Role of HOX and MEIS1 genes in induction of acute myeloid leukemia. Thorsteinsdottir U, Kroon E, Jerome L, Blasi F, Sauvageau G.

The human t(1;19) translocation in pre-B ALL produces multiple nuclear E2A-Pbx1 fusion proteins with differing transforming potentials. Kamps MP, Look AT, Baltimore D.

Molecular cloning, expression pattern, and chromosomal localization of human CDKN2D/INK4d, an inhibitor of cyclin D-dependent kinases. Okuda T, Hirai H, Valentine VA, Shurtleff SA, Kidd VJ, Lahti JM, Sherr CJ, Downing JR.

Meis1, a PBX1-related homeobox gene involved in myeloid leukemia in BXH-2 mice. Moskow JJ, Bullrich F, Huebner K, Daar IO, Buchberg AM.

The t(1;19)(q23;p13) results in consistent fusion of E2A and PBX1 coding sequences in acute lymphoblastic leukemias. Hunger SP, Galili N, Carroll AJ, Crist WM, Link MP, Cleary ML.

The E2A gene, at 19p13.3, is fused with two different molecular partners, PBX1 and HLF, following two chromosome translocations recurrent in childhood pre-B ALL.  Bruckner R, Jentsch-Ullrich K, Franke A, Wieacker P, Stumm M.

Studies provide the first genetic evidence that Pbx1-related genes cooperate with Hox genes in leukaemia formation and identify a number of new murine myeloid leukaemia genes. Nakamura T, Largaespada DA, Shaughnessy JD Jr, Jenkins NA, Copeland NG

E2A-Pbx1 the t(1;19) translocation protein of human pre-B-cell acute lymphocytic leukemia, causes acute myeloid leukemia in mice. Kamps MP, Baltimore D.

Clinical implications of recurring chromosomal and associated molecular abnormalities in acute lymphoblastic leukemia. Ferrando AA, Look AT.

Complex genetic and biochemical interactions between HOX proteins and members of the TALE (i.e., PBX and MEIS) family have been identified in embryonic development, and some of these interactions also appear to be important for leukemic transformation Thorsteinsdottir U, Kroon E, Jerome L, Blasi F, Sauvageau G.

A carboxy-terminal deletion mutant of Notch1 accelerates lymphoid oncogenesis in E2A-PBX1 transgenic mice. Feldman BJ, Hampton T, Cleary ML.

the E2A-Pbx1 fusion protein activates the expression of a novel WNT gene McWhirter JR, Neuteboom ST, Wancewicz EV, Monia BP, Downing JR, Murre C.

E2A gene, at 19p13.3, is fused with two different molecular partners, PBX1 and HLF, following two chromosome translocations recurrent in childhood pre-B ALL Brambillasca F, Mosna G, Colombo M, Rivolta A, Caslini C, Minuzzo M, Giudici G, Mizzi L, Biondi A, Privitera E.

p53 inactivation in ALL of B cell lineage is restricted to cases carrying a rearrangement of MLL or c-MYC, whereas it is consistently negative in other molecular subgroups Lanza C, Gaidano G, Cimino G, Lo Coco F, Basso G, Sainati L, Pastore C, Nomdedeu J, Volpe G, Parvis G, et al.

Molecular evidence of minimal residual disease after treatment for leukaemia and lymphoma Potter MN, Cross NC, van Dongen JJ, Saglio G, Oakhill A, Bartram CR, Goldman JM.

The t(1;19) chromosomal translocation of pediatric pre-B cell leukemia produces chimeric oncoprotein E2a-Pbx1, which contains the N-terminal transactivation domain of the basic helix-loop-helix (bHLH) transcription factor, E2a, joined to the majority of the homeodomain protein, Pbx1 Knoepfler PS, Bergstrom DA, Uetsuki T, Dac-Korytko I, Sun YH, Wright WE, Tapscott SJ, Kamps MP.

The Meis1 homeobox gene has 44% identity to Pbx within the homeodomain and was identified as a common site of viral integration in myeloid leukemias arising in BXH-2 mice Shen WF, Montgomery JC, Rozenfeld S, Moskow JJ, Lawrence HJ, Buchberg AM, Largman C

Heterodimerization of Hox proteins with Pbx1 and oncoprotein E2a-Pbx1 generates unique DNA-binding specifities at nucleotides predicted to contact the N-terminal arm of the Hox homeodomain--demonstration of Hox-dependent targeting of E2a-Pbx1 in vivo. Lu Q, Kamps MP.

