Impact of BTK Inhibition on Monocytic Myeloid-Derived Suppressor Cells in CLL

Arantxa Romero-Toledo, PhD
Published: Monday, Oct 07, 2019



Arantxa Romero-Toledo, PhD student, at the Centre for Haemato-Oncology, Barts Cancer Institute, discusses the impact of BTK inhibition on monocytic myeloid-derived suppressor cells (MDSCs) in chronic lymphocytic leukemia (CLL).

In a study led by Romero-Toledo, investigators sought to evaluate MDSCs in CLL using a mouse model. First, investigators assessed granulocytic and monocytic MDSC populations upon progression. However, unlike in humans, the MDSC populations were lost upon disease progression, says Romero-Toledo; this was surprising as these populations were expected to accumulate. Investigators attributed this to the granulocytic population in peripheral blood.

After treatment with acalabrutinib (Calquence) and ibrutinib (Imbruvica), investigators reported that the monocytic population regrew in the spleen. As such, investigators believe there is a role for ITK inhibition in this population. However, ITK inhibition has only been reported with ibrutinib, not acalabrutinib. However, in terms of macrophages, acalabrutinib restored the population of macrophages in spleens, contrary to prior findings.
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Arantxa Romero-Toledo, PhD student, at the Centre for Haemato-Oncology, Barts Cancer Institute, discusses the impact of BTK inhibition on monocytic myeloid-derived suppressor cells (MDSCs) in chronic lymphocytic leukemia (CLL).

In a study led by Romero-Toledo, investigators sought to evaluate MDSCs in CLL using a mouse model. First, investigators assessed granulocytic and monocytic MDSC populations upon progression. However, unlike in humans, the MDSC populations were lost upon disease progression, says Romero-Toledo; this was surprising as these populations were expected to accumulate. Investigators attributed this to the granulocytic population in peripheral blood.

After treatment with acalabrutinib (Calquence) and ibrutinib (Imbruvica), investigators reported that the monocytic population regrew in the spleen. As such, investigators believe there is a role for ITK inhibition in this population. However, ITK inhibition has only been reported with ibrutinib, not acalabrutinib. However, in terms of macrophages, acalabrutinib restored the population of macrophages in spleens, contrary to prior findings.

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