S. Willis

发表

Phylogenetic and physiological comparisons of PAH-degrading bacteria from geographically diverse soils

S. E. Lantz, J. Mueller, Suzanne E. Lantz, 1997, Antonie van Leeuwenhoek.

RNAi screen for rapid therapeutic target identification in leukemia patients

B. Druker, M. Heinrich, M. Deininger, 2009, Proceedings of the National Academy of Sciences.

The JAK2V617F activating mutation occurs in chronic myelomonocytic leukemia and acute myeloid leukemia, but not in acute lymphoblastic leukemia or chronic lymphocytic leukemia.

M. Loh, S. Armstrong, E. Estey, 2005, Blood.

Molecular Phylogenetic and Biogeochemical Studies of Sulfate-Reducing Bacteria in the Rhizosphere ofSpartina alterniflora

J. Rooney-Varga, R. Devereux, S. Willis, 1999, Applied and Environmental Microbiology.

Genome Sizes of Desulfovibrio desulfuricans, Desulfovibrio vulgaris, and Desulfobulbus propionicus Estimated by Pulsed-Field Gel Electrophoresis of Linearized Chromosomal DNA

R. Devereux, S. Willis, M. Hines, 1997, Current Microbiology.

Absence of Skp2 Expression Attenuates Bcr-abl-induced

K. Nakayama, B. Druker, A. Corbin, 2008 .

leukemia or chronic lymphocytic leukemia leukemia and acute myeloid leukemia, but not in acute lymphoblastic The JAK2V617F activating mutation occurs in chronic myelomonocytic

Avis J. Thomas, M. Loh, S. Armstrong, 2013 .

The JAK 2 V 617 F activating mutation occurs in chronic myelomonocytic leukemia and acute myeloid leukemia , but not in acute lymphoblastic leukemia or chronic lymphocytic leukemia

M. Loh, S. Armstrong, E. Estey, 2005 .

acute lymphoblastic The JAK 2 V 617 F activating mutation occurs in chronic myelomonocytic

M. Loh, S. Armstrong, E. Estey, 2005 .

mutations in myeloid leukemia patients High-throughput sequencing screen reveals novel, transforming RAS

B. Druker, M. Heinrich, D. Gilliland, 2013 .

BCR-ABL Kinase Domain Mutations in Chronic Myeloid Leukemia: Not Quite Enough to Cause Resistance to Imatinib Therapy?

M. Deininger, S. Willis, T. Lange, 2005, Cell cycle.

In vitro efficacy of combined treatment depends on the underlying mechanism of resistance in imatinib-resistant Bcr-Abl-positive cell lines.

J. Melo, B. Druker, A. Corbin, 2004, Blood.

A Half-Log Increase in BCR-ABL RNA Predicts a Higher Risk of Relapse in Patients with Chronic Myeloid Leukemia with an Imatinib-Induced Complete Cytogenetic Response

B. Druker, M. Deininger, M. Mauro, 2007, Clinical Cancer Research.

High-sensitivity detection of BCR-ABL kinase domain mutations in imatinib-naive patients: correlation with clonal cytogenetic evolution but not response to therapy.

S. McWeeney, B. Druker, M. Deininger, 2005, Blood.

Detection of ABL kinase domain mutations with denaturing high-performance liquid chromatography

B. Druker, M. Heinrich, L. McGreevey, 2004, Leukemia.

A single nucleotide polymorphism in the coding region of ABL and its effects on sensitivity to imatinib

M. Heinrich, A. Corbin, S. Willis, 2005, Leukemia.

patients on imatinib BCR-ABL SH3-SH2 domain mutations in chronic myeloid leukemia

G. Superti-Furga, O. Hantschel, I. Kaupe, 2011 .

Identification of Seven TreponemaSpecies in Health- and Disease-Associated Dental Plaque by Nested PCR

S. Willis, L. Gapter, G. Riviere, 1999, Journal of Clinical Microbiology.

Phenotypic and Genotypic Heterogeneity among Cultivable Pathogen-Related Oral Spirochetes and Treponema vincentii

S. Willis, G. Riviere, K. Smith, 1999, Journal of Clinical Microbiology.

Characterization of BCR-ABL deletion mutants from patients with chronic myeloid leukemia

G. Superti-Furga, O. Hantschel, I. Kaupe, 2008, Leukemia.

Imatinib resistant BCR‐ABL1 mutations at relapse in children with Ph+ALL: a Children's Oncology Group (COG) study

B. Druker, S. Hunger, N. Winick, 2012, British journal of haematology.

High-throughput sequencing screen reveals novel, transforming RAS mutations in myeloid leukemia patients.

