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A polymorphism in NFKB1 is associated with improved effect of interferon-alpha maintenance treatment of patients with multiple myeloma after high-dose treatment with stem cell support. / Vangsted, Annette J; Klausen, Tobias W; Gimsing, Peter; Andersen, Niels F; Abildgaard, Niels; Gregersen, Henrik; Vogel, Ulla Birgitte.

In: Haematologica, Vol. 94, No. 9, 2009, p. 1274-1281.

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Vangsted, Annette J ; Klausen, Tobias W ; Gimsing, Peter ; Andersen, Niels F ; Abildgaard, Niels ; Gregersen, Henrik ; Vogel, Ulla Birgitte. / A polymorphism in NFKB1 is associated with improved effect of interferon-alpha maintenance treatment of patients with multiple myeloma after high-dose treatment with stem cell support. In: Haematologica. 2009 ; Vol. 94, No. 9. pp. 1274-1281.

Bibtex

@article{00898f3f9c214ed1816417e9af62c083,
title = "A polymorphism in NFKB1 is associated with improved effect of interferon-alpha maintenance treatment of patients with multiple myeloma after high-dose treatment with stem cell support",
abstract = "Background: Maintenance therapy with interferon- after high-dose treatment with stem cell support in multiple myeloma has been intensively debated. In this study, we evaluated the response to treatment with interferon- in relation to genetic variation in genes related to inflammation. Design and Methods: In a retrospective study of 296 patients with multiple myelom undergoing high-dose therapy between 1994 and 2004, 146 patients were treated with interferon- as maintenance therapy. We tested the polymorphisms IL1B T-31C, IL6 G-174C, NFKB1-94ins/delATTG, CD3EAP G-21A and PPP1R13L IVS1 A4364G for associations with time to treatment failure and overall survival with and without interferon- treatment. Results: The wild type ins-allele of polymorphism NFKB1-94 ins/delATTG was, by multivariate Cox analysis, associated with longer time to treatment failure (p=0.01) and overall survival (p=0.0084) when tested between treatment arms and in the subgroup of patients treated with interferon- the wild type ins-allele was associated with longer overall survival (p=0.002). In the absence of interferon- treatment, there was no association between the polymorphisms and treatment outcome, except for patients homozygous for the wild type G allele of IL6 G-174C who survived longer (p= 0.0074) than variant allele carriers. There was no association between the polymorphisms IL1B T-31C, CD3EAP G-21A and PPP1R13L IVS1 A4364G and treatment outcome for interferon-. Conclusions: Patients who are homozygous carriers of the wild type ins-allele of the NFKB1 -94ins/delATTG polymorphism may benefit from treatment with interferon-, in contrast to patients carrying the variant allele. This result may indicate that the effect of interferon- treatment is dependent on the availability of nuclear factor-B and the polymorphism in NFKB1 may, therefore, be a good prognostic marker for multiple myeloma patients on maintenance treatment with interferon- after high-dose therapy. A prospective study of interferon- treatment in relation to NFKB1 -94ins/delATTG is highly warranted.",
author = "Vangsted, {Annette J} and Klausen, {Tobias W} and Peter Gimsing and Andersen, {Niels F} and Niels Abildgaard and Henrik Gregersen and Vogel, {Ulla Birgitte}",
note = "polymorphism, multiple myeloma, interferon, NF-B, treatment outcome",
year = "2009",
doi = "10.3324/haematol.2008.004572",
language = "English",
volume = "94",
pages = "1274--1281",
journal = "Haematologica",
issn = "0390-6078",
publisher = "Ferrata Storti Foundation",
number = "9",

}

RIS

TY - JOUR

T1 - A polymorphism in NFKB1 is associated with improved effect of interferon-alpha maintenance treatment of patients with multiple myeloma after high-dose treatment with stem cell support