Both Pbx1 and E2A-Pbx1 bind the DNA motif ATCAATCAA cooperatively with the products of multiple murine Hox genes, some of which are themselves oncogenes. Lu Q, Knoepfler PS, Scheele J, Wright DD, Kamps MP

Role of HOX and MEIS1 genes in induction of acute myeloid leukemia. Thorsteinsdottir U, Kroon E, Jerome L, Blasi F, Sauvageau G.

Role for homodimerization in growth deregulation by E2a fusion proteins. Bayly R, LeBrun DP.

mAngiogenin-3, a target gene of oncoprotein E2a-Pbx1, encodes a new angiogenic member of the angiogenin family. Fu X, Roberts WG, Nobile V, Shapiro R, Kamps MP.

Distinct in vivo engraftment and growth patterns of t(1;19)+/E2A-PBX1+ and t(9;22)+/BCR-ABL+ human leukemia cells in SCID mice. Waurzyniak BJ, Heerema N, Sensel MG, Gaynon PS, Kraft P, Sather HN, Chelstrom L, Reaman GH, Uckun FM.

G-CSFr gene is a target for deregulation by E2A-Pbx1. de Lau WB, Hurenkamp J, Berendes P, Touw IP, Clevers HC, van Dijk MA.

Meis1 and pKnox1 bind DNA cooperatively with Pbx1 utilizing an interaction surface disrupted in oncoprotein E2a-Pbx1. Knoepfler PS, Calvo KR, Chen H, Antonarakis SE, Kamps MP.

Hyperdiploidy and E2A-PBX1 fusion in an adult with t(1;19)+ acute lymphoblastic leukemia: case report and review of the literature. Hunger SP, Sun T, Boswell AF, Carroll AJ, McGavran L.

Pim1 and E2a-Pbx1 cooperate in T lineage lymphomagenesis but they are not sufficient and the role of Pim1 is more likely to be associated with tumor progression. Feldman BJ, Reid TR, Cleary ML.

Expression of BCR-ABL, E2A-PBX1, and MLL-AF4 fusion transcripts in newly diagnosed children with acute lymphoblastic leukemia Gaynon PS, Crotty ML, Sather HN, Bostrom BC, Nachman JB, Steinherz PG, Heerema NA, Sarquis M, Tuel-Ahlgren L, Uckun FM.

E2A-Pbx1 induces growth, blocks differentiation, and interacts with other homeodomain proteins regulating normal differentiation. Kamps MP.

A carboxy-terminal deletion mutant of Notch1 accelerates lymphoid oncogenesis in E2A-PBX1 transgenic mice. Feldman BJ, Hampton T, Cleary ML.

Pbx1 and E2A-Pbx1 bind the DNA motif ATCAATCAA cooperatively with the products of multiple murine Hox genes, some of which are themselves oncogenes. Lu Q, Knoepfler PS, Scheele J, Wright DD, Kamps MP.

Meis1 and pKnox1 bind DNA cooperatively with Pbx1 utilizing an interaction surface disrupted in oncoprotein E2a-Pbx1. Knoepfler PS, Calvo KR, Chen H, Antonarakis SE, Kamps MP

The E2a-Pbx1 fusion protein expressed in pre-B cells having this translocation will activate, in response to cAMP, transcription of genes not normally expressed in these cells leading to arrest of differentiation at the pre-B cell stage.  Ogo A, Waterman MR, Kamps MP, Kagawa N.

The leukemogenic transcription factor E2a-Pbx1 induces expression of the putative N-myc and p53 target gene NDRG1 in Ba/F3 cells. Rutherford MN, Bayly GR, Matthews BP, Okuda T, Dinjens WM, Kondoh H, LeBrun DP.

The p16INK4A (p16) and p15INK4B (p15) tumor suppressor genes are inactivated by homozygous gene deletion and p15 promoter hypermethylation in a significant proportion of childhood acute lymphoblastic leukemias  Maloney KW, McGavran L, Odom LF, Hunger SP.

G-CSFr gene is a target for deregulation by E2A-Pbx1. de Lau WB, Hurenkamp J, Berendes P, Touw IP, Clevers HC, van Dijk MA.

Expression of BCR-ABL, E2A-PBX1, and MLL-AF4 fusion transcripts in newly diagnosed children with acute lymphoblastic leukemia  Gaynon PS, Crotty ML, Sather HN, Bostrom BC, Nachman JB, ဠ Ƞ Steinherz PG, Heerema NA, Sarquis M, Tuel-Ahlgren L, Uckun FM.

In childhood acute lymphoblastic leukaemia (ALL), cytogenetics plays an essential role in diagnosis and prediction of outcome Harrison CJ.

Hyperdiploidy and E2A-PBX1 fusion in an adult with t(1;19)+ acute lymphoblastic leukemia: case report and review of the literature. Hunger SP, Sun T, Boswell AF, Carroll AJ, McGavran L.