SERUM RESISTIN IN RELATION TO B-CELL CHRONIC LYMPHOCYTIC LEUKEMIA RISK AND ITS CORRELATIONS WITH PROGNOSTIC BIOMARKERS
(Abstract release date: 05/19/16)
EHA Library. Lekka A. 06/09/16; 134695; PB1795
Prof. Dr. Antigoni Lekka
Contributions
Contributions
Abstract
Abstract: PB1795
Type: Publication Only
Background
Excess weight and insulin resistance are now considered risk factors for many types of malignancies, including leukemia and lymphoma. Potential mechanisms that may link obesity and insulin resistance to B-cell chronic lymphocytic leukemia (B-CLL) include also the abnormal secretion of adipocytokines. Resistin, an adipocytokine belonging to the family of resistin-like molecules, was originally discovered as a molecule enhancing insulin resistance or impaired hepatic sensitivity to insulin and provoking hyperglycemia without affecting peripheral insulin sensitivity. However, data in humans are controversial.
Aims
In this cross-sectional study, we attempted to investigate the contribution of resistinemia to B-CLL risk taking into account potential important confounders including the family history of lymphohematopoietic cancer (LHC), body mass index (BMI), serum insulin and other adipocytokines. We also attempted to ascertain whether a relationship between serum resistin and prognostic markers exists amongst patients with B-CLL diagnosis.
Methods
Blood samples were collected from 95 cases with incident B-CLL and 95 hospital controls, admitted for non-neoplastic and non-infectious conditions, matched on gender, age and year/month of diagnosis (±1 month) between 2001 and 2007. Informed consent was obtained from all study participants. Serum resistin was determined using a commercially available ELISA assay (Phoenix, CA, USA). Furthermore, serum lactate dehydrogenase (LDH), β2-microglobulin (BMG), lymphocyte morphology and the surface expression of CD38 in >30% of B-CLL lymphocytes were assessed. The statistical analysis of the data was performed using IBM-SPSS® version 23 for Windows.
Results
Patients with B-CLL had on average a higher BMI as compared to control participants (27.8 vs. 26.7 kg/m2; p<0.01). Significantly, more patients than controls presented a positive family history of LHC (13 vs. 3 controls; p<0.01). In univariate analysis, circulating levels of resistin were statistically significantly elevated in cases as compared with controls (10.43 ± 5.42 versus 8.12 ± 4.88 ng/mL respectively, p=0.002). However, although serum higher resistin was associated with B-CLL risk in unadjusted analyses, in multivariable analyses controlling for age, gender, date of diagnosis, family history of LHC, BMI, serum insulin, leptin and adiponectin levels, serum resistin presented a borderline statistical significance with B-CLL occurrence (OR: 1.08, 95% CI: 0.99-1.16, p=0.06). Amid patients, serum resistin was not associated with Binet stage (p=0.85) and absolute lymphocyte count (p=0.55). Nevertheless, circulating resistin presented a borderline negative correlation with BMG (p=0.07) and CD38 (p=0.07).
Conclusion
Circulating resistin was found to be elevated among cases as compared to controls in univariate analysis. It has been recently shown that hyperesistinemia is linked to the risk for many malignancies. These results need to be confirmed in larger study populations using a prospective study design; but if reproduced in adjusted analyses they may suggest that resistin may be upregulated and/or upregulate the synthesis of other inflammatory factors etiologically linked to B-CLL etiopathogenetic process.
Session topic: E-poster
Keyword(s): B cell chronic lymphocytic leukemia, Cytokine, Obesity, Prognostic factor
Type: Publication Only
Background
Excess weight and insulin resistance are now considered risk factors for many types of malignancies, including leukemia and lymphoma. Potential mechanisms that may link obesity and insulin resistance to B-cell chronic lymphocytic leukemia (B-CLL) include also the abnormal secretion of adipocytokines. Resistin, an adipocytokine belonging to the family of resistin-like molecules, was originally discovered as a molecule enhancing insulin resistance or impaired hepatic sensitivity to insulin and provoking hyperglycemia without affecting peripheral insulin sensitivity. However, data in humans are controversial.
Aims
In this cross-sectional study, we attempted to investigate the contribution of resistinemia to B-CLL risk taking into account potential important confounders including the family history of lymphohematopoietic cancer (LHC), body mass index (BMI), serum insulin and other adipocytokines. We also attempted to ascertain whether a relationship between serum resistin and prognostic markers exists amongst patients with B-CLL diagnosis.
