CHRONIC MYELOMONOCYTIC LEUKEMIA IS CHARACTERIZED BY HYPOADIPONECTINEMIA AND HYPORESISTINEMIA INDEPENDENTLY FROM THE IGF-I SYSTEM: A CROSS-SECTIONAL STUDY
(Abstract release date: 05/21/15)
EHA Library. Lekka A. 06/12/15; 102590; PB1837
Prof. Dr. Antigoni Lekka
Contributions
Contributions
Abstract
Abstract: PB1837
Type: Publication Only
Background
Aims
In this cross-sectional study, we investigated the association of circulating adiponectin and resistin with CMML in relation to insulin-like growth factor-I (IGF-I), a hormonal system which is implicated in several human malignancies including leukemia.
Methods
Blood samples were collected from 14 cases with incident, histologically confirmed CMML and 70 healthy controls (1 patient versus 5 controls) who came for an annual check-up examination without any neoplastic and infectious conditions, matched on gender, age and year/month of diagnosis (±1 month) between 2004 and 2012. Informed consent was obtained from all participants. Serum adiponectin and resistin were determined respectively by radioimmunoassay (LINCO Research Institute, St Louis, MO). High molecular weight (HMW) adiponectin was measured using ELISA (ALPCO Diagnostics, Salem). IGF-I and IGFBP-3 concentrations were measured using an immunoradiometric assay kit (DSL, Webster, TX) The statistical analysis of the data was performed using IBM-SPSS® version 22 for Windows.
Results
CMML cases presented significantly higher height and weight than control subjects (p<0.001), while differences of body mass index (BMI) were only of borderline significance (p=0.10). Lower serum total or HMW adiponectin and/or resistin levels were independently associated with higher risk of CMML adjusting for age, gender, BMI and serum IGF-I levels (p≤0.05). In particular, CMML was characterized by hypoadiponectinemia (total adiponectin in CMML patients: 12.5 ± 8.8 μg/dL versus controls: 16.3 ± 7.9 μg/dL, p=0.05) and hyporesistinemia (resistin in CMML patients: 12.1 ± 6.2 ng/mL versus controls: 21.9 ± 32.7 ng/mL, p=0.013). Total adiponectin exhibited a positive correlation with HMW adiponectin both in CMML cases and controls (r=0.83, p<0.001; r=0.88, p<0.001, respectively). Although, total and HMW adiponectin were both significantly reduced in CMML, HMW did not offer any substantial additional predictive value over total adiponectin. Serum IGF-I was not significantly and independently associated with CMML in multivariable analysis adjusting for age, gender, date of diagnosis, BMI and history of lymphohematopoietic cancer (p=0.56).
Summary
Total and HMW adiponectin may present a protective role in CMML by suppressing proliferation of myeloid cell lineage, whereas resistin levels may be decreased via a compensatory mechanism due to an upregulation of other inflammatory factors etiologically and ontologically linked to CMML. Further studies are needed to confirm these associations and to explore the mechanisms underlying adiponectin’s role in myelopoiesis and leukemogenesis
Keyword(s): Chronic myelomonocytic leukemia, Myeloproliferative disorder, Obesity
Type: Publication Only
Background
Accumulating evidence supports a role for obesity in the etiology of hematologic malignancies. Obesity may be also linked to chronic myelomonocytic leukemia (CMML), a hematologic malignancy combining proliferative and dysplastic characteristics, through altered adipokine secretion, one of which, adiponectin, presents a protective role in several malignancies, including leukemia and lymphoma.
Aims
In this cross-sectional study, we investigated the association of circulating adiponectin and resistin with CMML in relation to insulin-like growth factor-I (IGF-I), a hormonal system which is implicated in several human malignancies including leukemia.
