| Data suggest that PU.1 is a potent tumor suppressor in classical Hodgkin lymphoma (cHL) and that induction of PU.1 with demethylation agents and/or histone deacetylase inhibitors is a possible therapeutic option for patients with cHL. | lymphoma, |
| Epigenetic silencing of the tumor suppressor genes SPI1, PRDX2, KLF4, DLEC1, and DAPK1 in childhood and adolescent lymphomas | lymphoma, |
| an upstream regulatory element has an essential role in orchestrating the dynamic PU.1 expression pattern required for lymphoid development and tumor suppression. | None |
| PU.1 acts as tumor suppressor for myeloma cells through direct transcriptional repression of IRF4 | None |
| PU.1 has a role in tumor suppression in PEL and its down-regulation is associated with PEL development. | None |
| Oncogene cooperativity in Friend erythroleukemia: erythropoietin receptor activation by the env gene of SFFV leads to transcriptional upregulation of PU.1, independent of SFFV proviral insertion. | leukemia, |
| DNA hypomethylation caused by Lsh depletion is linked to transcriptional upregulation of retroviral elements and oncogenes such as PU.1 which in turn may promote the development of erythroleukemia in mice | leukemia, |
| Spi-1 oncogene activation in Rauscher and Friend murine virus-induced acute erythroleukemias. | leukemia, |
| Spi-1, Fli-1 and Fli-3 (miR-17-92) oncogenes contribute to a single oncogenic network controlling cell proliferation in friend erythroleukemia. | leukemia, |
| The putative oncogene Spi-1: murine chromosomal localization and transcriptional activation in murine acute erythroleukemias. | leukemia, |
| Characterization of Spi-B, a transcription factor related to the putative oncoprotein Spi-1/PU.1. | None |
| Spi-1/PU.1 oncoprotein affects splicing decisions in a promoter binding-dependent manner. | None |
| The human homologue of the putative proto-oncogene Spi-1: characterization and expression in tumors. | None |
| Downregulation of the Spi-1/PU.1 oncogene induces the expression of TRIM10/HERF1, a key factor required for terminal erythroid cell differentiation and survival. | None |
| Results suggest that the oncogenicity of Spi-1, Fli-1, and possibly other ETS transcription factors may involve their ability to stimulate ribosome biogenesis. | None |
| Subtle distinct regulations of late erythroid molecular events by PI3K/AKT-mediated activation of Spi-1/PU.1 oncogene autoregulation loop. | None |
| Spi-1/PU.1 oncogene accelerates DNA replication fork elongation and promotes genetic instability in the absence of DNA breakage. | None |
| The macrophage and B cell-specific transcription factor PU.1 is related to the ets oncogene. | None |
| Localization of the human oncogene SPI1 on chromosome 11, region p11.22. | None |
| The PU.1 transcription factor is the product of the putative oncogene Spi-1. | None |