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Differences between Peripheral Blood, Lymph Nodes and Bone Marrow in Expression of Integrins, ICAMs, CD38 and CD31 Correlate with Clinical Characteristics in B-CLL.
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Abstract
B-CLL patients have variable tumor mass distribution within major cell compartments, and as a consequence different clinical presentation. Adhesion molecules (AM) expression phenotype of integrins (CD11a, CD11b, CD11c, CD18, CD29, CD49c, CD49d and CD61), ICAMs (CD54, CD102 and CD50), CD38 and CD31 was determined in samples taken from peripheral blood (PB), bone marrow (BM) and lymph nodes (LN) by two/three color flow cytometry in 33 B-CLL patients. Differences for particular AM expression between compartments were quantified to express respective intensity and direction (gradients). We found following significant differences: stronger expression for CD11a and CD102 in PB than in BM, while CD54 was stronger in BM than in PB; CD11b and CD102 were stronger in PB than in LN, opposite to CD54 and CD38; CD102 was stronger in BM than in LN, while CD18, CD11a, CD11c and CD38 were stronger in LN then in BM. Observed gradients were compared with clinical and laboratory parameters: PB lymphocytosis, LN size, Spleen size, Total Tumor Mass score (TTM), TTM distribution (TD), BM failure (BMF), Rai and Binet stages. Peripheral blood lymphocytosis positively correlated with LN to PB gradient for CD11a, CD11b, CD18 and CD31 (p<0.05). Lymph node size negatively correlated with LN to PB gradient for CD11b and with BM to PB gradient for CD54 and CD61 (p<0.05). Spleen size negatively correlated with BM to PB gradient for CD11c and CD102 (p<0.05). TTM negatively correlated with BM to PB gradient for CD11c, CD61 and CD102 (p<0.05). TD positively correlated with LN to PB gradient for CD11b and CD102, and with BM to PB gradient for CD11c and CD102 (p<0.05). Isolated BMF irrespective of tumor load, as well as clinical stages that incorporate BMF (Rai and Binet) were associated with significant PB to BM gradient for CD18, CD11a, CD11c, CD49d, CD54 and CD102, and with PB to LN gradient for CD102 (p<0.05). Cluster analysis corroborated these findings. This study shows that expression of selected integrins, ICAMs, CD38 and CD31on B-CLL cells is significantly different among lymphoid compartments suggesting possible role in resulting clinical presentation. Taking together, this investigation disclosed yet unexplained interesting interactions and warrants further studies of AM role in B-CLL.
American Society of Hematology
Title: Differences between Peripheral Blood, Lymph Nodes and Bone Marrow in Expression of Integrins, ICAMs, CD38 and CD31 Correlate with Clinical Characteristics in B-CLL.
Description:
Abstract
B-CLL patients have variable tumor mass distribution within major cell compartments, and as a consequence different clinical presentation.
Adhesion molecules (AM) expression phenotype of integrins (CD11a, CD11b, CD11c, CD18, CD29, CD49c, CD49d and CD61), ICAMs (CD54, CD102 and CD50), CD38 and CD31 was determined in samples taken from peripheral blood (PB), bone marrow (BM) and lymph nodes (LN) by two/three color flow cytometry in 33 B-CLL patients.
Differences for particular AM expression between compartments were quantified to express respective intensity and direction (gradients).
We found following significant differences: stronger expression for CD11a and CD102 in PB than in BM, while CD54 was stronger in BM than in PB; CD11b and CD102 were stronger in PB than in LN, opposite to CD54 and CD38; CD102 was stronger in BM than in LN, while CD18, CD11a, CD11c and CD38 were stronger in LN then in BM.
Observed gradients were compared with clinical and laboratory parameters: PB lymphocytosis, LN size, Spleen size, Total Tumor Mass score (TTM), TTM distribution (TD), BM failure (BMF), Rai and Binet stages.
Peripheral blood lymphocytosis positively correlated with LN to PB gradient for CD11a, CD11b, CD18 and CD31 (p<0.
05).
Lymph node size negatively correlated with LN to PB gradient for CD11b and with BM to PB gradient for CD54 and CD61 (p<0.
05).
Spleen size negatively correlated with BM to PB gradient for CD11c and CD102 (p<0.
05).
TTM negatively correlated with BM to PB gradient for CD11c, CD61 and CD102 (p<0.
05).
TD positively correlated with LN to PB gradient for CD11b and CD102, and with BM to PB gradient for CD11c and CD102 (p<0.
05).
Isolated BMF irrespective of tumor load, as well as clinical stages that incorporate BMF (Rai and Binet) were associated with significant PB to BM gradient for CD18, CD11a, CD11c, CD49d, CD54 and CD102, and with PB to LN gradient for CD102 (p<0.
05).
Cluster analysis corroborated these findings.
This study shows that expression of selected integrins, ICAMs, CD38 and CD31on B-CLL cells is significantly different among lymphoid compartments suggesting possible role in resulting clinical presentation.
Taking together, this investigation disclosed yet unexplained interesting interactions and warrants further studies of AM role in B-CLL.
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