The systemic inflammatory response (SIR) sequestrated by the host-tumor interaction is integral to the establishment, development, and maintenance of the cancer state. Indeed the SIR is now a key target of tumouricidal therapies in several primary cancer types. Accompanying the progression of cancer in terms of metastatic development is nutritional deterioration and cancer cachexia. Progressive functional decline, loss of appetite, reduction in lean mass and fatigue are long established as the phenotype of advanced cancer yet the genesis of this has been unclear.
In the last decade, it has now been understood that the SIR is associated with reduced prognosis, quality of life, and loss of lean mass and appetite. Rather than the SIR merely being responsible for tumor development, it is likely that this is also a fundamental component of all that encompasses nutritional deterioration. At a superficial level, the SIR can be evidenced by raised inflammatory markers such as C-reactive protein or neutrophil count whilst at a cellular level cytokines such as Interleukin 1, 6, and Tumor Necrosis Factor-alpha have been shown to be related to nutrition-related deterioration.
However, despite our increased knowledge, much of our understanding of how inflammation results in nutritional deterioration and cachexia in cancer remains unknown. To illustrate, we do not comprehend if the magnitude of the SIR is related to the degree of nutritional symptoms, loss of lean mass, or level of functional decline. Further, a more detailed understanding of the specific roles of cellular messengers is needed and how, if indeed they do, relate to the clinical phenotype. In the clinical trial setting, consensus on endpoints needs to be reached, primarily informed by a mechanistic approach.
With these and other areas in mind, we hereby welcome submissions to this Research Topic ranging from basic science and animal work, through to clinical trials and reviews will be considered in the hope that we bring together key topics with the aim of moving the research agenda forward in this area.
The systemic inflammatory response (SIR) sequestrated by the host-tumor interaction is integral to the establishment, development, and maintenance of the cancer state. Indeed the SIR is now a key target of tumouricidal therapies in several primary cancer types. Accompanying the progression of cancer in terms of metastatic development is nutritional deterioration and cancer cachexia. Progressive functional decline, loss of appetite, reduction in lean mass and fatigue are long established as the phenotype of advanced cancer yet the genesis of this has been unclear.
In the last decade, it has now been understood that the SIR is associated with reduced prognosis, quality of life, and loss of lean mass and appetite. Rather than the SIR merely being responsible for tumor development, it is likely that this is also a fundamental component of all that encompasses nutritional deterioration. At a superficial level, the SIR can be evidenced by raised inflammatory markers such as C-reactive protein or neutrophil count whilst at a cellular level cytokines such as Interleukin 1, 6, and Tumor Necrosis Factor-alpha have been shown to be related to nutrition-related deterioration.
However, despite our increased knowledge, much of our understanding of how inflammation results in nutritional deterioration and cachexia in cancer remains unknown. To illustrate, we do not comprehend if the magnitude of the SIR is related to the degree of nutritional symptoms, loss of lean mass, or level of functional decline. Further, a more detailed understanding of the specific roles of cellular messengers is needed and how, if indeed they do, relate to the clinical phenotype. In the clinical trial setting, consensus on endpoints needs to be reached, primarily informed by a mechanistic approach.
With these and other areas in mind, we hereby welcome submissions to this Research Topic ranging from basic science and animal work, through to clinical trials and reviews will be considered in the hope that we bring together key topics with the aim of moving the research agenda forward in this area.
