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Dear Colleagues, Cancer survival rates and successful organ transplantation in patients continues to increase due to improvements in early diagnosis and treatments. Since immuno-suppressive therapies are frequently used, the mortality rate due to secondary infections has become an ever-increasing problem. Opportunistic fungal infections are probably the deadliest threat to these patients due to their difficult early diagnosis, the limited effect of antifungal drugs and the appearance of resistances. In recent years, a considerable effort has been devoted to investigating the role of many virulence traits in the pathogenic outcome of fungal infections. New virulence factors (hypoxia adaptation, CO2 sensing, pH regulation, micronutrient acquisition, secondary metabolites, immunity regulators, etc.) have been reported and their molecular mechanisms of action are being thoroughly investigated. The recent application of gene-editing technologies such as CRISPr-Cas9, has opened a whole new window to the discovery of new fungal virulence factors. Accurate fungal genotyping, Next Generation Sequencing and RNAseq approaches will undoubtedly provide new clues to interpret the plethora of molecular interactions controlling these complex systems. Unraveling their intimate regulatory details will provide insights for a more target-focused search or a rational design of more specific antifungal agents. This Special Issue is show significant discoveries, proofs of concept of new theories or relevant observations in fungal pathogenesis and its regulation. Dr. Fernando Leal Guest Editor
CO2 sensing --- Micronutrient acquisition --- Biofilm formation --- Secondary metabolites and toxins --- Criptococcus --- Fungal virulence --- Immune evasion --- pH regulation --- Pneumocysits --- Aspergillus --- Regulation of antifungals resistance --- Candida --- Fusarium --- Trehalose biosynthesis --- Fungal genotyping --- Scedosporium
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Reactive oxygen species (ROS) are produced by healthy cells and are maintained at physiological levels by antioxidant systems. However, when ROS increase in number, a condition of oxidative stress occurs, leading to many human diseases, including cancer. The relationship between oxidative stress and cancer is complex since ROS play a double-edged role in cancer development and under therapy response. This paradox represents a great challenge for researchers and needs to be investigated. The articles collected in this Special Issue can help to clarify the role of ROS modulation in cancer prevention and treatment, and to dissect the molecular mechanisms underlying its paradoxical role in order to counteract carcinogenesis or enhance sensitivity to anticancer therapy.
Medicine --- Oncology --- sonodynamic therapy --- carbon doped titanium dioxide --- sonosensitizers --- ultrasound --- cancer treatment --- breast cancer treatment --- radiotherapy --- hematological malignancies --- oxidative stress --- lymphoma --- leukemia --- multiple myeloma --- apoptosis --- mitochondria --- ultraviolet-C (UVC) --- withanolide --- combined treatment --- oral cancer --- DNA damage --- cancer therapy --- immune system --- Hypericum perforatum --- hyperforin --- reactive oxygen species --- pH regulation --- tumor prevention --- tumor therapy --- cancerogenesis --- inflammatory signaling --- natural compounds --- pancreatic cancer --- antitumor agents --- coordination polymers --- bioinorganic chemistry --- cold atmospheric plasma --- reactive oxygen and nitrogen species --- nitrite --- cancer stem cells --- chemoresistance --- glutathione --- lipid peroxidation --- ZEB-1 --- GPX4 --- ferroptosis --- HO-1 --- Nrf2 --- cancer progression --- patients --- therapy --- prognosis --- biomarker --- Eprenetapopt --- Erastin --- glutathione (GSH) --- SLC7A11 --- iron --- NRF2 --- n/a
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Reactive oxygen species (ROS) are produced by healthy cells and are maintained at physiological levels by antioxidant systems. However, when ROS increase in number, a condition of oxidative stress occurs, leading to many human diseases, including cancer. The relationship between oxidative stress and cancer is complex since ROS play a double-edged role in cancer development and under therapy response. This paradox represents a great challenge for researchers and needs to be investigated. The articles collected in this Special Issue can help to clarify the role of ROS modulation in cancer prevention and treatment, and to dissect the molecular mechanisms underlying its paradoxical role in order to counteract carcinogenesis or enhance sensitivity to anticancer therapy.