Methods
Blood samples were collected from 95 cases with incident B-CLL and 95 hospital controls, admitted for non-neoplastic and non-infectious conditions, matched on gender, age and year/month of diagnosis (±1 month) between 2001 and 2007. Informed consent was obtained from all study participants. Serum resistin was determined using a commercially available ELISA assay (Phoenix, CA, USA). Furthermore, serum lactate dehydrogenase (LDH), β2-microglobulin (BMG), lymphocyte morphology and the surface expression of CD38 in >30% of B-CLL lymphocytes were assessed. The statistical analysis of the data was performed using IBM-SPSS® version 23 for Windows.
Results
Patients with B-CLL had on average a higher BMI as compared to control participants (27.8 vs. 26.7 kg/m2; p<0.01). Significantly, more patients than controls presented a positive family history of LHC (13 vs. 3 controls; p<0.01). In univariate analysis, circulating levels of resistin were statistically significantly elevated in cases as compared with controls (10.43 ± 5.42 versus 8.12 ± 4.88 ng/mL respectively, p=0.002). However, although serum higher resistin was associated with B-CLL risk in unadjusted analyses, in multivariable analyses controlling for age, gender, date of diagnosis, family history of LHC, BMI, serum insulin, leptin and adiponectin levels, serum resistin presented a borderline statistical significance with B-CLL occurrence (OR: 1.08, 95% CI: 0.99-1.16, p=0.06). Amid patients, serum resistin was not associated with Binet stage (p=0.85) and absolute lymphocyte count (p=0.55). Nevertheless, circulating resistin presented a borderline negative correlation with BMG (p=0.07) and CD38 (p=0.07).
Conclusion
Circulating resistin was found to be elevated among cases as compared to controls in univariate analysis. It has been recently shown that hyperesistinemia is linked to the risk for many malignancies. These results need to be confirmed in larger study populations using a prospective study design; but if reproduced in adjusted analyses they may suggest that resistin may be upregulated and/or upregulate the synthesis of other inflammatory factors etiologically linked to B-CLL etiopathogenetic process.
Session topic: E-poster
Keyword(s): B cell chronic lymphocytic leukemia, Cytokine, Obesity, Prognostic factor
Abstract: PB1795
Type: Publication Only
Background
Excess weight and insulin resistance are now considered risk factors for many types of malignancies, including leukemia and lymphoma. Potential mechanisms that may link obesity and insulin resistance to B-cell chronic lymphocytic leukemia (B-CLL) include also the abnormal secretion of adipocytokines. Resistin, an adipocytokine belonging to the family of resistin-like molecules, was originally discovered as a molecule enhancing insulin resistance or impaired hepatic sensitivity to insulin and provoking hyperglycemia without affecting peripheral insulin sensitivity. However, data in humans are controversial.
Aims
In this cross-sectional study, we attempted to investigate the contribution of resistinemia to B-CLL risk taking into account potential important confounders including the family history of lymphohematopoietic cancer (LHC), body mass index (BMI), serum insulin and other adipocytokines. We also attempted to ascertain whether a relationship between serum resistin and prognostic markers exists amongst patients with B-CLL diagnosis.
Methods
Blood samples were collected from 95 cases with incident B-CLL and 95 hospital controls, admitted for non-neoplastic and non-infectious conditions, matched on gender, age and year/month of diagnosis (±1 month) between 2001 and 2007. Informed consent was obtained from all study participants. Serum resistin was determined using a commercially available ELISA assay (Phoenix, CA, USA). Furthermore, serum lactate dehydrogenase (LDH), β2-microglobulin (BMG), lymphocyte morphology and the surface expression of CD38 in >30% of B-CLL lymphocytes were assessed. The statistical analysis of the data was performed using IBM-SPSS® version 23 for Windows.
