Search Results - "Breeden, Megan"

Rapid clonal shifts in response to kinase inhibitor therapy in chronic myelogenous leukemia are identified by quantitation mutation assays by Yin, C. Cameron, Cortes, Jorge, Galbincea, John, Reddy, Neelima, Breeden, Megan, Jabbour, Elias, Luthra, Rajyalakshmi, Jones, Dan

“…Treatment of CML with the tyrosine kinase inhibitor (TKI) imatinib mesylate results in the emergence of point mutations within the kinase domain (KD) of the…”
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Aptamers: prospects in therapeutics and biomedicine by Yan, Amy C, Bell, Kathryn M, Breeden, Megan M, Ellington, Andrew D

“…Most biopolymer drugs to date have been proteins. However, the ability to select nucleic acid binding species (aptamers) has led to the development of protein…”
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Electrospray ionization of nucleic acid aptamer/small molecule complexes for screening aptamer selectivity by Keller, Karin M., Breeden, Megan M., Zhang, Junmei, Ellington, Andrew D., Brodbelt, Jennifer S.

“…Molecular recognition of small molecule ligands by the nucleic acid aptamers for tobramycin, ATP, and FMN has been examined using electrospray ionization mass…”
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Characteristics and outcomes of patients with chronic myeloid leukemia and T315I mutation following failure of imatinib mesylate therapy by Jabbour, Elias, Kantarjian, Hagop, Jones, Dan, Breeden, Megan, Garcia-Manero, Guillermo, O'Brien, Susan, Ravandi, Farhad, Borthakur, Gautam, Cortes, Jorge

“…Chronic myeloid leukemia (CML) with T315I mutation has been reported to have poor prognosis. We analyzed 27 patients with T315I, including 20 who developed…”
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Dynamics of BCR-ABL kinase domain mutations in chronic myeloid leukemia after sequential treatment with multiple tyrosine kinase inhibitors by Cortes, Jorge, Jabbour, Elias, Kantarjian, Hagop, Yin, C. Cameron, Shan, Jianqin, O'Brien, Susan, Garcia-Manero, Guillermo, Giles, Francis, Breeden, Megan, Reeves, Nubia, Wierda, William G., Jones, Dan

“…Dasatinib and nilotinib are potent tyrosine kinase inhibitors (TKIs) with activity against many imatinib-resistant chronic myeloid leukemia (CML) clones with…”
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Kinase domain point mutations in Philadelphia chromosome‐positive acute lymphoblastic leukemia emerge after therapy with BCR‐ABL kinase inhibitors by Jones, Dan, Thomas, Deborah, Yin, C. Cameron, O'Brien, Susan, Cortes, Jorge E., Jabbour, Elias, Breeden, Megan, Giles, Francis J., Zhao, Weiqiang, Kantarjian, Hagop M.

“…BACKGROUND. BCR‐ABL kinase domain (KD) mutations are detected in approximately 45% of patients with imatinib‐resistant chronic myeloid leukemia. Patterns of KD…”
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Splenic marginal zone lymphomas are characterized by loss of interstitial regions of chromosome 7q, 7q31.32 and 7q36.2 that include the protection of telomere 1 (POT1) and sonic hedgehog (SHH) genes by Vega, Francisco, Cho‐Vega, Jeong Hee, Lennon, Patrick A., Luthra, Madan G., Bailey, Jaime, Breeden, Megan, Jones, Dan, Medeiros, L. Jeffrey, Luthra, Rajyalakshmi

“…Summary To further characterize the genotypic features of splenic (S) and nodal (N) marginal zone lymphomas (MZL) we compared eight SMZL and five NMZL by…”
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Characteristics and outcomes of patients with chronic myeloid leukemia and T315Ι mutation following failure of imatinib mesylate therapy by JABBOUR, Elias, KANTARJIAN, Hagop, JONES, Dan, BREEDEN, Megan, GARCIA-MANERO, Guillermo, O'BRIEN, Susan, RAVANDI, Farhad, BORTHAKUR, Gautam, CORTES, Jorge

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Kinase Domain Point Mutations in Ph+ Acute Lymphoblastic Leukemia (ALL) Emerge Following Therapy with BCR-ABL Kinase Inhibitors by Jones, Dan, Thomas, Deborah, Yin, C. Cameron, O'Brien, Susan, Cortes, Jorge E., Jabbour, Elias, Breeden, Megan, Giles, Francis J., Zhao, Weiqiang, Kantarjian, Hagop M.

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Kinase Domain Point Mutations in Ph+ Acute Lymphoblastic Leukemia (ALL) and Lymphoid Blast Crisis of Chronic Myeloid Leukemia (CML) and Their Emergence Following Therapy with Bcr-Abl Kinase Inhibitors by Jones, Dan, Luthra, Rayjalakshmi, Kantarjian, Hagop M., Breeden, Megan, O'Brien, Susan, Faderl, Stefan, Cortes, Jorge, Thomas, Deborah

“…Bcr-Abl kinase domain (KD) point mutations are detected in the dominant clone(s) in approximately 45% of CML at the time of disease resistance, developing…”
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