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The Cope rearrangement is classified as a [3,3] sigmatropic shift in 1,5-dienes, leading to a more stable, isomeric 1,5-diene. The reaction involves a concerted movement of six electrons, four from two π bonds and two from a σ bond, via an energetically favorable chair-like transition state.
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The Claisen rearrangement is a [3,3] sigmatropic rearrangement of allyl vinyl ethers to unsaturated carbonyl compounds. The rearrangement is a concerted pericyclic reaction proceeding via a chair-like transition state.
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Compounds bearing two hydroxyl groups are known as diols. When the hydroxyl groups are located on adjacent carbon atoms, the diols are called vicinal diols or glycols. Under acidic conditions, vicinal diols undergo a specific reaction called pinacol rearrangement.
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In the presence of an aqueous base and a halogen, primary amides can lose the carbonyl (as carbon dioxide) and undergo rearrangement to form primary amines. This reaction, called the Hofmann rearrangement, can produce primary amines (aryl and alkyl) in high yields without contamination by secondary and tertiary amines.
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Rationale for targeting BCL6 in MLL-rearranged acute lymphoblastic leukemia.

Christian Hurtz1,2, Lai N Chan1,2, Huimin Geng1,2

  • 1Department of Systems Biology, City of Hope Comprehensive Cancer Center, Monrovia, California 91016, USA.

Genes & Development
|August 10, 2019
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Summary

Mixed lineage leukemia (MLL) gene rearrangements in B-cell acute lymphoblastic leukemia (B-ALL) drive aberrant BCL6 expression, promoting cancer. Inhibiting BCL6 shows therapeutic potential against MLL-rearranged B-ALL.

Keywords:
B cellsBCL6BIMMLL

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Area of Science:

  • Molecular Biology
  • Oncology
  • Genetics

Background:

  • Chromosomal rearrangements of the mixed lineage leukemia (MLL) gene are found in approximately 10% of B-cell acute lymphoblastic leukemia (B-ALL) cases.
  • These MLL rearrangements are associated with poor patient outcomes and aberrant expression of the BCL6 transcription factor in bone marrow biopsies.
  • BCL6 is known to promote oncogenic B-cell transformation and contribute to drug resistance in B-ALL.

Purpose of the Study:

  • To investigate the functional relationship between MLL fusions and BCL6 expression in B-ALL.
  • To explore the therapeutic potential of targeting BCL6 in MLL-rearranged B-ALL.
  • To elucidate the role of BCL6 in regulating MLL-induced gene expression, including pro-apoptotic genes.

Main Methods:

  • Genetic analyses and chromatin immunoprecipitation sequencing (ChIP-seq) to identify direct binding of MLL fusions to the BCL6 promoter.
  • Studies on the effects of MLL and BCL6 expression on each other's mRNA levels.
  • Conditional deletion and pharmacological inhibition of BCL6 in mouse models and patient-derived samples; combination therapy studies with BCL6 and BIM inhibitors.

Main Results:

  • MLL-AF4 and MLL-ENL fusions directly up-regulate BCL6 expression by binding to its promoter.
  • A positive feedback loop exists between MLL and BCL6, where BCL6 induction increases MLL mRNA levels.
  • BCL6 inhibition compromises leukemogenesis in mice and restores chemotherapy sensitivity in patient samples, while also derepressing BIM and synergizing with ABT-199.

Conclusions:

  • MLL-dependent transcriptional activation of BCL6 is a critical factor in the malignant transformation of B-ALL.
  • BCL6 is identified as a novel therapeutic target for MLL-rearranged B-ALL.
  • Targeting BCL6 offers a promising strategy to overcome drug resistance and improve treatment outcomes in this leukemia subtype.