Topic
ETV6
About: ETV6 is a research topic. Over the lifetime, 343 publications have been published within this topic receiving 16261 citations. The topic is also known as: TEL & TEL/ABL.
Papers published on a yearly basis
Papers
TL;DR: Retroviral transfer of ETV6-NTRK3 (EN) into murine mammary epithelial cells resulted in transformed cells that readily formed tumors in nude mice, confirming that EN transformation is compatible with epithelial differentiation.
909 citations
TL;DR: JAK2 plays a central role in non-protein tyrosine kinase receptor signaling pathways, which could explain its involvement in malignancies of different hematologic lineages and in Drosophila no member of the JAK family has yet been implicated in tumorigenesis.
525 citations
St. Jude Children's Research Hospital1, University of New Mexico2, National Institutes of Health3, New York University4, University of Florida5, University of California, San Francisco6, George Washington University7, Children's Hospital of Wisconsin8, Boston Children's Hospital9, University of Colorado Denver10
TL;DR: Integrated analysis of 179 validated somatic sequence mutations with genome-wide copy number alterations and gene expression profiles revealed a high frequency of recurrent somatic alterations in key signaling pathways, including B-cell development/differentiation, the TP53/RB tumor suppressor pathway, and Ras signaling.
314 citations
Journal Article•
TL;DR: This review describes the translocations involving the AML1(CBFA2), MLL, and TEL gene on 11q23, and the TEL(ETV6) gene on 12p13, which account for a large proportion of patients with acute lymphoblastic leukemia (ALL) and acute myeloid leukemia (AML).
313 citations
TL;DR: Mouse chimeras generated with TEL-/- ES cells establish TEL as the first transcription factor required specifically for hematopoiesis within the bone marrow, as opposed to other sites of hematoietic activity during development.
Abstract: The TEL (translocation-Ets-leukemia or ETV6) locus, which encodes an Ets family transcription factor, is frequently rearranged in human leukemias of myeloid or lymphoid origins. By gene targeting in mice, we previously showed that TEL-/- mice are embryonic lethal because of a yolk sac angiogenic defect. TEL also appears essential for the survival of selected neural and mesenchymal populations within the embryo proper. Here, we have generated mouse chimeras with TEL-/- ES cells to examine a possible requirement in adult hematopoiesis. Although not required for the intrinsic proliferation and/or differentiation of adult-type hematopoietic lineages in the yolk sac and fetal liver, TEL function is essential for the establishment of hematopoiesis of all lineages in the bone marrow. This defect is manifest within the first week of postnatal life. Our data pinpoint a critical role for TEL in the normal transition of hematopoietic activity from fetal liver to bone marrow. This might reflect an inability of TEL-/- hematopoietic stem cells or progenitors to migrate or home to the bone marrow or, more likely, the failure of these cells to respond appropriately and/or survive within the bone marrow microenvironment. These data establish TEL as the first transcription factor required specifically for hematopoiesis within the bone marrow, as opposed to other sites of hematopoietic activity during development.
302 citations
Related Topics (5)
Performance Metrics
| Year | Papers |
|---|---|
| 2025 | 10 |
| 2024 | 24 |
| 2023 | 78 |
| 2022 | 76 |
| 2021 | 16 |
| 2020 | 19 |