Elevated Serum B-Lymphocyte Stimulator Levels in Patients With Familial Lymphoproliferative Disorders

Novak, Anne J.; Grote, Deanna M.; Ziesmer, Steven C.; Kline, Michael; Manske, Michelle K.; Slager, Susan L.; Witzig, Thomas E.; Shanafelt, Tait D.; Call, Timothy G.; Kay, Neil E.; Jelinek, Diane F.; Cerhan, James R.; Gross, Jane A.; Harder, Brandon; Dillon, Stacey R.; Ansell, Stephen M.

doi:10.1200/jco.2005.02.7938

Cited by 82 publications

(94 citation statements)

References 23 publications

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“…We performed restriction fragment length polymorphism analysis to evaluate the BAFF promoter genotype. The primers used for BAFF promoter amplification were 5Ј-GGCACAGTCAACATGGGAGT-3Ј (forward) and 5Ј-GCTAAGTGTTTTAGCATTGAATTG-3Ј (reverse) as previously described (6). The PCR products were subjected to a restriction enzyme-based screening of the Ϫ871 C/T using 20 units of Bsr BI restriction enzyme.…”

Section: Patientsmentioning

confidence: 99%

“…BAFF, a tumor necrosis factor ␣ (TNF␣) family member, is a key regulator of B cell differentiation, survival, and Ig secretion, and alterations in its expression have been initially associated with different autoimmune disorders, such as Sjögren's syndrome, SLE, and RA (5). Overexpression of BAFF in monocytes has been associated with the presence of a T allele at the polymorphic site Ϫ871 C/T of its promoter in patients with RA and familial lymphoproliferative disorders (6).…”

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confidence: 99%

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Genetic determinants in hepatitis C virus–associated mixed cryoglobulinemia: Role of polymorphic variants of BAFF promoter and Fcγ receptors

Gragnani¹,

Piluso²,

Giannini³

et al. 2011

Arthritis & Rheumatism

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Section: Patientsmentioning

confidence: 99%

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confidence: 99%

Genetic determinants in hepatitis C virus–associated mixed cryoglobulinemia: Role of polymorphic variants of BAFF promoter and Fcγ receptors

Gragnani¹,

Piluso²,

Giannini³

et al. 2011

Arthritis & Rheumatism

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“…1 Alkylating agents have long been considered to be part of the cause. [2][3][4][5] Some, but not all, smaller investigations have reported that higher cumulative melphalan dose and longer duration of melphalan therapy are associated with an increased risk of AML. 6,7 The role of nontreatmentrelated factors is largely unknown.…”

Section: Conflict Of Interestmentioning

confidence: 99%

“…4 This indicates that a single genetic variation might affect TACI activation by increasing BLyS levels. Whereas the rs3803800 G SNP in the APRIL gene is nonsynonymous and directly induces amino-acid changes (N96S), the rs11078355 T SNP in the TACI gene is synonymous (S277S).…”

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Phase 1b trial of atacicept, a recombinant protein binding BLyS and APRIL, in patients with chronic lymphocytic leukemia

Elter

et al. 2011

Leukemia

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aberrations, altered drug metabolism, and enhanced cellular repair processes. In contrast, the median OS for the 14 patients undergoing an ASCT was not reached, suggesting perhaps continued response to alkylator-based therapy.Among the 74 patients, 31 had high-risk disease based on the presence of one or more of the following abnormalities (Del 13 by metaphase cytogenetics, hypodiploidy, del 17p, t(4;14) or t(14;16)). The median OS from the time of progression was 9.5 months for the high-risk group compared with 14.7 months for the rest; P ¼ 0.4. The higher than average proportion of patients with high-risk disease likely reflects a selection bias in favor of patients relapsing rapidly after currently available treatments.Our study represents a unique description of response to salvage therapies and outcome of patients progressing on pomalidomide, the latest IMiD to reach clinical trials. Several important conclusions can be derived from these clinical results. It confirms poor outcome of the patients relapsing after novel therapies. We also provide evidence of retained activity of lenalidomide in a proportion of patients relapsing on pomalidomide, suggesting that a trial of lenalidomide in these patients is justified. Finally, even in this relapsed and refractory population, ASCT when feasible is associated with high response rates.

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Serum BLyS levels increase after rituximab as initial therapy in patients with follicular grade 1 non‐Hodgkin lymphoma

Ansell¹,

Novak²,

Ziesmer³

et al. 2008

American J Hematol

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Serum B‐lymphocyte stimulator (BLyS) levels are elevated in a subset of non‐Hodgkin lymphoma (NHL) patients, particularly those with a family history of B‐cell malignancies or a polymorphism in the BLyS gene. BLyS promotes growth of malignant B‐cells and increased serum BLyS levels are associated with a poor clinical outcome. In this study, BLyS levels were measured before and after 4 weekly doses of rituximab in 30 patients with previously untreated follicular Grade 1 NHL. A significant increase was seen in the serum levels of BLyS (P = 0.0001) after rituximab therapy. The increase was independent of genetic variability in the BLyS gene. Am. J. Hematol., 2009. © 2008 Wiley‐Liss, Inc.

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Elevated Serum B-Lymphocyte Stimulator Levels in Patients With Familial Lymphoproliferative Disorders

Abstract: Our data suggest serum BLyS levels are elevated in patients with familial B-CLL and that elevated BLyS levels correlate with the presence of a T at -871 in the BLyS promoter.

Cited by 82 publications

References 23 publications

Genetic determinants in hepatitis C virus–associated mixed cryoglobulinemia: Role of polymorphic variants of BAFF promoter and Fcγ receptors

Genetic determinants in hepatitis C virus–associated mixed cryoglobulinemia: Role of polymorphic variants of BAFF promoter and Fcγ receptors

Phase 1b trial of atacicept, a recombinant protein binding BLyS and APRIL, in patients with chronic lymphocytic leukemia

Serum BLyS levels increase after rituximab as initial therapy in patients with follicular grade 1 non‐Hodgkin lymphoma

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