MLLr activates BCL-2 through H3K79 methylation rendering MLLr-ALL sensitive to selective BCL-2 inhibitor (venetoclax). In other subtypes of ALL, concurrent inhibition of both BCL-2 and BCL-XL is required for maximal antileukemia efficacy. Use of concurrent ALL chemotherapy that reduces MCL-1 and BCL-XL levels in combination with venetoclax may obviate the need for adding selective BCL-XL or dual BCL-2/BCL-XL inhibitors.

MLLr activates BCL-2 through H3K79 methylation rendering MLLr-ALL sensitive to selective BCL-2 inhibitor (venetoclax). In other subtypes of ALL, concurrent inhibition of both BCL-2 and BCL-XL is required for maximal antileukemia efficacy. Use of concurrent ALL chemotherapy that reduces MCL-1 and BCL-XL levels in combination with venetoclax may obviate the need for adding selective BCL-XL or dual BCL-2/BCL-XL inhibitors.

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