Methods
Blood samples were collected from 14 cases with incident, histologically confirmed CMML and 70 healthy controls (1 patient versus 5 controls) who came for an annual check-up examination without any neoplastic and infectious conditions, matched on gender, age and year/month of diagnosis (±1 month) between 2004 and 2012. Informed consent was obtained from all participants. Serum adiponectin and resistin were determined respectively by radioimmunoassay (LINCO Research Institute, St Louis, MO). High molecular weight (HMW) adiponectin was measured using ELISA (ALPCO Diagnostics, Salem). IGF-I and IGFBP-3 concentrations were measured using an immunoradiometric assay kit (DSL, Webster, TX) The statistical analysis of the data was performed using IBM-SPSS® version 22 for Windows.
Results
CMML cases presented significantly higher height and weight than control subjects (p<0.001), while differences of body mass index (BMI) were only of borderline significance (p=0.10). Lower serum total or HMW adiponectin and/or resistin levels were independently associated with higher risk of CMML adjusting for age, gender, BMI and serum IGF-I levels (p≤0.05). In particular, CMML was characterized by hypoadiponectinemia (total adiponectin in CMML patients: 12.5 ± 8.8 μg/dL versus controls: 16.3 ± 7.9 μg/dL, p=0.05) and hyporesistinemia (resistin in CMML patients: 12.1 ± 6.2 ng/mL versus controls: 21.9 ± 32.7 ng/mL, p=0.013). Total adiponectin exhibited a positive correlation with HMW adiponectin both in CMML cases and controls (r=0.83, p<0.001; r=0.88, p<0.001, respectively). Although, total and HMW adiponectin were both significantly reduced in CMML, HMW did not offer any substantial additional predictive value over total adiponectin. Serum IGF-I was not significantly and independently associated with CMML in multivariable analysis adjusting for age, gender, date of diagnosis, BMI and history of lymphohematopoietic cancer (p=0.56).
Summary
Total and HMW adiponectin may present a protective role in CMML by suppressing proliferation of myeloid cell lineage, whereas resistin levels may be decreased via a compensatory mechanism due to an upregulation of other inflammatory factors etiologically and ontologically linked to CMML. Further studies are needed to confirm these associations and to explore the mechanisms underlying adiponectin’s role in myelopoiesis and leukemogenesis
Keyword(s): Chronic myelomonocytic leukemia, Myeloproliferative disorder, Obesity
Abstract: PB1837
Type: Publication Only
Background
Aims
In this cross-sectional study, we investigated the association of circulating adiponectin and resistin with CMML in relation to insulin-like growth factor-I (IGF-I), a hormonal system which is implicated in several human malignancies including leukemia.
Methods
Blood samples were collected from 14 cases with incident, histologically confirmed CMML and 70 healthy controls (1 patient versus 5 controls) who came for an annual check-up examination without any neoplastic and infectious conditions, matched on gender, age and year/month of diagnosis (±1 month) between 2004 and 2012. Informed consent was obtained from all participants. Serum adiponectin and resistin were determined respectively by radioimmunoassay (LINCO Research Institute, St Louis, MO). High molecular weight (HMW) adiponectin was measured using ELISA (ALPCO Diagnostics, Salem). IGF-I and IGFBP-3 concentrations were measured using an immunoradiometric assay kit (DSL, Webster, TX) The statistical analysis of the data was performed using IBM-SPSS® version 22 for Windows.
Results
CMML cases presented significantly higher height and weight than control subjects (p<0.001), while differences of body mass index (BMI) were only of borderline significance (p=0.10). Lower serum total or HMW adiponectin and/or resistin levels were independently associated with higher risk of CMML adjusting for age, gender, BMI and serum IGF-I levels (p≤0.05). In particular, CMML was characterized by hypoadiponectinemia (total adiponectin in CMML patients: 12.5 ± 8.8 μg/dL versus controls: 16.3 ± 7.9 μg/dL, p=0.05) and hyporesistinemia (resistin in CMML patients: 12.1 ± 6.2 ng/mL versus controls: 21.9 ± 32.7 ng/mL, p=0.013). Total adiponectin exhibited a positive correlation with HMW adiponectin both in CMML cases and controls (r=0.83, p<0.001; r=0.88, p<0.001, respectively). Although, total and HMW adiponectin were both significantly reduced in CMML, HMW did not offer any substantial additional predictive value over total adiponectin. Serum IGF-I was not significantly and independently associated with CMML in multivariable analysis adjusting for age, gender, date of diagnosis, BMI and history of lymphohematopoietic cancer (p=0.56).
