Cancer and viruses have a long history that has evolved over many decades. Much information about the interplay between viruses and cell proliferation and metabolism has come from the history of clinical cases of patients infected with virus-induced cancer. In addition, information from viruses used to treat some types of cancer is valuable. Now, since the global coronavirus pandemic erupted almost a year ago, the scientific community has invested countless time and resources to slow down the infection rate and diminish the number of casualties produced by this highly infectious pathogen. A large percentage of cancer cases diagnosed are strongly related to dysregulations of the tyrosine kinase receptor (TKR) family and its downstream signaling pathways. As such, many therapeutic agents have been developed to strategically target these structures in order to hinder certain mechanisms pertaining to the phenotypic characteristics of cancer cells such as division, invasion or metastatic potential. Interestingly, several authors have pointed out that a correlation between coronaviruses such as the SARS-CoV-1 and -2 or MERS viruses and dysregulations of signaling pathways activated by TKRs can be established. This information may help to accelerate the repurposing of clinically developed anti-TKR cancer drugs in COVID-19 management. Because the need for treatment is critical, drug repurposing may be an advantageous choice in the search for new and efficient therapeutic compounds. This approach would be advantageous from a financial point of view as well, given that the resources used for research and development would no longer be required and can be potentially redirected towards other key projects. This review aims to provide an overview of how SARS-CoV-2 interacts with different TKRs and their respective downstream signaling pathway and how several therapeutic agents targeted against these receptors can interfere with the viral infection. Additionally, this review aims to identify if SARS-CoV-2 can be repurposed to be a potential viral vector against different cancer types.

Glioblastoma (GBM) is an aggressive brain tumor characterized by molecular complexity and resistance to conventional treatments, including surgery, radiation, and chemotherapy. Despite these challenges, advancements in receptor tyrosine kinase (RTK) research, combined with multi-omics approaches, hold promise for improving patient outcomes and survivability. RTKs are central to GBM progression, influencing cell proliferation, survival, and angiogenesis. However, the complexity of RTK signaling necessitates a broader, integrative perspective, which has been enabled by the emergence of -omics sciences. Multi-omics technologies—including genomics, transcriptomics, proteomics, and metabolomics—offer unprecedented insights into the molecular landscape of GBM and its RTK-driven pathways. Genomic studies have revealed mutations and amplifications in RTK-related genes, while transcriptomics has uncovered alterations in gene expression patterns, providing a clearer picture of how these aberrations drive tumor behavior. Proteomics has further delineated changes in protein expression and post-translational modifications linked to RTK signaling, highlighting novel therapeutic targets. Metabolomics complements these findings by identifying RTK-associated metabolic reprogramming, such as shifts in glycolysis and lipid metabolism, which sustain tumor growth and therapy resistance. The integration of these multi-omics layers enables a comprehensive understanding of RTK biology in GBM. For example, studies have linked metabolic alterations with RTK activity, offering new biomarkers for tumor classification and therapeutic targeting. Additionally, single-cell transcriptomics has unveiled intratumoral heterogeneity, a critical factor in therapy resistance. This article highlights the transformative potential of multi-omics in unraveling the complexity of RTK signaling in GBM. By combining these approaches, researchers are paving the way for precision medicine strategies that may significantly enhance diagnostic accuracy and treatment efficacy, providing new hope for patients facing this devastating disease.

The COVID-19 pandemic has significantly accelerated the adoption of telemedicine and digital health technologies, revealing their immense potential in managing cancer patients effectively. This article explores the impact of recent technological developments and widened consumer perspectives on personalised healthcare and patient awareness, particularly in oncology. Smartphones and wearable devices have become integral to daily life, promoting healthy lifestyles and supporting cancer patients through remote monitoring and health management. The widespread use of these devices presents an unprecedented opportunity to transform clinical trials and patient care by offering convenient and accessible means of collecting health data continuously and non-invasively. However, to fully harness their potential, it is crucial to establish standardised methods for measuring patient metrics to ensure data reliability and validity. This article also addresses the challenges of integrating these technologies into clinical practice, such as cost, patient and professional reluctance, and technological oversaturation. It emphasises the need for continuous innovation, the development of robust digital infrastructures, and the importance of fostering a supportive environment to integrate these advancements permanently. Ultimately, the convergence of technological innovation and personalised healthcare promises to enhance patient outcomes, improve quality of life, and revolutionise cancer management in the post-COVID era.

Glioblastoma (GBM) is an aggressive brain tumor characterized by its molecular complexity and resistance to conventional treatments, including surgery, radiation, and chemotherapy. Despite these challenges, advancements in receptor tyrosine kinase (RTK) research, combined with multi-omics approaches, hold promise for improving patient outcomes and survivability. RTKs, are central to GBM progression, influencing cell proliferation, survival, and angiogenesis. However, the complexity of RTK signaling necessitates a broader, integrative perspective, which has been enabled by the emergence of -omics sciences. Multi-omics technologies—including genomics, transcriptomics, proteomics, and metabolomics—offer unprecedented insights into the molecular landscape of GBM and its RTK-driven pathways. Genomic studies reveal mutations and amplifications in RTK-related genes, while transcriptomics uncovers alterations in gene expression patterns, providing a clearer picture of how these aberrations drive tumor behavior. Proteomics further delineates changes in protein expression and post-translational modifications linked to RTK signaling, highlighting novel therapeutic vulnerabilities. Metabolomics complements these findings by identifying RTK-associated metabolic reprogramming, such as shifts in glycolysis and lipid metabolism, which sustain tumor growth and therapy resistance. The integration of these multi-omics layers enables a comprehensive understanding of RTK biology in GBM. For example, studies have linked metabolic alterations with RTK activity, offering new biomarkers for tumor classification and therapeutic targeting. Additionally, single-cell transcriptomics has unveiled intratumoral heterogeneity, a critical factor in therapy resistance. This article highlights the transformative potential of multi-omics in unraveling the complexity of RTK signaling in GBM. By combining these approaches, researchers are paving the way for precision medicine strategies that may significantly enhance diagnostic accuracy and treatment efficacy, providing new hope for patients facing this devastating disease.