Publications by authors named "Ji Yanrong"

This study reports a significant clinical outcome following the use of bronchoscopic interventional therapy combined with pembrolizumab for treating pulmonary large cell neuroendocrine carcinoma (LCNEC), showcasing a novel approach in managing this aggressive cancer.

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Enhancing diversity and inclusion in clinical trial recruitment, especially for historically marginalized populations including Black, Indigenous, and People of Color individuals, is essential. This practice ensures that generalizable trial results are achieved to deliver safe, effective, and equitable health and healthcare. However, recruitment is limited by two inextricably linked barriers - the inability to recruit and retain enough trial participants, and the lack of diversity amongst trial populations whereby racial and ethnic groups are underrepresented when compared to national composition.

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Motivation: Molecular subtyping by integrative modeling of multi-omics and clinical data can help the identification of robust and clinically actionable disease subgroups; an essential step in developing precision medicine approaches.

Results: We developed a novel outcome-guided molecular subgrouping framework, called Deep Multi-Omics Integrative Subtyping by Maximizing Correlation (DeepMOIS-MC), for integrative learning from multi-omics data by maximizing correlation between all input -omics views. DeepMOIS-MC consists of two parts: clustering and classification.

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Motivation: Deciphering the language of non-coding DNA is one of the fundamental problems in genome research. Gene regulatory code is highly complex due to the existence of polysemy and distant semantic relationship, which previous informatics methods often fail to capture especially in data-scarce scenarios.

Results: To address this challenge, we developed a novel pre-trained bidirectional encoder representation, named DNABERT, to capture global and transferrable understanding of genomic DNA sequences based on up and downstream nucleotide contexts.

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Defining traits of platinum-tolerant cancer cells could expose new treatment vulnerabilities. Here, new markers associated with platinum-tolerant cells and tumors were identified using and ovarian cancer models treated repetitively with carboplatin and validated in human specimens. Platinum-tolerant cells and tumors were enriched in ALDH cells, formed more spheroids, and expressed increased levels of stemness-related transcription factors compared with parental cells.

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-Methyladenosine (mA) is the most abundant modification of mammalian mRNAs. RNA methylation fine tunes RNA stability and translation, altering cell fate. The fat mass- and obesity-associated protein (FTO) is an mA demethylase with oncogenic properties in leukemia.

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Identifying and evaluating the right target are the most important factors in early drug discovery phase. Most studies focus on one protein ignoring the multiple splice-variant or protein-isoforms, which might contribute to unexpected therapeutic activity or adverse side effects. Here, we present computational analysis of cancer drug-target interactions affected by alternative splicing.

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Purpose: Molecular cancer subtyping is an important tool in predicting prognosis and developing novel precision medicine approaches. We developed a novel platform-independent gene expression-based classification system for molecular subtyping of patients with high-grade serous ovarian carcinoma (HGSOC).

Methods: Unprocessed exon array (569 tumor and nine normal) and RNA sequencing (RNA-seq; 376 tumor) HGSOC data sets, with clinical annotations, were downloaded from the Genomic Data Commons portal.

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Article Synopsis
  • Mutations or increased expression of isocitrate dehydrogenases 1 and 2 (IDH1 and IDH2) are linked to cancer progression through changes in metabolism and gene expression. !* -
  • IDH3α, a subunit of the IDH3 enzyme, is found at higher levels in glioblastoma (GBM) samples and contributes to tumor growth in mouse models. !* -
  • IDH3α influences cellular energy production and nucleotide availability during DNA replication while its loss affects methionine metabolism, indicating a new metabolic adaptation mechanism in GBM. !*
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