Search

Your search keyword '"Zehnder, James L."' showing total 762 results
Start Over Author "Zehnder, James L."
762 results on '"Zehnder, James L."'

203. Interlaboratory Performance of a Microarray-Based Gene Expression Test to Determine Tissue of Origin in Poorly Differentiated and Undifferentiated Cancers

Author

Dumur, Catherine I., primary, Lyons-Weiler, Maureen, additional, Sciulli, Christin, additional, Garrett, Carleton T., additional, Schrijver, Iris, additional, Holley, Tara K., additional, Rodriguez-Paris, Juan, additional, Pollack, Jonathan R., additional, Zehnder, James L., additional, Price, Melissa, additional, Hagenkord, Jill M., additional, Rigl, C. Ted, additional, Buturovic, Ljubomir J., additional, Anderson, Glenda G., additional, and Monzon, Federico A., additional

Published
2008
Full Text
View/download PDF

216. Granulocyte–Macrophage Progenitors as Candidate Leukemic Stem Cells in Blast-Crisis CML

Author

Jamieson, Catriona H.M., primary, Ailles, Laurie E., additional, Dylla, Scott J., additional, Muijtjens, Manja, additional, Jones, Carol, additional, Zehnder, James L., additional, Gotlib, Jason, additional, Li, Kevin, additional, Manz, Markus G., additional, Keating, Armand, additional, Sawyers, Charles L., additional, and Weissman, Irving L., additional

Published
2004
Full Text
View/download PDF

224. The role of CD8+T-cell clones in immune thrombocytopenia

Author

Malik, Amna, Sayed, Anwar A., Han, Panpan, Tan, Michelle M. H., Watt, Eleanor, Constantinescu-Bercu, Adela, Cocker, Alexander T. H., Khoder, Ahmad, Saputil, Rocel C., Thorley, Emma, Teklemichael, Ariam, Ding, Yunchuan, Hart, Alice C. J., Zhang, Haiyu, Mitchell, Wayne A., Imami, Nesrina, Crawley, James T. B., Salles-Crawley, Isabelle I., Bussel, James B., Zehnder, James L., Adams, Stuart, Zhang, Bing M., and Cooper, Nichola

Abstract

•Patients with chronic ITP had clonal expansions of disease-associated TEMRA CD8+T cells.•CD8+T cells bind to platelets and cause their activation and apoptosis, defining an antibody-independent mechanism of platelet destruction.

Published
2023
Full Text
View/download PDF

225. Reply from the Authors

Author

Wrone, Elizabeth M., primary, Zehnder, James L., additional, Hornberger, John M., additional, McCann, Linda M., additional, Coplon, Norman S., additional, and Fortmann, Stephen P., additional

Published
2002
Full Text
View/download PDF

231. A study of the mutational landscape of pediatric-type follicular lymphoma and pediatric nodal marginal zone lymphoma

Author

Ozawa, Michael G, Bhaduri, Aparna, Chisholm, Karen M, Baker, Steven A, Ma, Lisa, Zehnder, James L, Luna-Fineman, Sandra, Link, Michael P, Merker, Jason D, Arber, Daniel A, and Ohgami, Robert S

Abstract

Pediatric-type follicular lymphoma and pediatric marginal zone lymphoma are two of the rarest B-cell lymphomas. These lymphomas occur predominantly in the pediatric population and show features distinct from their more common counterparts in adults: adult-type follicular lymphoma and adult-type nodal marginal zone lymphoma. Here we report a detailed whole-exome deep sequencing analysis of a cohort of pediatric-type follicular lymphomas and pediatric marginal zone lymphomas. This analysis revealed a recurrent somatic variant encoding p.Lys66Arg in the transcription factor interferon regulatory factor 8 (IRF8) in 3 of 6 cases (50%) of pediatric-type follicular lymphoma. This specific point mutation was not detected in pediatric marginal zone lymphoma or in adult-type follicular lymphoma. Additional somatic point mutations in pediatric-type follicular lymphoma were observed in genes involved in transcription, intracellular signaling, and cell proliferation. In pediatric marginal zone lymphoma, no recurrent mutation was identified; however, somatic point mutations were observed in genes involved in cellular adhesion, cytokine regulatory elements, and cellular proliferation. A somatic variant in AMOTL1, a recurrently mutated gene in splenic marginal zone lymphoma, was also identified in a case of pediatric marginal zone lymphoma. The overall non-synonymous mutational burden was low in both pediatric-type follicular lymphoma and pediatric marginal zone lymphoma (4.6 mutations per exome). Altogether, these findings support a distinctive genetic basis for pediatric-type follicular lymphoma and pediatric marginal zone lymphoma when compared with adult subtypes and to one another. Moreover, identification of a recurrent point mutation in IRF8provides insight into a potential driver mutation in the pathogenesis of pediatric-type follicular lymphoma with implications for novel diagnostic or therapeutic strategies.

