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Tissue fibrosis may occur for unknown causes or be the consequence of many pathological conditions including chronic inflammatory or infectious diseases, autoimmune disorders, graft rejection, or malignancy. On the other hand, malignant tumors have been identified in fibrotic tissues decades ago, and now accumulating evidence suggests that fibrotic lesions enhance the risk of cancer in several organs such as liver, lungs, and breast. Disruption of an organ parenchymal cells and of its normal structural scaffold during tissue fibrogenesis appears to induce loss of cell polarity, promoting uncontrolled cell proliferation that may eventually lead to cancer development. Many cellular and molecular abnormalities including aberrant expression of microRNAs, genetic and epigenetic alterations, evasion or delayed apoptosis, unregulated intracellular signal pathways, and dysregulation or defective intercellular communications have been proposed to explain this link between fibrogenesis and carcinogenesis. However, the precise mechanisms of this fibrosis-to-cancer transition remain unclear. This book presents a collection of reviews and original articles summarizing recent advances in understanding the molecular mechanisms of cancer development in fibrotic organs.

bleomycin --- n/a --- regeneration --- antitumor efficacy --- lung cancer --- SOX2 --- leiomyosarcoma --- lung cancer (LC) --- nanoparticles --- cytokines --- hepatocellular carcinoma --- metabolic reprogramming --- hepatic stellate cells --- angiogenesis --- transforming growth factor-? --- anaplastic lymphoma kinase --- idiopathic pulmonary fibrosis --- growth factor --- pathogenesis --- cancer-associated fibroblasts --- fibrosis --- lipopolysaccharide --- DHA --- lncRNA --- SREBP-1 --- YAP --- protein S --- non-small cell lung cancer (NSCLC) --- omega-3 fatty acid --- inflammation --- metastasis --- clinical symptoms --- miRNA --- smooth muscle tumor of uncertain malignant potential --- Wnt --- interstitial fluid pressure --- heterogeneity --- hepatocytes --- myometrium --- tumor necrosis factor ? --- tumor --- tumor microenvironment --- extracellular matrix --- TAZ --- carcinogenesis --- cystic formation --- pulmonary fibrosis --- HBV --- cytokine --- genetic instability --- diagnosis --- EMT --- crizotinib --- Hippo pathway --- GPR120 --- marker --- HCV --- non-alcoholic steatohepatitis --- pathology --- common pathways --- apoptosis --- type I collagen --- GPR40 --- acute lung injury --- uterine fibroid --- renal injury --- pathophysiology --- reactive oxygen species --- immunohistochemistry --- SMAD --- butylidenephthalide --- leiomyoma --- cirrhosis --- Erk1/2 --- targeted therapy --- TGF-? --- mechanotransduction --- therapy --- breast cancer --- hepatocellular carcinoma (HCC) --- hepatic stellate cells (HSCs) --- idiopathic pulmonary fibrosis (IPF) --- cancer-associated fibroblasts (CAFs) --- cancer --- signal pathway --- tumor stiffness

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Fibroblast growth factor (FGF) signal transmission has an essential function in embryonic development and tissue repair, and is dysregulated in the vast majority of malignancies studied. The FGF signaling in the tumor cells is usually increased by autocrine and paracrine mechanisms and gives them a high growth potential, resistance to apoptosis, neoangiogenesis and metastasis, all essential parameters relevant for tumor progression. This makes FGFs, and their tyrosine kinase receptors FGFRs, valuable targets for therapeutic interventions. This book is a collection of 15 recent articles—both original work and reviews—that summarize the current research state effectively. The content covers FGF signaling aspects in gastric, skin, liver, esophageal cancer, melanoma, mesothelioma and glioblastoma, including one article that addresses the role of FGF in the tumor-microenvironment cross-talk. Several reports describe the development of compounds targeting FGFRs, their structure and interaction with the receptor molecules, and their effectivity in preclinical and clinical testing. In summary, the papers demonstrate the complexity of the topic, with various FGF ligands and receptors involved and the need for further research. They also present results that fuel hope that targeting cancer with dysfunctional FGF signaling can become a realistic treatment option.

