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Deutsch, A. J.

Publications and source records attributed to Deutsch, A. J..

3 recordsLinked to original sources

Exploring the Anti-Tumor Effects of Brusatol in Aggressive B-Cell Lymphomas

Aggressive B-cell lymphomas are the most common lymphoid malignancies in adults, with an increasing incidence. Diffuse large B-cell lymphoma (DLBCL) is the most prevalent and highly heterogeneous type, often exhibiting poor responses to standard immuno-chemotherapy. One third of patients experience primary refractory disease or relapse, particularly those with high c-MYC and BCL-2 expression levels, which drive aggressiveness and resistance to treatment. Therefore, the development of new therapies is urgently needed. This study explores the anti-tumor properties of brusatol, both as single agent and in combination with the BCL-2 inhibitor, venetoclax, for the treatment of aggressive lymphoma cells. Brusatol inhibited lymphoma cell growth in a concentration-dependent manner in various cell lines. Further analysis revealed that brusatol is able to efficiently induce cell death in the lymphoma cells in vitro, as well as in patient-derived samples. Importantly, the effect of brusatol was strongly reduced in non-malignant lymphoid cells compared to lymphoma cells. We discovered that lymphoma cell lines highly sensitive to brusatol have elevated c-MYC expression. Brusatol treatment rapidly reduced protein expression of c-MYC and MCL-1. Protein biosynthesis analysis confirmed that brusatol induced translational inhibition in aggressive lymphoma cells. Furthermore, the combination of brusatol and venetoclax synergistically enhanced lymphoma cell death, particularly in samples with low c-MYC protein levels. Our findings suggest that brusatol has significant potential for the development of novel therapeutic strategies for aggressive lymphomas, especially for cases with high c-MYC content. Additionally, its combination with venetoclax represents a promising approach to improve treatment outcomes.

cancer biology↗

A statistical genetics guide to identifying HLA alleles driving complex disease

The human leukocyte antigen (HLA) locus is associated with more human complex diseases than any other locus. In many diseases it explains more heritability than all other known loci combined. Investigators have now demonstrated the accuracy of in silico HLA imputation methods. These approaches enable rapid and accurate estimation of HLA alleles in the millions of individuals that are already genotyped on microarrays. HLA imputation has been used to define causal variation in autoimmune diseases, such as type I diabetes, and infectious diseases, such as HIV infection control. However, there are few guidelines on performing HLA imputation, association testing, and fine-mapping. Here, we present comprehensive statistical genetics guide to impute HLA alleles from genotype data. We provide detailed protocols, including standard quality control measures for input genotyping data and describe options to impute HLA alleles and amino acids including a web-based Michigan Imputation Server. We updated the HLA imputation reference panel representing global populations (African, East Asian, European and Latino) available at the Michigan Imputation Server (n = 20,349) and achived high imputation accuracy (mean dosage correlation r = 0.981). We finally offer best practice recommendations to conduct association tests in order to define the alleles, amino acids, and haplotypes affecting human traits. This protocol will be broadly applicable to the large-scale genotyping data and contribute to defining the role of HLA in human diseases across global populations.

genetics↗

Fasting reverses drug-resistance in hepatocellular carcinoma through p53-dependent metabolic synergism

Cancer cells voraciously consume nutrients to support their growth, exposing a metabolic vulnerability that can be therapeutically exploited. Here we show in hepatocellular carcinoma (HCC) cells, xenografts, and in patient-derived HCC organoids that fasting can synergistically sensitize resistant HCC to sorafenib. Mechanistically, sorafenib acts non-canonically as an inhibitor of mitochondrial respiration, causing resistant cells to depend on glycolysis for survival. Fasting, through reduction in glucose and impeded AKT/mTOR-signaling, prevents this Warburg shift. Regulating glucose transporter and pro-apoptotic protein expression, p53 is necessary and sufficient for the sorafenib-sensitizing effect of fasting. p53 is also crucial for fasting-mediated improvement of sorafenib efficacy in an orthotopic HCC mouse model. Together, our data suggest intermittent fasting and sorafenib as rational combination therapy for HCC with intact p53 signaling. As HCC therapy is currently severely limited by resistance, these results should instigate clinical studies aimed at improving therapy response in advanced-stage, and possibly even early-stage, HCC. HIGHLIGHTSO_LIFasting sensitizes resistant HCC xenografts and patient-derived organoids to sorafenib C_LIO_LISorafenib-mediated Warburg shift is prevented by glucose limitation upon fasting C_LIO_LIFasting synergistically improves sorafenib efficacy in non-resistant models C_LIO_LIp53 is required for synergism by regulating glucose uptake and apoptosis C_LI GRAPHICAL ABSTRACT O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=167 SRC="FIGDIR/small/430545v2_ufig1.gif" ALT="Figure 1"> View larger version (40K): org.highwire.dtl.DTLVardef@1c0bf9org.highwire.dtl.DTLVardef@15638b4org.highwire.dtl.DTLVardef@1a4b322org.highwire.dtl.DTLVardef@1ec863a_HPS_FORMAT_FIGEXP M_FIG C_FIG

cancer biology↗