cell growth in check. The public catalogues list it as a tumour suppressor, and it is called a cancer driver by mutation analysis of patient cohorts. Tied to Breast cancer and Cutaneous squamous cell carcinoma.
Major structural protein of tissues such as aorta and nuchal ligament, which must expand rapidly and recover completely. Molecular determinant of the late arterial morphogenesis, stabilising arterial structure by regulating proliferation and organisation of vascular smooth muscle.
IntOGen calls it a driver in 2 cohorts (0 activating, 2 loss-of-function), covering Invasive Breast Carcinoma, Cutaneous Squamous Cell Carcinoma.
In plain words · ELN (Elastin) is a gene whose normal job is to hold cell growth in check. The public catalogues list it as a tumour suppressor, and it is called a cancer driver by mutation analysis of patient cohorts. Tied to Breast cancer and Cutaneous squamous cell carcinoma.
ELN (Elastin) is a gene whose normal job is to hold cell growth in check. The public catalogues list it as a tumour suppressor, and it is called a cancer driver by mutation analysis of patient cohorts. Tied to Breast cancer and Cutaneous squamous cell carcinoma.
Major structural protein of tissues such as aorta and nuchal ligament, which must expand rapidly and recover completely.
No product in this corpus aims at ELN yet. Because the protein is lost rather than overactive, drugs either restore its function or exploit the weakness its loss leaves (synthetic lethality).
First described 1987. Earliest sequence paper UniProt cites for the protein: Indik et al, Proc. Natl. Acad. Sci. U.S.A, 1987, "Alternative splicing of human elastin mRNA indicated by sequence analysis of cloned genomic and complementary DNA". Source.
Sources: HGNC HGNC:3327 (approved symbol, name, aliases, locus and cross-references (hgnc_complete_set.txt)); UniProt P15502 (protein name, function text, keywords and locations (REST API)); IntOGen ELN (driver in 2 cohorts (Act 0, LoF 2); Compendium_Cancer_Genes.tsv release 20240920, CC0 1.0)
Major structural protein of tissues such as aorta and nuchal ligament, which must expand rapidly and recover completely. Molecular determinant of the late arterial morphogenesis, stabilising arterial structure by regulating proliferation and organisation of vascular smooth muscle. Location: Secreted, extracellular space, extracellular matrix (UniProt). Locus 7q11.23 (HGNC).
Query for this target: (TITLE:"ELN" OR ABSTRACT:"ELN" OR TITLE:"elastin" OR ABSTRACT:"elastin" OR TITLE:"Elastin" OR ABSTRACT:"Elastin") AND (cancer OR tumor OR tumour OR oncology OR carcinoma OR lymphoma OR leukemia OR leukaemia OR myeloma OR sarcoma OR melanoma OR glioma). Results are unfiltered search hits about ELN, not a curated reading list.
Shares Cutaneous squamous cell carcinoma, IntOGen.
Shares Cutaneous squamous cell carcinoma, IntOGen.
Shares Cutaneous squamous cell carcinoma, IntOGen.
Shares Cutaneous squamous cell carcinoma, Breast cancer (all types).