Medicine --- FGFR4 --- FGF19 --- gene regulation --- cancer signaling --- anticancer --- FRS2 --- FGFR --- NVP-BGJ398 --- LY2874455 --- sarcoma --- cancer-associated fibroblasts --- GPER --- breast cancer --- estrogen --- FGFR1 --- FGF2 --- optogenetics --- ERK --- AKT --- receptor kinase --- neurite outgrowth --- HEK293 --- PC12 --- fibroblast growth factor receptors --- signaling --- receptor cross-talk --- coreceptor --- membrane proteins --- FGFR2 --- ERK1/2 --- phosphorylation --- serine --- negative feedback loop --- cancer --- prognosis --- HCC --- inhibitors --- FGF --- fibroblast growth factor --- autocrine signaling --- skin --- melanoma --- squamous and basal cell carcinoma --- seborrheic keratosis --- targeted therapy --- resistance --- structure --- kinase inhibitor --- gastric cancer --- monoclonal antibody --- small molecule --- FGFR2c --- autophagy --- keratinocyte --- MTOR --- JNK1 --- review --- malignant glioma --- brain cancer --- astrocytoma --- Sprouty proteins --- FGF-mediated signaling --- tumor suppressor --- tumor promoter --- malignant pleural mesothelioma --- overall survival --- immunohistochemistry --- infigratinib sensitivity --- FGF8 --- FGF18 --- adenocarcinoma of the esophagogastric junction --- neoadjuvant therapy --- FGFR4 --- FGF19 --- gene regulation --- cancer signaling --- anticancer --- FRS2 --- FGFR --- NVP-BGJ398 --- LY2874455 --- sarcoma --- cancer-associated fibroblasts --- GPER --- breast cancer --- estrogen --- FGFR1 --- FGF2 --- optogenetics --- ERK --- AKT --- receptor kinase --- neurite outgrowth --- HEK293 --- PC12 --- fibroblast growth factor receptors --- signaling --- receptor cross-talk --- coreceptor --- membrane proteins --- FGFR2 --- ERK1/2 --- phosphorylation --- serine --- negative feedback loop --- cancer --- prognosis --- HCC --- inhibitors --- FGF --- fibroblast growth factor --- autocrine signaling --- skin --- melanoma --- squamous and basal cell carcinoma --- seborrheic keratosis --- targeted therapy --- resistance --- structure --- kinase inhibitor --- gastric cancer --- monoclonal antibody --- small molecule --- FGFR2c --- autophagy --- keratinocyte --- MTOR --- JNK1 --- review --- malignant glioma --- brain cancer --- astrocytoma --- Sprouty proteins --- FGF-mediated signaling --- tumor suppressor --- tumor promoter --- malignant pleural mesothelioma --- overall survival --- immunohistochemistry --- infigratinib sensitivity --- FGF8 --- FGF18 --- adenocarcinoma of the esophagogastric junction --- neoadjuvant therapy

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Fibroblast growth factor (FGF) signal transmission has an essential function in embryonic development and tissue repair, and is dysregulated in the vast majority of malignancies studied. The FGF signaling in the tumor cells is usually increased by autocrine and paracrine mechanisms and gives them a high growth potential, resistance to apoptosis, neoangiogenesis and metastasis, all essential parameters relevant for tumor progression. This makes FGFs, and their tyrosine kinase receptors FGFRs, valuable targets for therapeutic interventions. This book is a collection of 15 recent articles—both original work and reviews—that summarize the current research state effectively. The content covers FGF signaling aspects in gastric, skin, liver, esophageal cancer, melanoma, mesothelioma and glioblastoma, including one article that addresses the role of FGF in the tumor-microenvironment cross-talk. Several reports describe the development of compounds targeting FGFRs, their structure and interaction with the receptor molecules, and their effectivity in preclinical and clinical testing. In summary, the papers demonstrate the complexity of the topic, with various FGF ligands and receptors involved and the need for further research. They also present results that fuel hope that targeting cancer with dysfunctional FGF signaling can become a realistic treatment option.

