These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.
Pubmed for Handhelds
PUBMED FOR HANDHELDS
Search MEDLINE/PubMed
Title: Poor response to intensive chemotherapy in de novo acute myeloid leukaemia with trilineage myelodysplasia. Japan Adult Leukaemia Study Group (JALSG). Author: Kuriyama K, Tomonaga M, Matsuo T, Kobayashi T, Miwa H, Shirakawa S, Tanimoto M, Adachi K, Emi N, Hiraoka A. Journal: Br J Haematol; 1994 Apr; 86(4):767-73. PubMed ID: 7918070. Abstract: The findings of morphologically dysplastic features in haemopoietic cells in de novo acute myeloid leukaemia (AML) has been named AML with trilineage myelodysplasia (AML/TMDS). We analysed the clinical data, karyotypes, and treatment outcomes of 230 de novo AML patients treated with the Japan Adult Leukaemia Study Group AML-87 protocol. 40 (17%) patients had AML/TMDS. Platelet count was significantly higher (P = 0.006) and bone marrow blasts were fewer (P = 0.01) in the AML/TMDS group than in the AML without TMDS. Abnormal karyotype was shown in 12/30 patients (40%) analysed. The complete remission (CR) rate for AML/TMDS was significantly lower than AML without TMDS (63% v 81%) (P = 0.01). The overall survival curves showed that the 40 patients with TMDS had a significantly worse survival than the 190 without TMDS (P = 0.0005). AML/TMDS also showed significantly worse disease-free survival (DFS) (P = 0.0001). Multivariate analysis revealed that the absence of TMDS in AML was the most significant factor in obtaining CR (P = 0.01) and a significant factor in predicting longer DFS (P = 0.04). Our data suggest that AML/TMDS responds poorly to intensive chemotherapy. Further study is required to determine the best treatment strategy for AML/TMDS and the biological differences between AML/TMDS and other types of AML.[Abstract] [Full Text] [Related] [New Search]