CD62L shedding from T cells and increased plasma levels of soluble CD62L plasma levels at the time of diagnosis may be predictive of molecular response to tyrosine kinase inhibitor (TKI) therapy among patients with early chronic myeloid leukemia in chronic phase (CML-CP), according to a study published in the Journal of Clinical Oncology.1
Immunologic surveillance of minimal residual disease in patients with CML may be useful for long-term control, though limited evidence about the immunomodulatory effects of TKIs in vivo is available. Researchers therefore attempted to identify biomarkers that may be prognostic of molecular response in patients with CML treated with TKI therapy.
The authors conducted a prospective and comprehensive flow cytometry-based immunomonitoring program simultaneous to the phase 3b ENEST1, which evaluated the efficacy and safety of nilotinib among more than 1000 patients with newly diagnosed CML. The immunomonitoring program enrolled 52 nilotinib-naive patients with CML-CP.
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At diagnosis, T cells of patients expressed low CD62L (low L-selectin) levels. A low number of CD4+ and CD8+ T cells expressing CD62L was associated with a higher Sokal score, increased spleen size, and high leukocyte and peripheral-blood blast counts.
CD62L expression levels returned to those of healthy individuals at month 6 of nilotinib therapy. CD62L shedding from T cells was increased at diagnosis and significantly decreased during treatment with nilotinib.
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High CD62L+ expression on both CD4+ and CD8+ T cells and low levels of soluble CD62L levels at diagnosis correlated with superior molecular responses in patients with CML-CP.
Larger prospective studies are ongoing to reaffirm the prognostic impact of CD26L levels in this patient population.
Reference
- Sopper S, Mustjoki S, White D, et al. Reduced CD62L expression on T cells and increased soluble CD62L levels predict molecular response to tyrosine kinase inhibitor therapy in early chronic-phase chronic myelogenous leukemia. J Clin Oncol. 2016 Nov 7. doi: 10.1200/JCO.2016.67.0893 [Epub ahead of print]
