| the fusion VP16-Meis1 is spontaneously oncogenic, and leukemias harbor genetic activation of endogenous Hoxa9 and/or Hoxa7, suggesting that Hoxa gene activation represents a key event required for the oncogenic activity of VP16-Meis1 | leukemia, |
| HOXA9 activation is a novel, independent, and negative prognostic marker in GBM that is reversible through a PI3K-associated epigenetic mechanism. Findings suggest a transcriptional pathway through which PI3K activates oncogenic HOXA expression. | GBM, |
| Reversing HOXA9 oncogene activation by PI3K inhibition: epigenetic mechanism and prognostic significance in human glioblastoma. | glioblastoma, |
| HOXA9 acts as an oncogene in laryngeal squamous cell carcinoma, promoting tumor cell proliferation and migration. | laryngeal, |
| The role of HOXA9 in human laryngeal squamous cell carcinoma. | laryngeal, |
| The oncoprotein E2A-Pbx1a collaborates with Hoxa9 to acutely transform primary bone marrow cells. | None |
| The oncogene Nup98-HOXA9 induces gene transcription in myeloid cells. | None |
| HOXA9 modulates its oncogenic partner Meis1 to influence normal hematopoiesis. | None |
| Dissection of the transformation of primary human hematopoietic cells by the oncogene NUP98-HOXA9. | None |
| Amino-terminal enhancer of split (AES) interacts with the oncoprotein NUP98-HOXA9 and enhances its transforming ability. | None |