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893 results on '"Goodlad, John"'

1. Index

Author

Kridel, Craig, Bullough Jr., Robert V., and Goodlad, John I.

Published
2007

2. Cover

Author

Kridel, Craig, Bullough Jr., Robert V., and Goodlad, John I.

Published
2007

4. Abbreviations

Author

Kridel, Craig, Bullough Jr., Robert V., and Goodlad, John I.

Published
2007

5. Frontmatter

Author

Kridel, Craig, Bullough Jr., Robert V., and Goodlad, John I.

Published
2007

6. Glossary

Author

Kridel, Craig, Bullough Jr., Robert V., and Goodlad, John I.

Published
2007

7. Notes

Author

Kridel, Craig, Bullough Jr., Robert V., and Goodlad, John I.

Published
2007

11. Annotated Bibliography

Author

Kridel, Craig, Bullough Jr., Robert V., and Goodlad, John I.

Published
2007

33. Contents

Author

Basile, Carole G. and Goodlad, John I.

Published
2004

37. Appendices

Author

Basile, Carole G. and Goodlad, John I.

Published
2004

40. Foreword

Author

Basile, Carole G. and Goodlad, John I.

Published
2004

44. Bibliography

Author

Basile, Carole G. and Goodlad, John I.

Published
2004

46. Index

Author

Basile, Carole G. and Goodlad, John I.

Published
2004

48. The International Consensus Classification of Mature Lymphoid Neoplasms: a report from the Clinical Advisory Committee

Author

Campo, Elias, Jaffe, Elaine S., Cook, James R., Quintanilla-Martinez, Leticia, Swerdlow, Steven H., Anderson, Kenneth C., Brousset, Pierre, Cerroni, Lorenzo, de Leval, Laurence, Dirnhofer, Stefan, Dogan, Ahmet, Feldman, Andrew L., Fend, Falko, Friedberg, Jonathan W., Gaulard, Philippe, Ghia, Paolo, Horwitz, Steven M., King, Rebecca L., Salles, Gilles, San-Miguel, Jesus, Seymour, John F., Treon, Steven P., Vose, Julie M., Zucca, Emanuele, Advani, Ranjana, Ansell, Stephen, Au, Wing-Yan, Barrionuevo, Carlos, Bergsagel, Leif, Chan, Wing C., Cohen, Jeffrey I., d'Amore, Francesco, Davies, Andrew, Falini, Brunangelo, Ghobrial, Irene M., Goodlad, John R., Gribben, John G., Hsi, Eric D., Kahl, Brad S., Kim, Won-Seog, Kumar, Shaji, LaCasce, Ann S., Laurent, Camille, Lenz, Georg, Leonard, John P., Link, Michael P., Lopez-Guillermo, Armando, Mateos, Maria Victoria, Macintyre, Elizabeth, Melnick, Ari M., Morschhauser, Franck, Nakamura, Shigeo, Narbaitz, Marina, Pavlovsky, Astrid, Pileri, Stefano A., Piris, Miguel, Pro, Barbara, Rajkumar, Vincent, Rosen, Steven T., Sander, Birgitta, Sehn, Laurie, Shipp, Margaret A., Smith, Sonali M., Staudt, Louis M., Thieblemont, Catherine, Tousseyn, Thomas, Wilson, Wyndham H., Yoshino, Tadashi, Zinzani, Pier-Luigi, Dreyling, Martin, Scott, David W., Winter, Jane N., and Zelenetz, Andrew D.

Published
2022
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49. Enteropathy-associated T cell lymphoma subtypes are characterized by loss of function of SETD2

Author

Moffitt, Andrea B, Ondrejka, Sarah L, McKinney, Matthew, Rempel, Rachel E, Goodlad, John R, Teh, Chun Huat, Leppa, Sirpa, Mannisto, Susanna, Kovanen, Panu E, Tse, Eric, Au-Yeung, Rex KH, Kwong, Yok-Lam, Srivastava, Gopesh, Iqbal, Javeed, Yu, Jiayu, Naresh, Kikkeri, Villa, Diego, Gascoyne, Randy D, Said, Jonathan, Czader, Magdalena B, Chadburn, Amy, Richards, Kristy L, Rajagopalan, Deepthi, Davis, Nicholas S, Smith, Eileen C, Palus, Brooke C, Tzeng, Tiffany J, Healy, Jane A, Lugar, Patricia L, Datta, Jyotishka, Love, Cassandra, Levy, Shawn, Dunson, David B, Zhuang, Yuan, Hsi, Eric D, and Dave, Sandeep S