Summary
Total and HMW adiponectin may present a protective role in CMML by suppressing proliferation of myeloid cell lineage, whereas resistin levels may be decreased via a compensatory mechanism due to an upregulation of other inflammatory factors etiologically and ontologically linked to CMML. Further studies are needed to confirm these associations and to explore the mechanisms underlying adiponectin’s role in myelopoiesis and leukemogenesis
Keyword(s): Chronic myelomonocytic leukemia, Myeloproliferative disorder, Obesity
Type: Publication Only
Background
Accumulating evidence supports a role for obesity in the etiology of hematologic malignancies. Obesity may be also linked to chronic myelomonocytic leukemia (CMML), a hematologic malignancy combining proliferative and dysplastic characteristics, through altered adipokine secretion, one of which, adiponectin, presents a protective role in several malignancies, including leukemia and lymphoma.
Aims
In this cross-sectional study, we investigated the association of circulating adiponectin and resistin with CMML in relation to insulin-like growth factor-I (IGF-I), a hormonal system which is implicated in several human malignancies including leukemia.
Methods
Blood samples were collected from 14 cases with incident, histologically confirmed CMML and 70 healthy controls (1 patient versus 5 controls) who came for an annual check-up examination without any neoplastic and infectious conditions, matched on gender, age and year/month of diagnosis (±1 month) between 2004 and 2012. Informed consent was obtained from all participants. Serum adiponectin and resistin were determined respectively by radioimmunoassay (LINCO Research Institute, St Louis, MO). High molecular weight (HMW) adiponectin was measured using ELISA (ALPCO Diagnostics, Salem). IGF-I and IGFBP-3 concentrations were measured using an immunoradiometric assay kit (DSL, Webster, TX) The statistical analysis of the data was performed using IBM-SPSS® version 22 for Windows.
Results
CMML cases presented significantly higher height and weight than control subjects (p<0.001), while differences of body mass index (BMI) were only of borderline significance (p=0.10). Lower serum total or HMW adiponectin and/or resistin levels were independently associated with higher risk of CMML adjusting for age, gender, BMI and serum IGF-I levels (p≤0.05). In particular, CMML was characterized by hypoadiponectinemia (total adiponectin in CMML patients: 12.5 ± 8.8 μg/dL versus controls: 16.3 ± 7.9 μg/dL, p=0.05) and hyporesistinemia (resistin in CMML patients: 12.1 ± 6.2 ng/mL versus controls: 21.9 ± 32.7 ng/mL, p=0.013). Total adiponectin exhibited a positive correlation with HMW adiponectin both in CMML cases and controls (r=0.83, p<0.001; r=0.88, p<0.001, respectively). Although, total and HMW adiponectin were both significantly reduced in CMML, HMW did not offer any substantial additional predictive value over total adiponectin. Serum IGF-I was not significantly and independently associated with CMML in multivariable analysis adjusting for age, gender, date of diagnosis, BMI and history of lymphohematopoietic cancer (p=0.56).
Summary
Total and HMW adiponectin may present a protective role in CMML by suppressing proliferation of myeloid cell lineage, whereas resistin levels may be decreased via a compensatory mechanism due to an upregulation of other inflammatory factors etiologically and ontologically linked to CMML. Further studies are needed to confirm these associations and to explore the mechanisms underlying adiponectin’s role in myelopoiesis and leukemogenesis
Keyword(s): Chronic myelomonocytic leukemia, Myeloproliferative disorder, Obesity
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