Persistent inflammation caused by non-remitted infections, abnormal immune reactions to normal tissues (immune dysregulation), or obesity, can progress in neoplastic events. Over time, chronic inflammation at low grade can cause DNA damage and develop into neoplastic mutations. We are noticing that this phenomenon is appearing more frequently.
As already evident, many chronic inflammations can be involved in this switch towards cancer evolution. Some examples are: Chronic hepatitis B and C virus that are associated with hepatic fibrosis and development of hepatocellular carcinoma (HCC); Crohn’s disease and
Ulcerative colitis is more frequently associated with bowel cancer and colorectal cancer; Rheumatoid arthritis has long been linked with an increased risk of non-Hodgkin's lymphoma and further evidence supports its relationship to lung cancer; and last but not least, the inflammaging that has been proposed as a driver of age-related changes in Hematopoietic stem cells (HSCs) function and myeloid malignancy.
Moreover, another type of inflammation called metaflammation is characteristic of obesity-related metabolic disorders associated with Cardiometabolic diseases (CMD). Thus, not only obese patients with diabetes have a higher risk of infection but also show a dysbiosis that exacerbates the dysfunctional immunity with a real
risk of developing a tumour.
This special issue aims to highlight the emergent research in this field, evaluating new findings, methods, current therapeutic approaches, and studies addressing the role of advanced-age of low-grade inflammation in determining neoplastic events, or how chronic metabolic inflammation coming from overnutrition can
influence the tumour microenvironment.
We want to gather knowledge of on the following subtopics:
• The correlation between the oxidative stress, environmental stress and the effects of low-grade
inflammation in age related pathologies and cancer.
• Molecular mechanisms underlying interaction between chronic low-grade stimulation of the innate immune system and the trigging of neoplastic events.
• Identification of mediators implicated in metabolic diseases as new actors of neoplastic events.
• Understanding how inflammation coming from metabolic diseases and their active immune response could determine tumour progression.
• Understanding how innate immune memory could be involved in metaflammation and promote disease progression.
• Explorating new biomarkers and therapeutically targets involved in the prevention of dysfunctional immune response during the advance-age and CMD.
We are convinced that deep studies on this topic could be useful to the prevention and improvement outcomes of the patients. For this reason, we welcome the submissions of Original Research Articles, Reviews, Mini Reviews, Methods, and Perspectives.
Manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by validation (clinical cohort or biological validation in vitro or in vivo) are out of scope for this section.
Persistent inflammation caused by non-remitted infections, abnormal immune reactions to normal tissues (immune dysregulation), or obesity, can progress in neoplastic events. Over time, chronic inflammation at low grade can cause DNA damage and develop into neoplastic mutations. We are noticing that this phenomenon is appearing more frequently.
As already evident, many chronic inflammations can be involved in this switch towards cancer evolution. Some examples are: Chronic hepatitis B and C virus that are associated with hepatic fibrosis and development of hepatocellular carcinoma (HCC); Crohn’s disease and
Ulcerative colitis is more frequently associated with bowel cancer and colorectal cancer; Rheumatoid arthritis has long been linked with an increased risk of non-Hodgkin's lymphoma and further evidence supports its relationship to lung cancer; and last but not least, the inflammaging that has been proposed as a driver of age-related changes in Hematopoietic stem cells (HSCs) function and myeloid malignancy.
Moreover, another type of inflammation called metaflammation is characteristic of obesity-related metabolic disorders associated with Cardiometabolic diseases (CMD). Thus, not only obese patients with diabetes have a higher risk of infection but also show a dysbiosis that exacerbates the dysfunctional immunity with a real
risk of developing a tumour.
This special issue aims to highlight the emergent research in this field, evaluating new findings, methods, current therapeutic approaches, and studies addressing the role of advanced-age of low-grade inflammation in determining neoplastic events, or how chronic metabolic inflammation coming from overnutrition can
influence the tumour microenvironment.
We want to gather knowledge of on the following subtopics:
• The correlation between the oxidative stress, environmental stress and the effects of low-grade
inflammation in age related pathologies and cancer.
• Molecular mechanisms underlying interaction between chronic low-grade stimulation of the innate immune system and the trigging of neoplastic events.
• Identification of mediators implicated in metabolic diseases as new actors of neoplastic events.
• Understanding how inflammation coming from metabolic diseases and their active immune response could determine tumour progression.
• Understanding how innate immune memory could be involved in metaflammation and promote disease progression.
• Explorating new biomarkers and therapeutically targets involved in the prevention of dysfunctional immune response during the advance-age and CMD.
We are convinced that deep studies on this topic could be useful to the prevention and improvement outcomes of the patients. For this reason, we welcome the submissions of Original Research Articles, Reviews, Mini Reviews, Methods, and Perspectives.
Manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by validation (clinical cohort or biological validation in vitro or in vivo) are out of scope for this section.