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Prominent proteins in cancer
This is the list of significantly mutated genes (SMGs) and other proteins significantly involved in edgetic perturbations in THCA.
Perturbation typeGeneCitationCancer typeGene-disease relation
Top gainsGRAMD2B (Isoform switch) (GRAMD3)GDS1732 (GEO Profiles) (not yet published)THCADifferentially expressed in THCA patients compared to expression profiles in heathy controls
Top gainsGRAMD1C (Isoform switch)GDS1732 (GEO Profiles) (not yet published)THCADifferentially expressed in THCA patients compared to expression profiles in heathy controls
Top lossesANKS1B (Isoform switch)GDS1732 (GEO Profiles) (not yet published)THCADifferentially expressed in THCA patients compared to expression profiles in heathy controls
Top lossesERBB4 (Isoform switch)8640794THCACoexisting overexpression of epidermal growth factor receptor; c-erbB-2; c-erbB-3; and c-erbB-4 was demonstrated in 36 (64%) of 56 papillary thyroid carcinomas
Top cancer-specific gainsALK25501013THCAPathogenic ALK translocations are associated with papillary thyroid carcinoma.
Top cancer-specific gainsHIPK418575725THCADifferentially expressed in tumor samples compared to normal samples.
Top cancer-specific gainsRAB40A24423316THCADifferentially expressed in tumor samples compared to normal samples.
Top cancer-specific gainsPDZK118575725THCADifferentially expressed in tumor samples compared to normal samples.
Top cancer-specific gainsRAB40A18575725THCADifferentially expressed in tumor samples compared to normal samples.
Top lossesVEGFD17573672THCAAnalysis of micro‐dissected samples of the tumor and of the paired normal thyroid tissue revealed that RNA transcripts for VEGF‐D were significantly less numerous in the tumor tissue.
Top cancer-specific lossesCSAG124423316THCADifferentially expressed in tumor samples compared to normal samples.
SMGs within edgetic gains or lossesAKT121898122THCAThe expression of AKT1 was five to ten times higher than in benign samples.
PRKAR1A22514108THCAThe loss of Prkar1a in the thyroid glands leads to thyroid hyperfunction and the formation of follicular thyroid cancer in mice.

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