| Gene information | Literature | Expression | lncRNA | Mutation | Homolog |
Basic Information | |
|---|---|
Gene ID | 2066 |
Name | ERBB4 |
Synonymous | erb-b2 receptor tyrosine kinase 4;ERBB4;erb-b2 receptor tyrosine kinase 4 |
Definition | avian erythroblastic leukemia viral (v-erb-b2) oncogene homolog 4|human epidermal growth factor receptor 4|proto-oncogene-like protein c-ErbB-4|receptor tyrosine-protein kinase erbB-4|tyrosine kinase-type cell surface receptor HER4|v-erb-a erythroblastic |
Position | 2q33.3-q34 |
Gene type | protein-coding |
Title | Abstract |
| HER4 and its cytoplasmic isoforms are associated with progression-free survival of malignant melanoma. | HER4 belongs to the epidermal growth factor (EGF) family. mutations in HER4 are associated with malignant melanoma. This points to HER4 as an important receptor in malignant melanoma and also raises the question of whether the other receptors in the EGF system could be involved. RT-qPCR mRNA quantification was carried out of ALL four EGF receptors (EGFR, HER2, HER3, and HER4) and the HER4 cytoplasmic isoforms in lymph node metastases from patients with malignant melanoma. We related their expression to progression of the disease. HER4 expression was found to be an indicator of short progression-free survival (P=0.0340). Interestingly, of the two cytoplasmic splice variants of HER4, the association of CYT1 (P=0.0176) with progression-free survival was more pronounced than that for CYT2 (P=0.0458). Also, HER3 was associated with progression-free survival (P=0.0169), whereas no association was found for EGFR or HER2 with time to progression. Our results further emphasize the role of HER4 as an important oncogene in malignant melanoma and point to HER4 as a possible drug target in this disease. |
| Absence of EGFR, ERBB2 and ERBB4 mutation homologous to the oncogenic ERBB3 Val-104 mutation in colorectal cancers. | OBJECTIVE: The oncoprotein, gankyrin, is known to facilitate cell proliferation through phosphorylation and degradation of retinoblastoma protein. In the present study, we evaluated the expression of gankyrin and phosphorylated retinoblastoma protein in human testis and testicular germ cell tumors. METHODS: The effects of suppression of gankyrin by locked nucleic acid on phosphorylation status of retinoblastoma and cell proliferation were analyzed using western blot analysis and testicular tumor cell line NEC8. The expressions of gankyrin, retinoblastoma and retinoblastoma protein were analyzed in 93 testicular germ cell tumor samples and five normal human testis by immunohistochemistry. The retinoblastoma protein expression was determined using an antibody to retinoblastoma protein, Ser795. RESULTS: Gankyrin was expressed in NEC8 cells as well as a normal human testis and testicular tumors. Suppression of gankyrin by locked nucleic acid led to suppression of retinoblastoma protein and cell proliferation in NEC8 cells. Immunohistochemistry of normal testis showed that gankyrin is expressed dominantly in spermatocytes. In testicular germ cell tumors, high expressions of gankyrin and phosphorylated-retinoblastoma protein were observed in seminoma and embryonal carcinoma, whereas the expressions of both proteins were weak in histological subtypes of non-seminoma. Growing teratoma and testicular malignant transformation tissues expressed phosphorylated-retinoblastoma protein strongly, but gankyrin faintly. CONCLUSION: Gankyrin is dominantly expressed in normal spermatocytes and seminoma/embryonal carcinoma, and its expression correlates well with retinoblastoma protein expression except in the growing teratoma and testicular malignant transformation cases. These data provide new insights into the molecular mechanisms of normal spermatogenesis and pathogenesis of testicular germ cell tumors. |