Molecular Research of Chronic Lymphocytic Leukemia (CLL)

Dear Colleagues,

Chronic lymphocytic leukemia is unique among non-Hodgkin lymphomas with respect to the ability of its malignant cells to be present in large numbers in both blood and tissues. Current thinking supports a paradigm whereby CLL cells cyclically traffic from secondary lymphoid and bone marrow environments to the blood and back again. Importantly, CLL cells in tissues receive signals for survival and proliferation. However, when they are in the blood, they are destined for death unless they can re-enter tissues in a timely way. Moreover, the longer CLL cells remain in tissues, the more likely it is that disease will be progressive and resistant to therapy. We know that a principal regulator of CLL cell tissue residency is the expression of the integrin α4β1. We also know that a driver of CLL pathogenesis, engagement of the B cell receptor (BCR), is important for activating α4β1-mediated adhesion to its ligands VCAM and fibronectin. This has therapeutic implications because inhibitors of BCR signaling, such as idelalisib (targeting phosphatidylinositol 3 kinase δ) and ibrutinib (targeting Bruton’s tyrosine kinase), induce the release of CLL cells from tissues into the blood. What is unclear is how CLL cells make decisions to remain, leave, or even re-enter tissues, and whether pathogenetic features such as constitutive signals, chromosomal deletions, and/or the mutation of key genes contribute to this decision making. This Special Issue invites research articles and reviews to advance our knowledge of CLL cell biology and broaden our understanding of progressive disease.

Prof. Dr. Joseph Slupsky
Guest Editor

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• chronic lymphocytic leukemia
• B cell receptor (BCR) signaling
• chromosomal abnormality (del13q14, Trisomy 12, del11q23, del17p13)
• integrins [α4β1 (CD49d/CD29), CD11c/CD18, CD11a/CD18]
• cell adhesion
• cell migration
• cell trafficking
• signal transduction
• epithelial mesenchymal transition
• cell transformation