Published
2016
Full Text
View/download PDF

232. Germ line variants predispose to both JAK2 V617F clonal hematopoiesis and myeloproliferative neoplasms

Author

Hinds, David A., Barnholt, Kimberly E., Mesa, Ruben A., Kiefer, Amy K., Do, Chuong B., Eriksson, Nicholas, Mountain, Joanna L., Francke, Uta, Tung, Joyce Y., Nguyen, Huong (Marie), Zhang, Haiyu, Gojenola, Linda, Zehnder, James L., and Gotlib, Jason

Abstract

We conducted a genome-wide association study (GWAS) to identify novel predisposition alleles associated with Philadelphia chromosome-negative myeloproliferative neoplasms (MPNs) and JAK2 V617F clonal hematopoiesis in the general population. We recruited a web-based cohort of 726 individuals with polycythemia vera, essential thrombocythemia, and myelofibrosis and 252 637 population controls unselected for hematologic phenotypes. Using a single-nucleotide polymorphism (SNP) array platform with custom probes for the JAK2 V617F mutation (V617F), we identified 497 individuals (0.2%) among the population controls who were V617F carriers. We performed a combined GWAS of the MPN cases plus V617F carriers in the control population (n = 1223) vs the remaining controls who were noncarriers for V617F (n = 252 140). For these MPN cases plus V617F carriers, we replicated the germ line JAK2 46/1 haplotype (rs59384377: odds ratio [OR] = 2.4, P = 6.6 × 10−89), previously associated with V617F-positive MPN. We also identified genome-wide significant associations in the TERT gene (rs7705526: OR = 1.8, P = 1.1 × 10−32), in SH2B3 (rs7310615: OR = 1.4, P = 3.1 × 10−14), and upstream of TET2 (rs1548483: OR = 2.0, P = 2.0 × 10−9). These associations were confirmed in a separate replication cohort of 446 V617F carriers vs 169 021 noncarriers. In a joint analysis of the combined GWAS and replication results, we identified additional genome-wide significant predisposition alleles associated with CHEK2, ATM, PINT, and GFI1B. All SNP ORs were similar for MPN patients and controls who were V617F carriers. These data indicate that the same germ line variants endow individuals with a predisposition not only to MPN, but also to JAK2 V617F clonal hematopoiesis, a more common phenomenon that may foreshadow the development of an overt neoplasm.

Published
2016
Full Text
View/download PDF

233. Germ line variants predispose to both JAK2V617F clonal hematopoiesis and myeloproliferative neoplasms

Author

Hinds, David A., Barnholt, Kimberly E., Mesa, Ruben A., Kiefer, Amy K., Do, Chuong B., Eriksson, Nicholas, Mountain, Joanna L., Francke, Uta, Tung, Joyce Y., Nguyen, Huong (Marie), Zhang, Haiyu, Gojenola, Linda, Zehnder, James L., and Gotlib, Jason

Abstract

We conducted a genome-wide association study (GWAS) to identify novel predisposition alleles associated with Philadelphia chromosome-negative myeloproliferative neoplasms (MPNs) and JAK2V617F clonal hematopoiesis in the general population. We recruited a web-based cohort of 726 individuals with polycythemia vera, essential thrombocythemia, and myelofibrosis and 252 637 population controls unselected for hematologic phenotypes. Using a single-nucleotide polymorphism (SNP) array platform with custom probes for the JAK2V617F mutation (V617F), we identified 497 individuals (0.2%) among the population controls who were V617F carriers. We performed a combined GWAS of the MPN cases plus V617F carriers in the control population (n = 1223) vs the remaining controls who were noncarriers for V617F (n = 252 140). For these MPN cases plus V617F carriers, we replicated the germ line JAK246/1 haplotype (rs59384377: odds ratio [OR] = 2.4, P= 6.6 × 10−89), previously associated with V617F-positive MPN. We also identified genome-wide significant associations in the TERTgene (rs7705526: OR = 1.8, P= 1.1 × 10−32), in SH2B3(rs7310615: OR = 1.4, P= 3.1 × 10−14), and upstream of TET2(rs1548483: OR = 2.0, P= 2.0 × 10−9). These associations were confirmed in a separate replication cohort of 446 V617F carriers vs 169 021 noncarriers. In a joint analysis of the combined GWAS and replication results, we identified additional genome-wide significant predisposition alleles associated with CHEK2, ATM, PINT, and GFI1B. All SNP ORs were similar for MPN patients and controls who were V617F carriers. These data indicate that the same germ line variants endow individuals with a predisposition not only to MPN, but also to JAK2V617F clonal hematopoiesis, a more common phenomenon that may foreshadow the development of an overt neoplasm.

