Disease Biomarkers in the Precision Medicine Era: A Comprehensive Multi-omics Analysis

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Molecular and Translational Medicine".

Deadline for manuscript submissions: 31 July 2024 | Viewed by 680

Special Issue Editor

Special Issue Information

Dear Colleagues,

Late-stage diagnosis often leads to advanced tumors, resulting in unfavorable survival outcomes despite continuous research and advancements in treatment modalities. Precision medicine efforts in disease have been prominent due to a comprehensive understanding of the impact of genetic mutations on disease initiation and progression. The recent surge in precision medicine techniques represents a groundbreaking era, where advancements in measurement technologies enable the sequencing of thousands of exomes, whole genomes, and the exploration of entire genomes, transcriptomes, proteomes, and metabolites at the single-cell level. Precision medicine, currently undergoing a multi-omics revolution, leverages insights from both germline and somatic cell differences to tailor treatments for individual disease patients. Molecular characterization, enabled by the diverse assessment of multi-omics, offers clinicians valuable information for personalized treatment planning.

This Special Issue aims to achieve precision in disease medicine through a multi-omics approach, emphasizing the fundamental understanding of disease biology. We welcome submissions that utilize multi-omics methodologies to uncover novel findings or identify new targets in disease research. The focus is on effectively generating, analyzing, and interpreting multi-omics data to inform decisions based on precision medicine. Authors are encouraged to submit research and review papers covering various aspects of the field, such as the basic understanding of genomics and signaling pathways, diagnostic and prognostic biomarkers, pharmacogenomic biomarkers, molecular diagnosis through gene expression profiling, molecular targets driving disease progression, drug development against these targets, clinical trials of new drugs, and investigations into disease epigenetics.

Dr. Chia-Jung Li
Guest Editor

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Keywords

  • personalized medicine
  • disease biomarkers: screening and diagnosis
  • multi-omics analysis
  • epidemiology

Published Papers (1 paper)

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Research

14 pages, 3345 KiB  
Article
Tumors Established in a Defective Immune Environment Reprogram the Oncogenic Signaling Pathways to Escalate Tumor Antigenicity
by Chiao-Hsu Ke, Hsin-Yi Wu, Yu-Shan Wang, Wei-Hsiang Huang and Chen-Si Lin
Biomedicines 2024, 12(4), 846; https://doi.org/10.3390/biomedicines12040846 - 11 Apr 2024
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Abstract
Tumors developed in immunocompromised hosts are more immunogenic. However, few studies have addressed the potential mechanisms underlying the high immunogenicity of tumors found in a suppressed immune system. Therefore, we aimed to elucidate the impacts of the immune system on tumor behaviors and [...] Read more.
Tumors developed in immunocompromised hosts are more immunogenic. However, few studies have addressed the potential mechanisms underlying the high immunogenicity of tumors found in a suppressed immune system. Therefore, we aimed to elucidate the impacts of the immune system on tumor behaviors and immunogenicity sculpting. A murine colorectal adenocarcinoma cell line, CT26wt, was administrated into immunocompetent (BALB/c) and immunocompromised (NOD.SCID) mice, respectively. On day 11, the CT26 cells slowly progressed in the NOD.SCID mice compared to the BALB/c mice. We then performed liquid chromatography–tandem mass spectrometry (LC-MS/MS) and analyzed the differentially expressed proteins (DEPs). The DEPs participated in numerous oncogenic pathways, PI3K/AKT/mTOR cell signaling, and the silencing of several tumor suppressors, such as PTEN and RBL1, during tumorigenesis. On day 34, the CT26/SCID tumors inversely became malignant counterparts; then the CT26/SCID tumors were harvested and re-inoculated into immunocompetent mice (CT26/SCID-Re tumors) to determine the immunogenicity. The CT26/SCID-Re tumor growth rate significantly decreased. Furthermore, increased infiltrations of dendritic cells and tumor-infiltrating T lymphocytes were found in the CT26/SCID-Re tumors. These findings suggest that immunogenic tumors might express multiple tumor rejection antigens, unlike wild-type tumors, and attract more immune cells, therefore decreasing the growth rate. Collectively, our study first revealed that in immunodeficient hosts, tumor suppressors were silenced and oncogenic signaling pathways were changed during the initial phase of tumor development. With tumor progression, the tumor antigens were overexpressed, exhibiting elevated immunogenicity. This study offers a hint on the mechanisms of tumorigenesis and provides a niche for investigating the interaction between host immunity and cancer development. Full article
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