sonodynamic therapy --- carbon doped titanium dioxide --- sonosensitizers --- ultrasound --- cancer treatment --- breast cancer treatment --- radiotherapy --- hematological malignancies --- oxidative stress --- lymphoma --- leukemia --- multiple myeloma --- apoptosis --- mitochondria --- ultraviolet-C (UVC) --- withanolide --- combined treatment --- oral cancer --- DNA damage --- cancer therapy --- immune system --- Hypericum perforatum --- hyperforin --- reactive oxygen species --- pH regulation --- tumor prevention --- tumor therapy --- cancerogenesis --- inflammatory signaling --- natural compounds --- pancreatic cancer --- antitumor agents --- coordination polymers --- bioinorganic chemistry --- cold atmospheric plasma --- reactive oxygen and nitrogen species --- nitrite --- cancer stem cells --- chemoresistance --- glutathione --- lipid peroxidation --- ZEB-1 --- GPX4 --- ferroptosis --- HO-1 --- Nrf2 --- cancer progression --- patients --- therapy --- prognosis --- biomarker --- Eprenetapopt --- Erastin --- glutathione (GSH) --- SLC7A11 --- iron --- NRF2 --- n/a
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Reactive oxygen species (ROS) are produced by healthy cells and are maintained at physiological levels by antioxidant systems. However, when ROS increase in number, a condition of oxidative stress occurs, leading to many human diseases, including cancer. The relationship between oxidative stress and cancer is complex since ROS play a double-edged role in cancer development and under therapy response. This paradox represents a great challenge for researchers and needs to be investigated. The articles collected in this Special Issue can help to clarify the role of ROS modulation in cancer prevention and treatment, and to dissect the molecular mechanisms underlying its paradoxical role in order to counteract carcinogenesis or enhance sensitivity to anticancer therapy.
Medicine --- Oncology --- sonodynamic therapy --- carbon doped titanium dioxide --- sonosensitizers --- ultrasound --- cancer treatment --- breast cancer treatment --- radiotherapy --- hematological malignancies --- oxidative stress --- lymphoma --- leukemia --- multiple myeloma --- apoptosis --- mitochondria --- ultraviolet-C (UVC) --- withanolide --- combined treatment --- oral cancer --- DNA damage --- cancer therapy --- immune system --- Hypericum perforatum --- hyperforin --- reactive oxygen species --- pH regulation --- tumor prevention --- tumor therapy --- cancerogenesis --- inflammatory signaling --- natural compounds --- pancreatic cancer --- antitumor agents --- coordination polymers --- bioinorganic chemistry --- cold atmospheric plasma --- reactive oxygen and nitrogen species --- nitrite --- cancer stem cells --- chemoresistance --- glutathione --- lipid peroxidation --- ZEB-1 --- GPX4 --- ferroptosis --- HO-1 --- Nrf2 --- cancer progression --- patients --- therapy --- prognosis --- biomarker --- Eprenetapopt --- Erastin --- glutathione (GSH) --- SLC7A11 --- iron --- NRF2
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Despite the efficiency of current cancer treatments, cancer is still a deadly disease for too many. In 2008, 7.6 million people died of cancer; with the current development, it is estimated that the annual cancer death number will grow to 13 million by 2030. There is clearly a need for not only more research but also more innovative and out of the mainstream scientific ideas to discover and develop even better cancer treatments. This book presents the collective works published in the recent Special Issue entitled “Killing Cancer: Discovery and Selection of New Target Molecules”. These articles comprise a selection of studies, ideas, and opinions that aim to facilitate knowledge, thoughts, and discussion about which biological and molecular mechanisms in cancer we should target and how we should target them.