Published
2016
Full Text
View/download PDF

239. Antibodies Against the First Ig-Like Domain of Human Platelet Endothelial Cell Adhesion Molecule-1 (PECAM-1) That Inhibit PECAM-1-Dependent Homophilic Adhesion Block In Vivo Neutrophil Recruitment

Author

Nakada, Marian T., primary, Amin, Kunjlata, additional, Christofidou-Solomidou, Melpo, additional, O’Brien, Christopher D., additional, Sun, Jing, additional, Gurubhagavatula, Indira, additional, Heavner, George A., additional, Taylor, Alexander H., additional, Paddock, Cathy, additional, Sun, Qi-Hong, additional, Zehnder, James L., additional, Newman, Peter J., additional, Albelda, Steven M., additional, and DeLisser, Horace M., additional

Published
2000
Full Text
View/download PDF

240. A Balanced Look at the Implications of Genomic (and Other "Omics") Testing for Disease Diagnosis and Clinical Care.

Author

Boyd, Scott D., Galli, Stephen J., Schrijver, Iris, Zehnder, James L., Ashley, Euan A., and Merker, Jason D.

Subjects
NUCLEOTIDE sequence, COMMERCIALIZATION, MEDICAL technology, GENOMICS, MEDICAL care
Abstract

The tremendous increase in DNA sequencing capacity arising from the commercialization of "next generation" instruments has opened the door to innumerable routes of investigation in basic and translational medical science. It enables very large data sets to be gathered, whose interpretation and conversion into useful knowledge is only beginning. A challenge for modern healthcare systems and academic medical centers is to apply these new methods for the diagnosis of disease and the management of patient care without unnecessary delay, but also with appropriate evaluation of the quality of data and interpretation, as well as the clinical value of the insights gained. Most critically, the standards applied for evaluating these new laboratory data and ensuring that the results and their significance are clearly communicated to patients and their caregivers should be at least as rigorous as those applied to other kinds of medical tests. Here, we present an overview of conceptual and practical issues to be considered in planning for the integration of genomic methods or, in principle, any other type of "omics" testing into clinical care. [ABSTRACT FROM AUTHOR]

Published
2014
Full Text
View/download PDF

241. Identification of recurrent SMO and BRAF mutations in ameloblastomas.

Author

Sweeney, Robert T, McClary, Andrew C, Myers, Benjamin R, Biscocho, Jewison, Neahring, Lila, Kwei, Kevin A, Qu, Kunbin, Gong, Xue, Ng, Tony, Jones, Carol D, Varma, Sushama, Odegaard, Justin I, Sugiyama, Toshihiro, Koyota, Souichi, Rubin, Brian P, Troxell, Megan L, Pelham, Robert J, Zehnder, James L, Beachy, Philip A, and Pollack, Jonathan R

Subjects
GENETIC mutation, AMELOBLASTOMA, ODONTOGENIC tumors, MITOGEN-activated protein kinases, ARSENIC trioxide
Abstract

Here we report the discovery of oncogenic mutations in the Hedgehog and mitogen-activated protein kinase (MAPK) pathways in over 80% of ameloblastomas, locally destructive odontogenic tumors of the jaw, by genomic analysis of archival material. Mutations in SMO (encoding Smoothened, SMO) are common in ameloblastomas of the maxilla, whereas BRAF mutations are predominant in tumors of the mandible. We show that a frequently occurring SMO alteration encoding p.Leu412Phe is an activating mutation and that its effect on Hedgehog-pathway activity can be inhibited by arsenic trioxide (ATO), an anti-leukemia drug approved by the US Food and Drug Administration (FDA) that is currently in clinical trials for its Hedgehog-inhibitory activity. In a similar manner, ameloblastoma cells harboring an activating BRAF mutation encoding p.Val600Glu are sensitive to the BRAF inhibitor vemurafenib. Our findings establish a new paradigm for the diagnostic classification and treatment of ameloblastomas. [ABSTRACT FROM AUTHOR]

Published
2014
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results