Protein profiles distinguish stable and progressive chronic lymphocytic leukemia

Patients with a stable chronic lymphocytic leukemia (CLL) double their blood lymphocyte count in >5 years, but may develop progressive disease with lymphocytes doubling in <12 months. To identify a protein signature for progressive CLL, whole cell extracts of peripheral blood mononuclear cells...

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Published inLeukemia & lymphoma Vol. 57; no. 5; pp. 1033 - 1043
Main Authors Huang, Pauline Y., Mactier, Swetlana, Armacki, Natalie, Giles Best, O., Belov, Larissa, Kaufman, Kimberley L., Pascovici, Dana, Mulligan, Stephen P., Christopherson, Richard I.
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Published United States Taylor & Francis 03.05.2016
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Abstract Patients with a stable chronic lymphocytic leukemia (CLL) double their blood lymphocyte count in >5 years, but may develop progressive disease with lymphocytes doubling in <12 months. To identify a protein signature for progressive CLL, whole cell extracts of peripheral blood mononuclear cells from patients with CLL (n = 27) were screened using iTRAQ (isobaric tags for relative and absolute quantification) analysis. A total of 84 differentially abundant proteins were identified from patients with stable and progressive CLL. Subsequently, 32 of these proteins were quantified by SRM (selected reaction monitoring) using extracts of purified CD19 + CLL cells from patients (n = 50). Hierarchical clustering of these protein profiles showed two clusters of patients that correlated with progressive and stable CLL, providing signatures that should be useful for triaging patients. Some of the proteins in the progressive cluster have not been linked with CLL, for example, glutamate dehydrogenase 1 and transcription intermediary factor 1-beta.
AbstractList Patients with a stable chronic lymphocytic leukemia (CLL) double their blood lymphocyte count in >5 years, but may develop progressive disease with lymphocytes doubling in <12 months. To identify a protein signature for progressive CLL, whole cell extracts of peripheral blood mononuclear cells from patients with CLL (n = 27) were screened using iTRAQ (isobaric tags for relative and absolute quantification) analysis. A total of 84 differentially abundant proteins were identified from patients with stable and progressive CLL. Subsequently, 32 of these proteins were quantified by SRM (selected reaction monitoring) using extracts of purified CD19 + CLL cells from patients (n = 50). Hierarchical clustering of these protein profiles showed two clusters of patients that correlated with progressive and stable CLL, providing signatures that should be useful for triaging patients. Some of the proteins in the progressive cluster have not been linked with CLL, for example, glutamate dehydrogenase 1 and transcription intermediary factor 1-beta.
Patients with a stable chronic lymphocytic leukemia (CLL) double their blood lymphocyte count in >5 years, but may develop progressive disease with lymphocytes doubling in <12 months. To identify a protein signature for progressive CLL, whole cell extracts of peripheral blood mononuclear cells from patients with CLL (n=27) were screened using iTRAQ (isobaric tags for relative and absolute quantification) analysis. A total of 84 differentially abundant proteins were identified from patients with stable and progressive CLL. Subsequently, 32 of these proteins were quantified by SRM (selected reaction monitoring) using extracts of purified CD19+ CLL cells from patients (n=50). Hierarchical clustering of these protein profiles showed two clusters of patients that correlated with progressive and stable CLL, providing signatures that should be useful for triaging patients. Some of the proteins in the progressive cluster have not been linked with CLL, for example, glutamate dehydrogenase 1 and transcription intermediary factor 1-beta.
Patients with a stable chronic lymphocytic leukemia (CLL) double their blood lymphocyte count in &gt;5 years, but may develop progressive disease with lymphocytes doubling in &lt;12 months. To identify a protein signature for progressive CLL, whole cell extracts of peripheral blood mononuclear cells from patients with CLL (n=27) were screened using iTRAQ (isobaric tags for relative and absolute quantification) analysis. A total of 84 differentially abundant proteins were identified from patients with stable and progressive CLL. Subsequently, 32 of these proteins were quantified by SRM (selected reaction monitoring) using extracts of purified CD19+ CLL cells from patients (n=50). Hierarchical clustering of these protein profiles showed two clusters of patients that correlated with progressive and stable CLL, providing signatures that should be useful for triaging patients. Some of the proteins in the progressive cluster have not been linked with CLL, for example, glutamate dehydrogenase 1 and transcription intermediary factor 1-beta.
Author Giles Best, O.
Huang, Pauline Y.
Pascovici, Dana
Mactier, Swetlana
Belov, Larissa
Armacki, Natalie
Kaufman, Kimberley L.
Christopherson, Richard I.
Mulligan, Stephen P.
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mass spectrometry
Chronic lymphocytic leukemia
prognostic markers
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selected reaction monitoring
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Snippet Patients with a stable chronic lymphocytic leukemia (CLL) double their blood lymphocyte count in >5 years, but may develop progressive disease with lymphocytes...
Patients with a stable chronic lymphocytic leukemia (CLL) double their blood lymphocyte count in &gt;5 years, but may develop progressive disease with...
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SubjectTerms Biomarkers, Tumor
Chromatography, Liquid
Chronic lymphocytic leukemia
Cluster Analysis
Disease Progression
Humans
Immunophenotyping
iTRAQ
Leukemia, Lymphocytic, Chronic, B-Cell - diagnosis
Leukemia, Lymphocytic, Chronic, B-Cell - metabolism
Leukemia, Lymphocytic, Chronic, B-Cell - pathology
mass spectrometry
Neoplasm Staging
Phenotype
Prognosis
prognostic markers
Proteome
proteomics
Proteomics - methods
selected reaction monitoring
Tandem Mass Spectrometry
Title Protein profiles distinguish stable and progressive chronic lymphocytic leukemia
URI https://www.tandfonline.com/doi/abs/10.3109/10428194.2015.1094692
https://www.ncbi.nlm.nih.gov/pubmed/26422656
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Volume 57
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