R. Levine, B. Druker, M. Heinrich, 2009, Blood.

A gene expression signature of CD34+ cells to predict major cytogenetic response in chronic-phase chronic myeloid leukemia patients treated with imatinib.

Beth Wilmot, Shannon K McWeeney, Jennifer L. Snead, 2010, Blood.

Comparison of imatinib mesylate, dasatinib (BMS-354825), and nilotinib (AMN107) in an N-ethyl-N-nitrosourea (ENU)-based mutagenesis screen: high efficacy of drug combinations.

B. Druker, F. Lee, M. Deininger, 2006, Blood.

domain mutation in patients with chronic myeloid leukemia on imatinib Determining the rise in BCR-ABL RNA that optimally predicts a kinase

M. Mauro, S. Willis, J. Laudadio, 2013 .

Determining the rise in BCR-ABL RNA that optimally predicts a kinase domain mutation in patients with chronic myeloid leukemia on imatinib.

M. Deininger, M. Mauro, S. Willis, 2009, Blood.

acute myeloid leukemia RNAi screening of the tyrosine kinome identifies therapeutic targets in

B. Druker, M. Heinrich, A. Corbin, 2013 .

RNAi screening of the tyrosine kinome identifies therapeutic targets in acute myeloid leukemia.

B. Druker, M. Heinrich, A. Corbin, 2008, Blood.

Absence of SKP 2 expression attenuates BCR-ABL-induced

K. Nakayama, B. Druker, A. Corbin, 2008 .

BCR-ABL SH3-SH2 domain mutations in chronic myeloid leukemia patients on imatinib.

G. Superti-Furga, O. Hantschel, I. Kaupe, 2010, Blood.

Amplification of ribosomal RNA sequences

R. Devereux, S. Willis, 1995 .

Catalytic domains of tyrosine kinases determine the phosphorylation sites within c‐Cbl

A. Corbin, S. Willis, A. Grossmann, 2004, FEBS letters.

Phylogenetic and physiological diversity of sulphate-reducing bacteria isolated from a salt marsh sediment.

B. Genthner, J. Rooney-Varga, R. Devereux, 1998, Systematic and applied microbiology.

Comparison of Imatinib, AMN107 and Dasatinib in an Accelerated Cell-Based Mutagenesis Screen.

B. Druker, M. Deininger, S. Willis, 2005 .

Functional characterization of an activating TEK mutation in acute myeloid leukemia: a cellular context-dependent activating mutation

B. Druker, H. Erickson, J. Tyner, 2009, Leukemia.

RNAi Screening of the Tyrosine Kinome Identifies Therapeutic Targets

B. Druker, M. Heinrich, A. Corbin, 2008 .

Determining the Rise in BCR-ABL RNA That Optimally Predicts a Kinase Domain Mutation in Patients with CML on Imatinib.

M. Deininger, M. Mauro, S. Willis, 2008 .

Abstract 2809: Pathway dependence on the tyrosine kinase TYK2 in T-cell acute lymphoblastic leukemia

L. Staudt, A. Look, N. Gray, 2011 .

High-throughput mutational screen of the tyrosine kinome in chronic myelomonocytic leukemia

H. Erickson, J. Tyner, M. Loriaux, 2009, Leukemia.

Absolute quantitative detection of ABL tyrosine kinase domain point mutations in chronic myeloid leukemia using a novel nanofluidic platform and mutation-specific PCR

J. Radich, F. McCormick, M. Unger, 2009, Leukemia.

Detection of Imatinib-Resistant BCR-ABL Mutants in Drug-Naïve Patients: Correlation with Disease Phase and Clonal Evolution but Not with Response to Treatment.

S. McWeeney, B. Druker, M. Deininger, 2004 .

High-sensitivity detection of BCR-ABL kinase domain mutations in imatinib-naive patients: correlation with clonal cytogenetic evolution but not response to therapy.

S. McWeeney, B. Druker, M. Deininger, 2005, Blood.

Absence of SKP2 expression attenuates BCR-ABL-induced myeloproliferative disease.

K. Nakayama, B. Druker, A. Corbin, 2008, Blood.