v-erbA cooperates with sarcoma oncogenes in leukemic cell transformation.
The v-erbB, v-src, v-fps, v-sea, and v-Ha-ras oncogenes induce avian erythroid progenitor cells to self-renew in an erythropoietin-independent manner. These transformed erythroblasts retain both their capacity to differentiate into erythrocytes and their requirement for complex growth media. However, previous studies showed that erythroblasts transformed by v-erbB plus v-erbA (which by itself is not oncogenic) are blocked in differentiation and grow in standard media. Here we show that the introduction of v-erbA into erythroblasts transformed with v-src, v-fps, v-sea, or v-Ha-ras likewise induces a fully transformed phenotype. It also reduces the capacity of ts sea- and ts erbB-transformed erythroblasts to differentiate terminally in an erythropoietin-dependent manner after a temperature shift. Cooperativity involving v-erbA also occurs in vivo since chicks infected with a retroviral construct encoding v-erbA and v-src develop both acute erythroblastosis and sarcomas.
D001355:Alpharetrovirus / Q000235:genetics*; D000818:Animals; D001354:Avian Leukosis Virus / Q000235:genetics*; D002454:Cell Differentiation; D002472:Cell Transformation, Viral; D004920:Erythropoiesis; D004921:Erythropoietin / Q000494:pharmacology; D005786:Gene Expression Regulation; D009857:Oncogenes; D012513:Sarcoma, Experimental / Q000235:genetics*
D004921:Erythropoietin