Gastrointestinal Cancers (GCs) comprise about 4.8 million new cases per year and 3.4 million deaths worldwide, representing more than one-quarter of the global cancer incidence. The cancer of the stomach is the most diffuse pathology followed by the liver, esophagus, pancreas, and colorectal, all sharing common risk factors such as alcohol consumption, tobacco smoking, unbalanced diet, and obesity. However, although external stimuli play an important role in boosting cancer incidence it is important to remark that genetic differences and geographical origin account equally as important risk factors. Even if earlier diagnosis and better therapies have recently improved the overall survival, GCs are often diagnosed at an advanced stage when the tumor is inoperable and only chemotherapy can be useful.
One of the major causal factors in both carcinogenesis and tumor development is oxidative stress. Excessive reactive oxygen species and reactive nitrogen species (ROS/RNS) production in the gastrointestinal tract may induce oxidative stress and damage epithelial cell DNA, promoting carcinogenesis. International guidelines commonly recommend a first-line chemotherapy regimen containing a platinum agent (cisplatin or oxaliplatin) and fluoropyrimidines to treat advanced GCs. In particular, cisplatin is a drug whose action mechanism is based on the production of active oxygen species triggering and stimulating apoptosis via p53 activation and cytochrome C release. In this context, mitochondria are the perfect cross point between the cancer cells redox potential and their metabolic characteristic to be metabolically involved in the oxidative phosphorylation. This efficient ATP production pathway, is commonly deregulated in cancer cells favoring a typical Warburg phenotype, where glycolysis is the dominant biochemical circuit producing a high amount of lactic acid, promoting a pro-tumoral milieu, and inducing the formation of metastatic niches.
We welcome Original Research articles, short communications, and Review articles focused on improving the current knowledge in the field and dispelling the unclear points on the complex pathway of the redox circuits and the metabolic behavior of gastrointestinal cancers. We also aim to boost the generation of new anti-cancer therapies based on redox modulation and targeting crucial metabolic enzymes, metabolic abnormalities in GI/liver cancer, and treating GI/liver cancer by targeting the key metabolic disturbances.
Gastrointestinal Cancers (GCs) comprise about 4.8 million new cases per year and 3.4 million deaths worldwide, representing more than one-quarter of the global cancer incidence. The cancer of the stomach is the most diffuse pathology followed by the liver, esophagus, pancreas, and colorectal, all sharing common risk factors such as alcohol consumption, tobacco smoking, unbalanced diet, and obesity. However, although external stimuli play an important role in boosting cancer incidence it is important to remark that genetic differences and geographical origin account equally as important risk factors. Even if earlier diagnosis and better therapies have recently improved the overall survival, GCs are often diagnosed at an advanced stage when the tumor is inoperable and only chemotherapy can be useful.
One of the major causal factors in both carcinogenesis and tumor development is oxidative stress. Excessive reactive oxygen species and reactive nitrogen species (ROS/RNS) production in the gastrointestinal tract may induce oxidative stress and damage epithelial cell DNA, promoting carcinogenesis. International guidelines commonly recommend a first-line chemotherapy regimen containing a platinum agent (cisplatin or oxaliplatin) and fluoropyrimidines to treat advanced GCs. In particular, cisplatin is a drug whose action mechanism is based on the production of active oxygen species triggering and stimulating apoptosis via p53 activation and cytochrome C release. In this context, mitochondria are the perfect cross point between the cancer cells redox potential and their metabolic characteristic to be metabolically involved in the oxidative phosphorylation. This efficient ATP production pathway, is commonly deregulated in cancer cells favoring a typical Warburg phenotype, where glycolysis is the dominant biochemical circuit producing a high amount of lactic acid, promoting a pro-tumoral milieu, and inducing the formation of metastatic niches.
We welcome Original Research articles, short communications, and Review articles focused on improving the current knowledge in the field and dispelling the unclear points on the complex pathway of the redox circuits and the metabolic behavior of gastrointestinal cancers. We also aim to boost the generation of new anti-cancer therapies based on redox modulation and targeting crucial metabolic enzymes, metabolic abnormalities in GI/liver cancer, and treating GI/liver cancer by targeting the key metabolic disturbances.