Subjects
Genetics, Cancer, Hematology, Lymphoma, Rare Diseases, Clinical Research, Biotechnology, Digestive Diseases, 2.1 Biological and endogenous factors, Aetiology, Animals, DNA Copy Number Variations, Enteropathy-Associated T-Cell Lymphoma, Female, Gene Expression Profiling, Gene Silencing, Histone-Lysine N-Methyltransferase, Humans, Male, Mice, Knockout, Middle Aged, Mutation, Sequence Analysis, DNA, T-Lymphocytes, Medical and Health Sciences, Immunology
Abstract

Enteropathy-associated T cell lymphoma (EATL) is a lethal, and the most common, neoplastic complication of celiac disease. Here, we defined the genetic landscape of EATL through whole-exome sequencing of 69 EATL tumors. SETD2 was the most frequently silenced gene in EATL (32% of cases). The JAK-STAT pathway was the most frequently mutated pathway, with frequent mutations in STAT5B as well as JAK1, JAK3, STAT3, and SOCS1 We also identified mutations in KRAS, TP53, and TERT Type I EATL and type II EATL (monomorphic epitheliotropic intestinal T cell lymphoma) had highly overlapping genetic alterations indicating shared mechanisms underlying their pathogenesis. We modeled the effects of SETD2 loss in vivo by developing a T cell-specific knockout mouse. These mice manifested an expansion of γδ T cells, indicating novel roles for SETD2 in T cell development and lymphomagenesis. Our data render the most comprehensive genetic portrait yet of this uncommon but lethal disease and may inform future classification schemes.

Published
2017

50. B-Cell and Classical Hodgkin Lymphomas Associated With Immunodeficiency: 2015 SH/EAHP Workshop Report-Part 2.

Author

de Jong, Daphne, Roemer, Margaretha, Chan, John, Goodlad, John, Gratzinger, Dita, Chadburn, Amy, Jaffe, Elaine, Said, Jonathan, and Natkunam, Yasodha

Subjects
9p24, Autoimmunity, Classical Hodgkin lymphoma, Iatrogenic immunodeficiency, Large B-cell lymphoma, Marginal zone lymphoma, PD-L1, Posttransplant lymphoproliferative disorder, Primary immunodeficiency, T-cell/histiocyte-rich B-cell lymphoma, Education, Epstein-Barr Virus Infections, Female, Hodgkin Disease, Humans, Immunologic Deficiency Syndromes, Lymphoma, B-Cell, Male
Abstract

OBJECTIVES: The 2015 Workshop of the Society for Hematopathology/European Association for Haematopathology submitted small and large B-cell lymphomas (BCLs), including classical Hodgkin lymphoma (CHL), in the context of immunodeficiency. METHODS: Clinicopathologic and molecular features were studied to explore unifying concepts in malignant B-cell proliferations across immunodeficiency settings. RESULTS: Cases submitted to the workshop spanned small BCLs presenting as nodal or extranodal marginal zone lymphoma and lymphoplasmacytic lymphoma, Epstein-Barr virus (EBV) positive in 75% of cases. Submitted large BCLs formed a spectrum from diffuse large B-cell lymphoma (DLBCL) to CHL across immunodeficiency settings. Additional studies demonstrated overexpression of PD-L1 and molecular 9p24 alterations in the large BCL spectrum and across different immunodeficiency settings. CONCLUSIONS: Small BCLs occur in all immunodeficiency settings, and EBV positivity is essential for their recognition as immunodeficiency related. Large BCLs include a spectrum from DLBCL to CHL across all immunodeficiency settings; immunohistochemical and molecular features are suggestive of shared pathogenetic mechanisms involving PD-L1 immune checkpoints.

Published
2017

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