Results
Patients with B-CLL had on average a higher BMI as compared to control participants (27.8 vs. 26.7 kg/m2; p<0.01). Significantly, more patients than controls presented a positive family history of LHC (13 vs. 3 controls; p<0.01). In univariate analysis, circulating levels of resistin were statistically significantly elevated in cases as compared with controls (10.43 ± 5.42 versus 8.12 ± 4.88 ng/mL respectively, p=0.002). However, although serum higher resistin was associated with B-CLL risk in unadjusted analyses, in multivariable analyses controlling for age, gender, date of diagnosis, family history of LHC, BMI, serum insulin, leptin and adiponectin levels, serum resistin presented a borderline statistical significance with B-CLL occurrence (OR: 1.08, 95% CI: 0.99-1.16, p=0.06). Amid patients, serum resistin was not associated with Binet stage (p=0.85) and absolute lymphocyte count (p=0.55). Nevertheless, circulating resistin presented a borderline negative correlation with BMG (p=0.07) and CD38 (p=0.07).
Conclusion
Circulating resistin was found to be elevated among cases as compared to controls in univariate analysis. It has been recently shown that hyperesistinemia is linked to the risk for many malignancies. These results need to be confirmed in larger study populations using a prospective study design; but if reproduced in adjusted analyses they may suggest that resistin may be upregulated and/or upregulate the synthesis of other inflammatory factors etiologically linked to B-CLL etiopathogenetic process.
Session topic: E-poster
Keyword(s): B cell chronic lymphocytic leukemia, Cytokine, Obesity, Prognostic factor
Type: Publication Only
Background
Excess weight and insulin resistance are now considered risk factors for many types of malignancies, including leukemia and lymphoma. Potential mechanisms that may link obesity and insulin resistance to B-cell chronic lymphocytic leukemia (B-CLL) include also the abnormal secretion of adipocytokines. Resistin, an adipocytokine belonging to the family of resistin-like molecules, was originally discovered as a molecule enhancing insulin resistance or impaired hepatic sensitivity to insulin and provoking hyperglycemia without affecting peripheral insulin sensitivity. However, data in humans are controversial.
Aims
In this cross-sectional study, we attempted to investigate the contribution of resistinemia to B-CLL risk taking into account potential important confounders including the family history of lymphohematopoietic cancer (LHC), body mass index (BMI), serum insulin and other adipocytokines. We also attempted to ascertain whether a relationship between serum resistin and prognostic markers exists amongst patients with B-CLL diagnosis.
Methods
Blood samples were collected from 95 cases with incident B-CLL and 95 hospital controls, admitted for non-neoplastic and non-infectious conditions, matched on gender, age and year/month of diagnosis (±1 month) between 2001 and 2007. Informed consent was obtained from all study participants. Serum resistin was determined using a commercially available ELISA assay (Phoenix, CA, USA). Furthermore, serum lactate dehydrogenase (LDH), β2-microglobulin (BMG), lymphocyte morphology and the surface expression of CD38 in >30% of B-CLL lymphocytes were assessed. The statistical analysis of the data was performed using IBM-SPSS® version 23 for Windows.
Results
Patients with B-CLL had on average a higher BMI as compared to control participants (27.8 vs. 26.7 kg/m2; p<0.01). Significantly, more patients than controls presented a positive family history of LHC (13 vs. 3 controls; p<0.01). In univariate analysis, circulating levels of resistin were statistically significantly elevated in cases as compared with controls (10.43 ± 5.42 versus 8.12 ± 4.88 ng/mL respectively, p=0.002). However, although serum higher resistin was associated with B-CLL risk in unadjusted analyses, in multivariable analyses controlling for age, gender, date of diagnosis, family history of LHC, BMI, serum insulin, leptin and adiponectin levels, serum resistin presented a borderline statistical significance with B-CLL occurrence (OR: 1.08, 95% CI: 0.99-1.16, p=0.06). Amid patients, serum resistin was not associated with Binet stage (p=0.85) and absolute lymphocyte count (p=0.55). Nevertheless, circulating resistin presented a borderline negative correlation with BMG (p=0.07) and CD38 (p=0.07).
Conclusion
Circulating resistin was found to be elevated among cases as compared to controls in univariate analysis. It has been recently shown that hyperesistinemia is linked to the risk for many malignancies. These results need to be confirmed in larger study populations using a prospective study design; but if reproduced in adjusted analyses they may suggest that resistin may be upregulated and/or upregulate the synthesis of other inflammatory factors etiologically linked to B-CLL etiopathogenetic process.
Session topic: E-poster
Keyword(s): B cell chronic lymphocytic leukemia, Cytokine, Obesity, Prognostic factor
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