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Dive into the research topics where Melinda S. Gordon is active.

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Featured researches published by Melinda S. Gordon.


Proceedings of the National Academy of Sciences of the United States of America | 2003

Somatic hypermutation of the B cell receptor genes B29 (Igβ, CD79b) and mb1 (Igα, CD79a)

Melinda S. Gordon; Cindy M. Kanegai; Jeanette R. Doerr; Randolph Wall

Somatic hypermutation (SHM), coupled to selection by antigen, generates high-affinity antibodies during germinal center (GC) B cell maturation. SHM is known to affect Bcl6, four additional oncogenes in diffuse large B cell lymphoma, and the CD95/Fas gene and is regarded as a major mechanism of B cell tumorigenesis. We find that mutations in the genes encoding the B cell receptor (BCR) accessory proteins B29 (Igβ, CD79b) and mb1 (Igα, CD79a) occur as often as Ig genes in a broad spectrum of GC- and post-GC-derived malignant B cell lines, as well as in normal peripheral B cells. These B29 and mb1 mutations are typical SHM consisting largely of single nucleotide substitutions targeted to hotspots. The B29 and mb1 mutations appear at frequencies similar to those of other non-Ig genes but lower than Ig genes. The distribution of mb1 mutations followed the characteristic pattern found in Ig and most non-Ig genes. In contrast, B29 mutations displayed a bimodal distribution resembling the CD95/Fas gene, in which promoter distal mutations conferred resistance to apoptosis. Distal B29 mutations in the cytoplasmic domain may contribute to B cell survival by limiting BCR signaling. B29 and mb1 are mutated in a much broader spectrum of GC-derived B cells than any other known somatically hypermutated non-Ig gene. This may be caused by the common cis-acting regulatory sequences that control the requisite coexpression of the B29, mb1, and Ig chains in the BCR.


British Journal of Haematology | 2007

Antimyeloma effects of arsenic trioxide are enhanced by melphalan, bortezomib and ascorbic acid

Richard A. Campbell; Eric Sanchez; Jeffrey A. Steinberg; Stavroula Baritaki; Melinda S. Gordon; Cathy S Wang; Dror Shalitin; Haiming Chen; Shen Pang; Benjamin Bonavida; Jonathan W. Said; James R. Berenson

Arsenic trioxide (ATO) induces apoptosis of malignant plasma cells through multiple mechanisms, including inhibition of DNA binding by nuclear factor kappa‐B, a key player in the development of chemoresistance in multiple myeloma (MM). This activity suggests that ATO may be synergistic when combined with other active antimyeloma drugs. To evaluate this, we examined the antimyeloma effects of ATO alone and in combination with bortezomib, melphalan and ascorbic acid (AA) both in vitro and in vivo using a severe combined immunodeficient (SCID)‐hu murine myeloma model. Marked synergistic antimyeloma effects were demonstrated when human MM Los Angeles xenograft IgG lambda light chain (LAGλ‐1) cells were treated in vitro with ATO and any one of these agents. SCID mice bearing human MM LAGλ‐1 tumours were treated with single‐agent ATO, bortezomib, melphalan, or AA, or combinations of ATO with either bortezomib or melphalan and AA. Animals treated with any of these drugs alone showed tumour growth and increases in paraprotein levels similar to control mice, whereas animals treated with ATO‐containing combinations showed markedly suppressed tumour growth and significantly reduced serum paraprotein levels. These in vitro and in vivo results suggest that addition of ATO to other antimyeloma agents may result in improved outcomes for patients with relapsed or refractory MM.


British Journal of Haematology | 2006

Serum pleiotrophin levels are elevated in multiple myeloma patients and correlate with disease status

Howard Yeh; Haiming Chen; Steven J. Manyak; Regina A. Swift; Richard A. Campbell; Cathy S Wang; Mingjie Li; Hee Jin Lee; Gabriel N. Waterman; Melinda S. Gordon; Jonathan Ma; Benjamin Bonavida; James R. Berenson

Pleiotrophin (PTN), a tightly regulated angiogenic and mitogenic heparin‐binding protein, is markedly elevated in a variety of aggressive solid tumours. The role of PTN in haematological malignancies, however, has not been previously evaluated. This study demonstrated that PTN serum levels were elevated in multiple myeloma (MM) patients when compared with healthy subjects (P < 0·0001). Serum levels of this protein significantly increased during progression of disease, and decreased during response to anti‐MM therapy (P < 0·001). These results suggest that serum PTN may be a new biomarker for monitoring the disease status and therapeutic response of MM patients.


Journal of Molecular Biology | 2005

Patterned CpG Methylation of Silenced B Cell Gene Promoters in Classical Hodgkin Lymphoma-derived and Primary Effusion Lymphoma Cell Lines

Jeanette R. Doerr; Cindy S. Malone; Francesca Fike; Melinda S. Gordon; Shahe V. Soghomonian; Roman K. Thomas; Qian Tao; Paul G. Murray; Volker Diehl; Michael A. Teitell; Randolph Wall


Proceedings of the National Academy of Sciences of the United States of America | 2000

Aberrant B cell receptor signaling from B29 (Igβ, CD79b) gene mutations of chronic lymphocytic leukemia B cells

Melinda S. Gordon; Roberta M. Kato; Frederick Lansigan; Alexis A. Thompson; Randolph Wall; David J. Rawlings


International Journal of Oncology | 2006

LAGλ-1: A clinically relevant drug resistant human multiple myeloma tumor murine model that enables rapid evaluation of treatments for multiple myeloma

Richard A. Campbell; Steven J. Manyak; Honghao H. Yang; Nelida N. Sjak-Shie; Haiming Chen; Dorina Gui; Laura M. Popoviciu; Cathy S Wang; Melinda S. Gordon; Shen Pang; Benjamin Bonavida; Jonathan W. Said; James R. Berenson


Blood | 2007

Pleiotrophin is highly expressed by myeloma cells and promotes myeloma tumor growth

Haiming Chen; Melinda S. Gordon; Richard A. Campbell; Mingjie Li; Cathy S Wang; Hee Jin Lee; Eric Sanchez; Steven J. Manyak; Dorina Gui; Dror Shalitin; Jonathan W. Said; Yunchao Chang; Thomas F. Deuel; Stavroula Baritaki; Benjamin Bonavida; James R. Berenson


Archive | 2005

Methods of regulating differentiation and treating of multiple myeloma

James R. Berenson; Chen Haiming; Melinda S. Gordon


Genomics | 1996

Alternatively spliced exons encode the tissue-specific 5' termini of leukocyte pp52 and stromal cell S37 mRNA isoforms.

Alexis A. Thompson; Sidne A. Omori; Michael J. Gilly; William A. May; Melinda S. Gordon; William J. Wood; Erina Miyoshi; Cindy S. Malone; Jeff Gimble; Christopher T. Denny; Randolph Wall


Blood | 2006

Anti-VEGF Antibody Treatment Markedly Inhibits Tumor Growth in SCID-hu Models of Human Multiple Myeloma.

Richard A. Campbell; Eric Sanchez; Haiming Chen; Lauren Turker; Olivia Trac; Mingjie Li; Dror Shalitin; Melinda S. Gordon; Shen Pang; Benjamin Bonavida; Jonathan W. Said; Gregory D. Plowman; Germaine Fuh; James R. Berenson

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Haiming Chen

University of California

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Mingjie Li

University of California

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Hee Jin Lee

University of California

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Cathy S Wang

University of California

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Dror Shalitin

University of California

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Eric Sanchez

University of California

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