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Ruff, S. M.

Publications and source records attributed to Ruff, S. M..

2 recordsLinked to original sources

A simple circuit to sustain intact tumor microenvironments for complex drug interrogations

Deep learning and large language models can integrate complex datasets to uncover biological insights that are often undetectable through conventional analyses. With application to translational cancer research, these computational tools have positioned 3D patient-derived tumor avatars front and center as crucial data input sources. However, a major challenge remains: the lack of standardization in media composition in 3D patient-derived tumor models unpredictably affects cell behavior and limit the utility beyond predicting treatment responses. To address this unmet need, we developed a simple, reproducible perfusion circuit system to approximate in vivo physiology using autologous patient plasma. With peritoneal metastases and core needle biopsies across multiple tumor histologies, we demonstrate preservation of the tumor microenvironment for up to 48 hours using multi-modal interrogation techniques. With proof-of-concept experiments, we display the systems ability to unveil complex drug-dependent biology within this time window. Standardizable, physiologically relevant platforms for 3D patient-derived tumor avatars will yield unprecedented insights through the integration of data from broad groups of patients and the use of an expanding armamentarium of artificial intelligence capabilities.

cancer biology↗

Upregulation of GREB1 in colorectal cancer ovarian metastases may be a potential therapeutic target

IntroductionClassification of ovarian metastases (OM) in colorectal cancer (CRC) as peritoneal metastasis (PM) remains controversial. OM demonstrate resistance to systemic therapy, suggesting distinct molecular tumorigenesis. Gene expression profiling and transcriptomic analysis were performed to distinguish OM, PM, and primary CRC (pCRC) and identify potential therapeutic targets. MethodsRNA sequencing data were obtained from the Total Cancer Care database. After filtering out low-expressed genes, raw counts of retained genes were normalized in trimmed mean of M-values and then log2-transformed. Genes with a |Log2FC|>0.58 and adjusted p-value <0.05 were considered dysregulated. In silico motif enrichment analysis of estrogen receptor 1 (ESR1) on growth regulating estrogen receptor binding 1 (GREB1) was conducted. ResultsThere were 115 patients with tissue from OM (n=6), PM (n=4), and pCRC (n=105). Among upregulated genes, LAMC3, SCUBE1, and GREB1 had the highest differential expression in OM compared to PM, and PEG3, C7, and GREB1 had the highest differential expression in OM compared to pCRC (all p<0.001). GREB1 was upregulated in OM compared to PM and pCRC. There are two estrogen response element (ERE) sites within the promoter region of GREB1. ESR1 transcription factor was shown to bind to these ERE (p<0.001). ConclusionsTranscriptomic analysis demonstrated clear molecular distinction between OM, PM and pCRC. We identified upregulation of GREB1 in OM compared to PM and pCRC. GREB1 contains both ERE and ESR1 in the upstream promoter regions implying potential upstream transcription regulation mediated by ESR1. GREB1 may represent a novel, hormonal target in treatment of OM in CRC.

cancer biology↗