1,034 results on '"Branford, Susan"'
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202. Single Molecule Real Time (SMRT™) Sequencing Sensitively Detects the Evolution of Polyclonal and Compound BCR-ABL Mutations in Patients Who Relapse On Kinase Inhibitor Therapy
203. BCR-ABL1 doubling times more reliably assess the dynamics of CML relapse compared with the BCR-ABL1 fold rise: implications for monitoring and management
204. ASXL1 and BIM germ line variants predict response and identify CML patients with the greatest risk of imatinib failure
205. ASXL1and BIMgerm line variants predict response and identify CML patients with the greatest risk of imatinib failure
206. The allosteric inhibitor ABL001 enables dual targeting of BCR–ABL1
207. Nilotinib in Imatinib-Resistant or -Intolerant Patients (pts) with Chronic Myeloid Leukemia in Chronic Phase (CML-CP): 48-Month Follow-up Results of a Phase 2 Study,
208. Complete Molecular Response (CMR) Rate with Nilotinib in Patients (pts) with Chronic Myeloid Leukemia in Chronic Phase (CML-CP) without CMR After ≥ 2 Years on Imatinib: Preliminary Results From the Randomized ENESTcmr Trial of Nilotinib 400 Mg Twice Daily (BID) Vs Imatinib
209. Multiple Low Level Mutations Identifies Imatinib Resistant CML Patients At Risk of Poor Response to Second-Line Inhibitor Therapy, Irrespective of the Resistance Profile of the Mutations
210. Upfront Imatinib Therapy in CML Patients with Rapid Switching to Nilotinib for Failure to Achieve Molecular Targets or Intolerance Achieves High Overall Rates of Molecular Response and a Low Risk of Progression - An Update of the TIDEL-II Trial
211. Imatinib Dose Interruption in Responding CML Patients Is Associated with Characteristic BCR-ABL Kinetics, Which Could Help to Differentiate Non-Adherence From Drug Resistance
212. Sensitive Detection of BCR-ABL1 Mutations in Patients With Chronic Myeloid Leukemia After Imatinib Resistance Is Predictive of Outcome During Subsequent Therapy
213. BCR–ABL Transcript Dynamics Support the Hypothesis That Leukemic Stem Cells Are Reduced during Imatinib Treatment
214. Harmonization of molecular monitoring of chronic myeloid leukemia therapy in Japan
215. Molecular methods in diagnosis and monitoring of haematological malignancies
216. SHP-1 expression accounts for resistance to imatinib treatment in Philadelphia chromosome–positive cells derived from patients with chronic myeloid leukemia
217. Dynamics of chronic myeloid leukemia response to long-term targeted therapy reveal treatment effects on leukemic stem cells
218. Minimal residual disease: the advantages of digital over analog polymerase chain reaction
219. Chronic Myelogenous Leukemia: Monitoring Response to Therapy
220. Mutational analysis in chronic myeloid leukemia: when and what to do?
221. Practical advice for determining the role of BCR-ABL mutations in guiding tyrosine kinase inhibitor therapy in patients with chronic myeloid leukemia
222. Establishment of the first World Health Organization International Genetic Reference Panel for quantitation of BCR-ABL mRNA
223. A Review of Mutation Analysis In the TOPS Trial of Standard Dose Versus High Dose IM In CML Suggests That Refinements to the ELN Recommendations for Mutation Screening May Be Appropriate
224. Selective Escalation of Imatinib Therapy and Early Switching to Nilotinib In De Novo Chronic Phase CML Patients: Interim Results From the TIDEL-II Trial
225. Towards DNA-Based Monitoring of Therapy In Chronic Myeloid Leukemia
226. Mutation Analysis of BCR-ABL Tyrosine Kinase Domain In New Chronic Phase-Chronic Myeloid Leukemia Patients with Suboptimal Response or Treatment Failure From Imatinib Treatment.
227. Detection of Low Level Nilotinib or Dasatinib Resistant BCR-ABL Mutations by Mass Spectrometry In CML Patients Who Fail Imatinib Is Highly Predictive of Their Subsequent Clonal Expansion When Treated with the Drug for Which Their Mutation Confers Resistance
228. Practical Considerations for Monitoring Patients With Chronic Myeloid Leukemia
229. Phase III, Randomized, Open-Label Study of Daily Imatinib Mesylate 400 mg Versus 800 mg in Patients With Newly Diagnosed, Previously Untreated Chronic Myeloid Leukemia in Chronic Phase Using Molecular End Points: Tyrosine Kinase Inhibitor Optimization and Selectivity Study
230. Selecting optimal second-line tyrosine kinase inhibitor therapy for chronic myeloid leukemia patients after imatinib failure: does the BCR-ABL mutation status really matter?