ferlin --- myoferlin --- dysferlin --- otoferlin --- C2 domain --- plasma membrane --- sulconazole --- NF-κB --- IL-8 --- mammosphere --- breast cancer stem cells --- AF1Q --- MLLT11 --- WNT --- STAT --- esophageal cancer --- prognosis --- mTORC1 --- mTORC2 --- metabolism --- rapalogs --- mTOR inhibitors --- cancer metabolism --- mTOR in immunotherapy --- nutrient metabolism --- kinase inhibitors --- mTOR signaling --- MAPK kinase --- ERK1 --- ERK2 --- CD domain --- Rolled --- SCH772984 --- VRT-11E --- sevenmaker --- cancer therapy --- EMT --- lysosome --- lysosome-mediated invasion --- MZF1 --- phosphorylation --- PAK4 --- SUMOylation --- transcription factor --- zinc finger --- glucocorticoids --- 3D growth --- nuclear factor kappa-light-chain-enhancer of activated B-cells (NF-κB) --- epithelial–mesenchymal transition --- anoikis --- proliferation --- targeted cancer therapy --- disulfiram --- NPL4 --- replication stress --- DNA damage --- BRCA1 --- BRCA2 --- ATR pathway --- PDAC --- TCIRG1 --- ATP6V0a3 --- invasion --- migration --- matrix degradation --- pH-regulation --- autophagy --- multidrug resistance in cancer --- drug efflux pumps --- ATP-binding cassette transporter --- breast cancer resistance protein (BCRP) --- ABCG2 --- pyrazolo-pyrimidine derivative --- SCO-201 --- colorectal cancer --- immunotherapy --- inflammation --- microsatellite instability --- oncofetal chondroitin sulfate --- chondroitin sulfate --- cancer --- solid tumors --- target --- pediatric cancer --- VAR2 --- dexamethasone --- thyroid cancer --- microgravity --- space environment --- n/a --- epithelial-mesenchymal transition
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Despite the efficiency of current cancer treatments, cancer is still a deadly disease for too many. In 2008, 7.6 million people died of cancer; with the current development, it is estimated that the annual cancer death number will grow to 13 million by 2030. There is clearly a need for not only more research but also more innovative and out of the mainstream scientific ideas to discover and develop even better cancer treatments. This book presents the collective works published in the recent Special Issue entitled “Killing Cancer: Discovery and Selection of New Target Molecules”. These articles comprise a selection of studies, ideas, and opinions that aim to facilitate knowledge, thoughts, and discussion about which biological and molecular mechanisms in cancer we should target and how we should target them.
Research & information: general --- Biology, life sciences --- ferlin --- myoferlin --- dysferlin --- otoferlin --- C2 domain --- plasma membrane --- sulconazole --- NF-κB --- IL-8 --- mammosphere --- breast cancer stem cells --- AF1Q --- MLLT11 --- WNT --- STAT --- esophageal cancer --- prognosis --- mTORC1 --- mTORC2 --- metabolism --- rapalogs --- mTOR inhibitors --- cancer metabolism --- mTOR in immunotherapy --- nutrient metabolism --- kinase inhibitors --- mTOR signaling --- MAPK kinase --- ERK1 --- ERK2 --- CD domain --- Rolled --- SCH772984 --- VRT-11E --- sevenmaker --- cancer therapy --- EMT --- lysosome --- lysosome-mediated invasion --- MZF1 --- phosphorylation --- PAK4 --- SUMOylation --- transcription factor --- zinc finger --- glucocorticoids --- 3D growth --- nuclear factor kappa-light-chain-enhancer of activated B-cells (NF-κB) --- epithelial-mesenchymal transition --- anoikis --- proliferation --- targeted cancer therapy --- disulfiram --- NPL4 --- replication stress --- DNA damage --- BRCA1 --- BRCA2 --- ATR pathway --- PDAC --- TCIRG1 --- ATP6V0a3 --- invasion --- migration --- matrix degradation --- pH-regulation --- autophagy --- multidrug resistance in cancer --- drug efflux pumps --- ATP-binding cassette transporter --- breast cancer resistance protein (BCRP) --- ABCG2 --- pyrazolo-pyrimidine derivative --- SCO-201 --- colorectal cancer --- immunotherapy --- inflammation --- microsatellite instability --- oncofetal chondroitin sulfate --- chondroitin sulfate --- cancer --- solid tumors --- target --- pediatric cancer --- VAR2 --- dexamethasone --- thyroid cancer --- microgravity --- space environment
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