ELN
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.
Overview
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.
- Target · the protein and the cell it sits on
- Drug · antibody, small molecule, cell or radioligand
- Effect · signal, damage or kill
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.
- 1 · What it is
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.
- 2 · What goes wrong in cancer
Major structural protein of tissues such as aorta and nuchal ligament, which must expand rapidly and recover completely.
- 3 · How drugs use it
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).
External identifiers
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)
Biology
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).
- Breast cancer: IntOGen driver in 1 cohort (BRCA)
- Cutaneous squamous cell carcinoma: IntOGen driver in 1 cohort (CSCC)
Notes
top- Written by scripts/fetch-cancer-genes.ts from CIViC, Open Targets, IntOGen, HGNC and UniProt; the function text is UniProt's, condensed and in UK spelling. Roles: IntOGen calls it a loss-of-function (LoF) driver in 2 cohorts. Evidence tier "cohort-driver" is the strongest of those signals.
- Prevalence not recorded: none of the sources gives a positivity rate.
Latest papers
topQuery 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.
Similar pages
not linked directly; found by shared links- TargetARHGEF10
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- TargetCNTRL
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- TargetACVR2A
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