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4. Base-Pair Resolution of Somatic and Germline-Derived Genome Rearrangement Breakpoints in Follicular Lymphoma.

Author

Mungall, Andrew J., primary, Chu, Andy, additional, Chiu, Readman, additional, Corbett, Richard, additional, Field, Matthew A., additional, Jackman, Shaun D., additional, Mungall, Karen L., additional, Wong, Kim, additional, Boyle, Merrill, additional, Carlsen, Rebecca, additional, Chan, Susanna Y., additional, Coope, Robin J.N., additional, Hirst, Carrie A., additional, Hirst, Martin, additional, Johnson, Nathalie, additional, Krzywinski, Martin, additional, Lee, Darlene, additional, Lin, Jasmine BingXue, additional, Moore, Richard, additional, Severson, Tesa, additional, Simpson, Jared T., additional, Steidl, Christian, additional, Zeng, Thomas, additional, Zhao, Yongjun, additional, Birol, Inanc, additional, Holt, Robert A., additional, Jones, Steven J., additional, Gascoyne, Randy D., additional, Horsman, Douglas E., additional, Connors, Joseph M., additional, Schein, Jacqueline E., additional, and Marra, Marco A., additional

Published
2009
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5. Towards the Human Cancer Genome Project: A Sequence-Ready Physical Map of a Follicular Lymphoma Genome.

Author

Marra, Marco A., primary, Krzywinski, Martin, primary, Chiu, Readman, primary, Field, Matthew, primary, Birol, Inanc, primary, D’Souza, Brian, primary, Bosdet, Ian, primary, Mathewson, Carrie, primary, Lee, Darlene, primary, Baross, Agnes, primary, Gascoyne, Randy D., primary, Horsman, Douglas, primary, Holt, Robert, primary, Schein, Jacqueline, primary, and Connors, Joseph M., primary

Published
2005
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6. Autosomal-dominant B-cell deficiency with alopecia due to a mutation in NFKB2that results in nonprocessable p100

Author

Lee, Cindy Eunhee, Fulcher, David A., Whittle, Belinda, Chand, Rochna, Fewings, Nicole, Field, Matthew, Andrews, Daniel, Goodnow, Christopher C., and Cook, Matthew C.

Abstract

Most genetic defects that arrest B-cell development in the bone marrow present early in life with agammaglobulinemia, whereas incomplete antibody deficiency is usually associated with circulating B cells. We report 3 related individuals with a novel form of severe B-cell deficiency associated with partial persistence of serum immunoglobulin arising from a missense mutation in NFKB2. Significantly, this point mutation results in a D865G substitution and causes a failure of p100 phosphorylation that blocks processing to p52. Severe B-cell deficiency affects mature and transitional cells, mimicking the action of rituximab. This phenotype appears to be due to disruption of canonical and noncanonical nuclear factor κB pathways by the mutant p100 molecule. These findings could be informative for therapeutics as well as immunodeficiency.

Published
2014
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