Editorial overview: Viruses and cancer

Gaglia, Marta Maria; Münger, Karl

doi:10.1016/j.coviro.2019.09.002

Cited by 6 publications

(5 citation statements)

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“…A tumor is formed by the abnormal proliferation of cells due to the loss of normal regulation of local tissue cells at the gene level under the action of various tumorigenic factors, such as viruses, pollution, tobacco, alcohol, and chemical carcinogens, 1 , 2 , 3 , 4 , 5 , 6 , 7 , 8 , 9 , 10 , 11 , 12 , 13 , 14 , 15 , 16 , 17 , 18 , 19 , 20 , 21 , 22 , 23 which is attributed to the action of these factors in stimulating or inactivating key signaling pathways and genes, such as the phosphoinositide 3‐kinase (PI3K)/AKT, Wnt/β‐catenin, Ras/extracellular signal‐regulated kinase (ERK), nuclear factor kappa B (NF‐κB), phospholipase C gamma (PLCγ), sting, signal transducer and activator of transcription (STAT), fibroblast growth factor (FGF)/fibroblast growth factor receptor (FGFR), c‐Myc, p53, and so on. 24 , 25 , 26 , 27 , 28 , 29 , 30 , 31 , 32 , 33 , 34 , 35 , 36 , 37 , 38 , 39 , 40 , 41 , 42 Among them, the FGF/FGFR pathway plays a significant role in maintaining normal physiological balance of the human body.…”

Section: Introductionmentioning

confidence: 99%

FGFR families: biological functions and therapeutic interventions in tumors

Liu,

Huang,

Yan

et al. 2023

MedComm

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There are five fibroblast growth factor receptors (FGFRs), namely, FGFR1–FGFR5. When FGFR binds to its ligand, namely, fibroblast growth factor (FGF), it dimerizes and autophosphorylates, thereby activating several key downstream pathways that play an important role in normal physiology, such as the Ras/Raf/mitogen‐activated protein kinase kinase/extracellular signal‐regulated kinase, phosphoinositide 3‐kinase (PI3K)/AKT, phospholipase C gamma/diacylglycerol/protein kinase c, and signal transducer and activator of transcription pathways. Furthermore, as an oncogene, FGFR genetic alterations were found in 7.1% of tumors, and these alterations include gene amplification, gene mutations, gene fusions or rearrangements. Therefore, FGFR amplification, mutations, rearrangements, or fusions are considered as potential biomarkers of FGFR therapeutic response for tyrosine kinase inhibitors (TKIs). However, it is worth noting that with increased use, resistance to TKIs inevitably develops, such as the well‐known gatekeeper mutations. Thus, overcoming the development of drug resistance becomes a serious problem. This review mainly outlines the FGFR family functions, related pathways, and therapeutic agents in tumors with the aim of obtaining better outcomes for cancer patients with FGFR changes. The information provided in this review may provide additional therapeutic ideas for tumor patients with FGFR abnormalities.

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Section: Introductionmentioning

confidence: 99%

FGFR families: biological functions and therapeutic interventions in tumors

Liu,

Huang,

Yan

et al. 2023

MedComm

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“…There is an emerging idea that viral infections could in principle contribute to cancer initiation and/or progression without being consistently detectable in every tumor cell ("hit-and-run") [14]. A study using three independent detection approaches (immunohistochemical visualization, flow cytometric analysis, and quantitative polymerase chain reaction) showed that HBV-HCC cells can express short HBV-specific mRNA without antibody detection of HBV antigens [15]. Selecting a viral antigen that is persistent in the tumor for engineered T cell immunotherapy is critical and remains a challenge.…”

Section: Involved In the Oncogenesis Of Virusesmentioning

confidence: 99%

“…By transfecting mRNA into cells, autologous T cells were made to express the selected TCRs, and these TCR T cells were adoptively transplanted into two patients in increasing quantities (1 × 10 4 –10 × 10 6 TCR‐T cells/kg) weekly for 112 days or 1 year, with no negative side effects. Five of six lung metastases in one patient showed volume reduction during the first year of the T‐cell treatment [15]. The few permanently infected hepatocytes that are present in these individuals may be the only target for CAR/TCR T cells [8].…”

Section: Studies Of Oncogenic Viral Antigen–specific Engineered T Cel...mentioning

confidence: 99%

Oncogenic viral antigens for engineered T cell immunotherapy: Challenges and opportunities

Zhang,

Chen,

Zhang

et al. 2023

Medicine Advances

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Viruses that cause malignancies such as hepatocellular carcinoma and cervical cancer are the cause of approximately 20% of all human cancers. In recent years, engineered T cell immunotherapy targeting tumor‐associated antigens (TAAs) has had some success against virus‐associated cancer, although these treatments are associated with side effects. TAA‐specific‐modified T cells may kill cancer cells but they also react with and damage healthy tissue. During an oncogenic virus infection, viral DNA integrates into the host genome, leading to the expression of viral‐specific antigens in the tumor in a restricted and durable manner. The cross‐reactive side‐effects of conventional TAA‐specific engineered T cell treatment can be avoided by creating engineered T cells that target oncogenic viral antigens. To chart a course for the discovery of additional viral‐specific antigens and their combination with immune checkpoint inhibition therapies, this review summarizes the development, preclinical research, and clinical application of oncogenic viral antigen–specific T cell immunotherapy. This review also addresses challenges such as virus mutation and diverse integration, which can result in the loss of the target.

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“…In particular, IFN stimulates proinflammatory immunity through diverse feedforward and feedback mechanisms, but chronic exposure could alleviate the host immunity that consequently promotes tumour initiation. 3,4 Interestingly, growing evidence also indicates that the viral infection gives rise to human tumourigenesis. Approximately, 10%-20% of all human cancers are attributed to viruses that are known as oncoviruses.…”

Section: Introductionmentioning

confidence: 99%

“…However, the long‐term virus infection (termed as latency) could suppress innate antiviral immunity and eliminate the adaptive immune system, therefore resulting in virus replication. In particular, IFN stimulates pro‐inflammatory immunity through diverse feedforward and feedback mechanisms, but chronic exposure could alleviate the host immunity that consequently promotes tumour initiation 3,4 . Interestingly, growing evidence also indicates that the viral infection gives rise to human tumourigenesis.…”

Section: Introductionmentioning

confidence: 99%

Long non‐coding RNAs in virus‐related cancers

Liu

Liu³

et al. 2022

Reviews in Medical Virology

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Some viral infections lead to tumourigenesis explained by a variety of underlying molecular mechanisms. Long non‐coding RNAs (lncRNAs) have the potential to be added to this list due to their diverse mechanisms in biological functions and disease processes via gene alternation, transcriptional regulation, protein modification, microRNA sponging and interaction with RNA/DNA/proteins. In this review, we summarise the dysregulation and mechanism of lncRNAs in virus‐related cancers focussing on Hepatitis B virus, Epstein‐Barr virus, Human Papillomavirus. We will also discuss the potential implications of lncRNAs in COVID‐19.

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Editorial overview: Viruses and cancer

Cited by 6 publications

References 0 publications

FGFR families: biological functions and therapeutic interventions in tumors

FGFR families: biological functions and therapeutic interventions in tumors

Oncogenic viral antigens for engineered T cell immunotherapy: Challenges and opportunities

Long non‐coding RNAs in virus‐related cancers

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