Medicine --- FGFR4 --- FGF19 --- gene regulation --- cancer signaling --- anticancer --- FRS2 --- FGFR --- NVP-BGJ398 --- LY2874455 --- sarcoma --- cancer-associated fibroblasts --- GPER --- breast cancer --- estrogen --- FGFR1 --- FGF2 --- optogenetics --- ERK --- AKT --- receptor kinase --- neurite outgrowth --- HEK293 --- PC12 --- fibroblast growth factor receptors --- signaling --- receptor cross-talk --- coreceptor --- membrane proteins --- FGFR2 --- ERK1/2 --- phosphorylation --- serine --- negative feedback loop --- cancer --- prognosis --- HCC --- inhibitors --- FGF --- fibroblast growth factor --- autocrine signaling --- skin --- melanoma --- squamous and basal cell carcinoma --- seborrheic keratosis --- targeted therapy --- resistance --- structure --- kinase inhibitor --- gastric cancer --- monoclonal antibody --- small molecule --- FGFR2c --- autophagy --- keratinocyte --- MTOR --- JNK1 --- review --- malignant glioma --- brain cancer --- astrocytoma --- Sprouty proteins --- FGF-mediated signaling --- tumor suppressor --- tumor promoter --- malignant pleural mesothelioma --- overall survival --- immunohistochemistry --- infigratinib sensitivity --- FGF8 --- FGF18 --- adenocarcinoma of the esophagogastric junction --- neoadjuvant therapy --- n/a

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Fibroblast growth factor (FGF) signal transmission has an essential function in embryonic development and tissue repair, and is dysregulated in the vast majority of malignancies studied. The FGF signaling in the tumor cells is usually increased by autocrine and paracrine mechanisms and gives them a high growth potential, resistance to apoptosis, neoangiogenesis and metastasis, all essential parameters relevant for tumor progression. This makes FGFs, and their tyrosine kinase receptors FGFRs, valuable targets for therapeutic interventions. This book is a collection of 15 recent articles—both original work and reviews—that summarize the current research state effectively. The content covers FGF signaling aspects in gastric, skin, liver, esophageal cancer, melanoma, mesothelioma and glioblastoma, including one article that addresses the role of FGF in the tumor-microenvironment cross-talk. Several reports describe the development of compounds targeting FGFRs, their structure and interaction with the receptor molecules, and their effectivity in preclinical and clinical testing. In summary, the papers demonstrate the complexity of the topic, with various FGF ligands and receptors involved and the need for further research. They also present results that fuel hope that targeting cancer with dysfunctional FGF signaling can become a realistic treatment option.

FGFR4 --- FGF19 --- gene regulation --- cancer signaling --- anticancer --- FRS2 --- FGFR --- NVP-BGJ398 --- LY2874455 --- sarcoma --- cancer-associated fibroblasts --- GPER --- breast cancer --- estrogen --- FGFR1 --- FGF2 --- optogenetics --- ERK --- AKT --- receptor kinase --- neurite outgrowth --- HEK293 --- PC12 --- fibroblast growth factor receptors --- signaling --- receptor cross-talk --- coreceptor --- membrane proteins --- FGFR2 --- ERK1/2 --- phosphorylation --- serine --- negative feedback loop --- cancer --- prognosis --- HCC --- inhibitors --- FGF --- fibroblast growth factor --- autocrine signaling --- skin --- melanoma --- squamous and basal cell carcinoma --- seborrheic keratosis --- targeted therapy --- resistance --- structure --- kinase inhibitor --- gastric cancer --- monoclonal antibody --- small molecule --- FGFR2c --- autophagy --- keratinocyte --- MTOR --- JNK1 --- review --- malignant glioma --- brain cancer --- astrocytoma --- Sprouty proteins --- FGF-mediated signaling --- tumor suppressor --- tumor promoter --- malignant pleural mesothelioma --- overall survival --- immunohistochemistry --- infigratinib sensitivity --- FGF8 --- FGF18 --- adenocarcinoma of the esophagogastric junction --- neoadjuvant therapy --- n/a

