They respond to 2GTKI therapy but not Chlormezanone
fully, and the level of BCR-ABL1 transcript reduction was not so much deep as that of patients with <1%IS. That is why they continue to lose the response to 2GTKI therapy, resulting in TF. However, our follow-up duration with 2GTKI was too short (i.e. 24?months) to observe occurrence of progression to advanced stage of disease. Although the PFS and OS of those with 1�C10%IS is not statistically significant from those with <1%IS, further follow-up will be necessary to see if the PFS and OS become significantly different between those with <1%IS vs. 1�C10%IS at 3?months in these patients. In conclusion, BCR-ABL1 transcript level at 3?months is the most relevant surrogate for response or long-term outcomes following 2GTKI therapy as 2nd/3rd line treatment after Imatinib failure for CML patients. Further study is strongly warranted to reach a clear conclusion on the prognostic role and the cutoff of BCR-ABL1 transcript level at 3?months in the 2nd/3rd line therapy setting for CML patients with Imatinib failure. DK, HL, SKL and JL performed the research, wrote the paper and approved the final version. DK and JL designed the research study. DK, SKL and JL analysed the data. None of the authors have any conflict of interest to declare. Table S1. Clinical outcomes of 2nd generation tyrosine kinase <a href="http://www.selleckchem.com/products/Fludarabine
(Fludara).html inhibitors after Imatinib failure according to BCR-ABL1 transcript levels at 3 or 6?months in the subgroup of patients resistant to previous Imatinib therapy Table S2. Serial changes of BCR-ABL1 transcript level according to the BCR-ABL1 transcript level at 3?months Figure S1. Comparison of response and treatment failure with 2GTKI therapy according to the BCR-ABL1 transcript level at 3?months with respect to complete cytogenetic (A), major molecular (B) and MR4��5 (C) as well as treatment failure (D) in overall population with CML in chronic phase. Figure S2. Comparison of response and treatment failure with 2GTKI therapy according to the BCR-ABL1 transcript level at 3?months with respect to complete cytogenetic (A), major molecular (B) and MR4��5 (C) as well as treatment failure (D) in resistant patients to previous imatinib therapy with CML in chronic phase. ""Lenalidomide (LEN) has been shown to yield red blood cell (RBC) transfusion independence Tamoxifen in vitro
in about 25% of lower risk myelodysplastic syndromes (MDS) without del(5q), but its efficacy in patients clearly refractory to erythropoiesis-stimulating agents (ESA) is not known. We report on 31 consecutive lower-risk non-del(5q) MDS patients with anaemia refractory to ESA and treated with LEN in a compassionate programme, 20 of whom also received an ESA. An erythroid response was obtained in 15 patients (48%), including 10 of the 27 (37%) previously transfusion-dependent (RBC-TD) patients, who became transfusion-independent (RBC-TI).