AU - Vangsted, Annette J

AU - Klausen, Tobias W

AU - Gimsing, Peter

AU - Andersen, Niels F

AU - Abildgaard, Niels

AU - Gregersen, Henrik

AU - Vogel, Ulla Birgitte

N1 - polymorphism, multiple myeloma, interferon, NF-B, treatment outcome

PY - 2009

Y1 - 2009

N2 - Background: Maintenance therapy with interferon- after high-dose treatment with stem cell support in multiple myeloma has been intensively debated. In this study, we evaluated the response to treatment with interferon- in relation to genetic variation in genes related to inflammation. Design and Methods: In a retrospective study of 296 patients with multiple myelom undergoing high-dose therapy between 1994 and 2004, 146 patients were treated with interferon- as maintenance therapy. We tested the polymorphisms IL1B T-31C, IL6 G-174C, NFKB1-94ins/delATTG, CD3EAP G-21A and PPP1R13L IVS1 A4364G for associations with time to treatment failure and overall survival with and without interferon- treatment. Results: The wild type ins-allele of polymorphism NFKB1-94 ins/delATTG was, by multivariate Cox analysis, associated with longer time to treatment failure (p=0.01) and overall survival (p=0.0084) when tested between treatment arms and in the subgroup of patients treated with interferon- the wild type ins-allele was associated with longer overall survival (p=0.002). In the absence of interferon- treatment, there was no association between the polymorphisms and treatment outcome, except for patients homozygous for the wild type G allele of IL6 G-174C who survived longer (p= 0.0074) than variant allele carriers. There was no association between the polymorphisms IL1B T-31C, CD3EAP G-21A and PPP1R13L IVS1 A4364G and treatment outcome for interferon-. Conclusions: Patients who are homozygous carriers of the wild type ins-allele of the NFKB1 -94ins/delATTG polymorphism may benefit from treatment with interferon-, in contrast to patients carrying the variant allele. This result may indicate that the effect of interferon- treatment is dependent on the availability of nuclear factor-B and the polymorphism in NFKB1 may, therefore, be a good prognostic marker for multiple myeloma patients on maintenance treatment with interferon- after high-dose therapy. A prospective study of interferon- treatment in relation to NFKB1 -94ins/delATTG is highly warranted.

AB - Background: Maintenance therapy with interferon- after high-dose treatment with stem cell support in multiple myeloma has been intensively debated. In this study, we evaluated the response to treatment with interferon- in relation to genetic variation in genes related to inflammation. Design and Methods: In a retrospective study of 296 patients with multiple myelom undergoing high-dose therapy between 1994 and 2004, 146 patients were treated with interferon- as maintenance therapy. We tested the polymorphisms IL1B T-31C, IL6 G-174C, NFKB1-94ins/delATTG, CD3EAP G-21A and PPP1R13L IVS1 A4364G for associations with time to treatment failure and overall survival with and without interferon- treatment. Results: The wild type ins-allele of polymorphism NFKB1-94 ins/delATTG was, by multivariate Cox analysis, associated with longer time to treatment failure (p=0.01) and overall survival (p=0.0084) when tested between treatment arms and in the subgroup of patients treated with interferon- the wild type ins-allele was associated with longer overall survival (p=0.002). In the absence of interferon- treatment, there was no association between the polymorphisms and treatment outcome, except for patients homozygous for the wild type G allele of IL6 G-174C who survived longer (p= 0.0074) than variant allele carriers. There was no association between the polymorphisms IL1B T-31C, CD3EAP G-21A and PPP1R13L IVS1 A4364G and treatment outcome for interferon-. Conclusions: Patients who are homozygous carriers of the wild type ins-allele of the NFKB1 -94ins/delATTG polymorphism may benefit from treatment with interferon-, in contrast to patients carrying the variant allele. This result may indicate that the effect of interferon- treatment is dependent on the availability of nuclear factor-B and the polymorphism in NFKB1 may, therefore, be a good prognostic marker for multiple myeloma patients on maintenance treatment with interferon- after high-dose therapy. A prospective study of interferon- treatment in relation to NFKB1 -94ins/delATTG is highly warranted.

U2 - 10.3324/haematol.2008.004572

DO - 10.3324/haematol.2008.004572

M3 - Journal article

VL - 94

SP - 1274

EP - 1281

JO - Haematologica

JF - Haematologica

SN - 0390-6078

IS - 9

ER -