A novel translocation, t(14;19)(q32;p13), involving IGH@ and the cytokine receptor for erythropoietin

Immunoglobulin heavy chain locus chromosomal translocations in B-cell precursor acute lymphoblastic leukemia: rare clinical curios or potent genetic drivers?

“…First, rare cases may exhibit chromosomal translocation t(14;19)(q32;p13), sometimes as the only detectable cytogenetic abnormality. 16 The translocation results in high-level EPOR expression. However, EPOR is also a transcriptional target gene for the ETV6-RUNX1 fusion protein resulting from t(12;21)(p13;q22) that occurs in approximately 25% of pediatric BCP-ALL.…”

“…Several previously unidentified IGH translocations have been reported in BCP-ALL over the past 3 years. [12][13][14][15][16][17] All are relatively rare events, occurring individually in less than 1% of all cases and many are probably sporadic. This is in marked contrast to the situation in mature B-cell malignancies, where specific IGH translocations are commonly found in most subtypes of disease and underlie disease pathogenesis.…”

EpCAM- AN OLD CANCER ANTIGEN, TURNED ONCOGENIC RECEPTOR AND ITS TAGETING IMMUNOTHERAPY

“…GHRH/GHRHR oncogenic signaling（pituitary tumors）; Oncogenic EPOR（PFCP) 16 , oncogenic EPOR-IGH/IGK fusion（BCP-ALL) 17 ;…”

B acute lymphoblastic leukemia with t(14;19)(q32;p13.1) involving IGH/EPOR: a clinically aggressive subset of disease

“…4 Recently, a small number of cases of B-ALL involving IGH and the erythropoietin receptor gene (EPOR) at 19p13.1 have been reported. 5,6 EPOR encodes a type 1 cytokine receptor involved in kinase signaling that is normally found on the surface of erythroid progenitor cells and is required for normal erythropoiesis. 5,7 B-ALL with genetic alterations involving cytokine and receptor signaling has been associated with an aggressive clinical course.…”

“…5,6 EPOR encodes a type 1 cytokine receptor involved in kinase signaling that is normally found on the surface of erythroid progenitor cells and is required for normal erythropoiesis. 5,7 B-ALL with genetic alterations involving cytokine and receptor signaling has been associated with an aggressive clinical course. 6 However, the clinicopathologic features of B-ALL with t(14;19) (q32;p13.1) remain incompletely described.…”