231. Dasatinib treatment of chronic-phase chronic myeloid leukemia: analysis of responses according to preexisting BCR-ABL mutations
232. Molecular Response at 3 Months On Nilotinib Therapy Predicts Response and Long-Term Outcomes in Patients with Imatinib-Resistant or -Intolerant Chronic Myeloid Leukemia in Chronic Phase (CML-CP).
233. 24 Months Update of the TOPS Study: a Phase III, Randomized, Open-Label Study of 400mg/d (SD-IM) Versus 800mg/d (HD-IM) of Imatinib Mesylate (IM) in Patients (Pts) with Newly Diagnosed, Previously Untreated Chronic Myeloid Leukemia in Chronic Phase (CML-CP).
234. Early Dose-Escalation in Chronic Myeloid Leukaemia Patients with Low Plasma Imatinib Levels Leads to Equivalent BCR-ABL Values and Drug Levels at 6 Months to Those with Optimal Drug Levels: First Analysis From the TIDEL II Trial of De-Novo Patients Treated with 600mg Imatinib.
235. Reduced Expression Level of SHP1 Gives An Additive Survival Advantage to the Ph+ Cells of Chronic Myeloid Leukemia (CML) Patients and Provides a Novel Pretreatment Predictor of Major Molecular Response Achievement in CML Patients.
236. Response and Outcomes to Nilotinib at 24 Months in Imatinib-Resistant Chronic Myeloid Leukemia Patients in Chronic Phase (CML-CP) and Accelerated Phase (CML-AP) with and without BCR-ABL Mutations.
237. Maintaining Imatinib ≥600 Mg Daily in the First 12 Months of Chronic Phase CML Treatment Is Associated with Superior Event-Free Survival at 5 Years.
238. Analysis of Molecular Data and the Emergence of Mutations for Chronic-Phase Chronic Myelogenous Leukemia (CML-CP) Patients Treated with Dasatinib After Imatinib Failure.
239. Measuring Minimal Residual Disease in Chronic Myeloid Leukemia: Fluorescence In Situ Hybridization and Polymerase Chain Reaction
240. Impact of Baseline BCR-ABL Mutations on Response to Nilotinib in Patients With Chronic Myeloid Leukemia in Chronic Phase
241. A Phase I/II study of nilotinib in Japanese patients with imatinib-resistant or -intolerant Ph+ CML or relapsed/refractory Ph+ ALL
242. Genomic translocation breakpoint sequences are conserved in BCR-ABL1 cell lines despite the presence of amplification
243. Monitoring disease response to tyrosine kinase inhibitor therapy in CML
244. Mathematical Simulation of BCR-ABL Real Time Quantitative Polymerase Chain Reaction (RQ-PCR) for Chronic Myeloid Leukemia (CML) Response Monitoring Provides Insight on the Basis of International Standardization.
245. DNA-Based Monitoring of Minimal Residual Disease(MRD) in Chronic Myeloid Leukemia(CML).
246. The Initial Molecular Response of Chronic Phase CML Patients Treated with Second Generation ABL Inhibitor Therapy after Imatinib Failure Can Predict Inadequate Response and Provide Indications for Rational Mutation Screening
247. Nilotinib Efficacy According to Baseline BCR-ABL Mutations in Patients with Imatinib-Resistant Chronic Myeloid Leukemia in Chronic Phase (CML-CP)
248. Reduction of BCR-ABL Transcript Levels at 6, 12, and 18 Months (mo) Correlates with Long-Term Outcomes on Imatinib (IM) at 72 Mo: An Analysis from the International Randomized Study of Interferon versus STI571 (IRIS) in Patients (pts) with Chronic Phase Chronic Myeloid Leukemia (CML-CP)
249. The Expression of shp-1 and SHP-2: A Novel Powerful Predictor of Major Molecular Response (MMR) Achievement in Chronic Myeloid Leukemia Gleevec-Treated Patients Enrolled into the TOPS Clinical Trial.
250. Dasatinib-Associated Major Molecular Responses Are Rapidly Achieved in Patients with Chronic Myeloid Leukemia in Chronic Phase (CML-CP) Following Resistance, Suboptimal Response, or Intolerance on Imatinib.
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