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Area of Science:

  • Bioinformatics
  • Oncology
  • Virology

Background:

  • Cancer patients exhibit heightened susceptibility to infections due to immunosuppression from malignancy and treatments.
  • The COVID-19 pandemic underscored this vulnerability, especially in aggressive cancers such as triple-negative breast cancer (TNBC) and clear cell renal cell carcinoma (ccRCC).
  • Molecular links between cancer progression and COVID-19 severity are not well understood.

Purpose of the Study:

  • To identify shared molecular signatures between COVID-19 and TNBC, breast cancer, and ccRCC.
  • To elucidate the molecular mechanisms underlying the interaction between cancer and COVID-19 severity.
  • To provide a framework for understanding virus-cancer interactions and potential therapeutic targets.

Main Methods:

  • In silico case-control analysis of publicly available transcriptomic datasets.
  • Identification of differentially expressed genes (DEGs) between mild/severe COVID-19 and cancer types.
  • Construction of protein-protein interaction (PPI) networks, Gene Ontology (GO), KEGG pathway, miRNA, and transcription factor (TF) analyses.

Main Results:

  • Identified shared hub genes (e.g., IGF1, MMP9, NOTCH1 in TNBC; TOP2A, PXN, CCNB1 in breast cancer; ASPM, TTK in ccRCC) linked to immune regulation, inflammation, and tumor progression.
  • Convergent pathways including MAPK signaling and cytokine-cytokine receptor interaction were revealed.
  • Key regulatory molecules (e.g., miR-145-5p, NFKB1, TP53) modulated both viral and oncogenic processes, with severe COVID-19 showing enhanced inflammatory signaling.

Conclusions:

  • Identified shared molecular and regulatory features linking severe COVID-19 with aggressive cancers.
  • Highlighted persistent immune activation and altered immune communication as common themes.
  • Provided a hypothesis-generating framework for virus-cancer interactions, potentially informing biomarker discovery and immune-focused therapies for vulnerable cancer populations.