Blood: BCL6 maintains the survival and self-renewal of AML's original cells, or may be a new therapeutic target.

BCL6 is a transcription inhibitor and primary cancer gene that play a vital role in congenital immune system, accessory immune system and lymphatic system tumors.
, its role in myelin malignancies remains unclear.
study, researchers explored the role of BCL6 in acute myeloid leukemia (AML).
the expression level of BCL6 in AML cells/samples is variable and usually high in AML cell line and primary AML samples.
addition to single-nucleocyte differentiated AML, AML with a high level of BCL6 expression is usually sensitive to the treatment of BCL6 inhibitors.
gene expression spectrum of AML cells treated with BCL6 inhibitors showed that the target gene suppressed by BCL6 and the transcription procedure associated with the DNA damage checkpoint were induced to activate, while the stem cell gene was reduced.
in-body, the treatment of primary AML cells with BCL6 inhibitors can induce apoptosis and reduce the ability of cluster formation, these effects are related to the expression level of BCL6.
important, inhibiting or knocking out BCL6 in primary AML cells significantly reduced leukemia start-up capacity in mice, indicating that the function of leukemia refilling cells was ablation.
, knocking out or suppressing the BCL6 gene does not inhibit the function of normal hematopoietic stem cells.
the proportion of human AML cells in mice treated with
BCL inhibitors and ARAC was significantly reduced and the expression of BCL6 was further induced with AraC therapy, and the degree of induction of BCL6 was related to the resistance of tumor cells to ARAC.
a heterogeneic transplantation (PDX) model of the source of AML patients treated with BCL6 inhibitors in a joint ARA-C, this joint application enhanced antileukemia activity.
, inhibiting BCL6 may provide a new treatment strategy for ablation of leukemia regenerative cells and improved response to chemotherapy.
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