Publications by authors named "Brian M Ho"
Article Synopsis
- Interferon gamma (IFNγ) is a proinflammatory cytokine that can cause bone marrow failure by activating and exhausting hematopoietic stem cells (HSCs), with bone marrow stromal antigen 2 (BST2) playing a crucial role in this activation process.
- Research using a murine model shows that knocking out BST2 doesn't impact immune responses or HSC localization in the bone marrow, but it does affect lipid raft polarity in response to IFNγ.
- The study concludes that BST2 is essential for HSC division by promoting cell polarization and essential ERK1/2 activation, which could be significant for future cancer and bone marrow failure treatment strategies.
Article Synopsis
- MYC is a critical driver of cancer that enhances gene expression and increases RNA production, contributing to tumor growth and survival.
- The study reveals that MYC triggers RNA degradation, leading to toxic byproducts that cause cancer cell death, indicating a new mechanism for targeting MYC-driven cancers.
- Therapeutic strategies that intensify the breakdown of RNA could serve as effective treatments for aggressive cancers like triple-negative breast cancer (TNBC) that rely on MYC.
Bacteriophage (phage) therapy is being explored as a possible response to the antimicrobial resistance public health emergency. Administering a mixture of different phage types as a cocktail is one proposed strategy for therapeutic applications, but the optimal method for formulating phage cocktails remains a major challenge. Each phage strain has complex pharmacokinetic/pharmacodynamic (PK/PD) properties which depend on the nano-scale size, target-mediated, self-dosing nature of each phage strain, and rapid selection of resistant subpopulations.
View Article and Find Full Text PDFBackground: Genome wide-association studies have successfully identified several hundred independent loci harboring common cancer susceptibility alleles that are distinct from the more than 110 cancer predisposition genes. The latter are generally characterized by disruptive mutations in coding genes that have been established as 'drivers' of cancer in large somatic sequencing studies. We set out to determine whether, similarly, common cancer susceptibility loci map to genes that have altered frequencies of mutation.
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