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In the era of precision medicine, the use of molecularly targeted therapies in selected patients has led to a paradigm change in cancer treatment. Multiple studies have demonstrated the benefits of therapies that are chosen based on the molecular profile of the tumor and also from the liquid biopsy. With genomics' increasing ability, a routine transcriptomics analysis of advanced/metastatic cancers is now feasible in most cancer hospitals, including community cancer centers. This is an unprecedented shift in the management of cancers irrespective of their organ types, which not only improved the outcome but also opened several new avenues in research and practice, such as immune-check-point inhibitors, tumor-TME co-evolution in the development of resistance, longitudinal liquid biopsies, biomarkers screening and the management of electronic medical records.This book brings together these crucial areas of investigation. The research presented here attempts to address the current issues to provoke thoughts for the future. The future of precision medicine will have to embrace a shift from in vitro, in vivo/PDX models for the mechanistic study to a more functional test based on the scientific interrogation of genomic data, in the form of functional precision medicine. We will also have to combat the element of noise in the multitudes of data and impart the regulatory structure to make judicious use of the data. The expectations for functional precision medicine are high. We aspire to witness a tremendous improvement in patient outcomes, from better to best, down the road that will match the clinical guidelines.

Medicine --- Oncology --- pediatric tumors --- tumor mutational burden --- TMB --- whole-exome sequencing --- gene panel sequencing --- immune checkpoint inhibitors --- glioblastoma prognosis --- overall survival --- extent of resection --- random forest --- Decision tree --- personalized precision oncology --- circulating free DNA --- liquid biopsy --- epidermal growth factor receptor --- tyrosine kinase inhibitor --- osimertinib --- comprehensive genomic profiling --- molecular genotyping --- intratumor heterogeneity --- multiple biopsies --- tumor evolution --- clonality classification --- strategic therapeutic intervention --- thymoma --- driver mutation --- sequencing --- molecular barcoding --- EGFR mutation --- EGFR-TKI --- cfDNA --- NGS --- digital enrichment --- next-generation sequencing --- solid cancer --- universal health-care system --- precision medicine --- presumed germline findings --- clinical guideline --- non-small cell lung cancer --- outcome --- adjuvant chemotherapy --- anaplastic lymphoma receptor tyrosine kinase --- HNSCC --- ctDNA --- tDNA --- DDR genes --- PARP inhibitors --- new drug development --- next-generation sequencing (NGS) --- open data --- regulatory reform --- tumor profiling test --- triple-negative breast cancer (TNBC) --- breast cancer --- targeted therapy --- TNBC subtypes --- immunotherapy --- cancer --- screening --- smoking --- electronic records --- PD-L1 --- cancer-associated fibroblasts --- resistance --- chemotherapy --- CTC --- immunocytochemistry --- parallel double-detection --- laboratory-friendly --- pediatric tumors --- tumor mutational burden --- TMB --- whole-exome sequencing --- gene panel sequencing --- immune checkpoint inhibitors --- glioblastoma prognosis --- overall survival --- extent of resection --- random forest --- Decision tree --- personalized precision oncology --- circulating free DNA --- liquid biopsy --- epidermal growth factor receptor --- tyrosine kinase inhibitor --- osimertinib --- comprehensive genomic profiling --- molecular genotyping --- intratumor heterogeneity --- multiple biopsies --- tumor evolution --- clonality classification --- strategic therapeutic intervention --- thymoma --- driver mutation --- sequencing --- molecular barcoding --- EGFR mutation --- EGFR-TKI --- cfDNA --- NGS --- digital enrichment --- next-generation sequencing --- solid cancer --- universal health-care system --- precision medicine --- presumed germline findings --- clinical guideline --- non-small cell lung cancer --- outcome --- adjuvant chemotherapy --- anaplastic lymphoma receptor tyrosine kinase --- HNSCC --- ctDNA --- tDNA --- DDR genes --- PARP inhibitors --- new drug development --- next-generation sequencing (NGS) --- open data --- regulatory reform --- tumor profiling test --- triple-negative breast cancer (TNBC) --- breast cancer --- targeted therapy --- TNBC subtypes --- immunotherapy --- cancer --- screening --- smoking --- electronic records --- PD-L1 --- cancer-associated fibroblasts --- resistance --- chemotherapy --- CTC --- immunocytochemistry --- parallel double-detection --- laboratory-friendly