TEL/AML1 shows dominant-negative effects over TEL as well as AML1.

The TEL/AML1 chimeric gene is generated by the t(12;21) translocation in pre-B cell acute lymphoblastic leukemia. TEL/AML1 consists of the helix-loop-helix (HLH) dimerization domain from TEL and almost the entire of AML1, but loses the ETS DNA-binding domain from TEL. Dominant-negative effects of TEL/AML1 over wild-type-AML1 are believed to trigger the development of this type of leukemia.

[Hypereosinophilic syndrome developing after prednisolone therapy for autoimmune hemolytic anemia].

A 26-year-old woman was diagnosed as having autoimmune hemolytic anemia in September 2002. Her eosinophil count was already high (2,190/microliter) at that time. She received prednisolone therapy with a good response and was released from the treatment in April 2003.

[Philadelphia chromosome-positive acute lymphoblastic leukemia showing normal karyotype at presentation].

21-year-old male was diagnosed as having acute lymphoblastic leukemia (ALL) in March 2001. Standard G-banding analysis revealed normal karyotype. He achieved complete remission after the first course of induction therapy and underwent allogeneic PBSCT in August 2001.

[WT1 gene expression in patients with acute myelogenous leukemia or high risk myelodysplastic syndrome successfully treated with the CAG regimen].

Ten patients with acute myelogenous leukemia or high risk myelodysplastic syndrome who had achieved complete remission following treatment with the CAG regimen were monitored for peripheral blood WT1 expression mRNA levels. Induction therapy with the CAG regimen did not seem to be enough to lower WT1 expression levels to the normal range. In comparison with patients who received intensive chemotherapy for post-remission therapy, those who received only CAG therapy showed higher levels of WT1 expression and more easily relapsed.