Choose an application

• Reference Manager
• EndNote
• RefWorks (Direct export to RefWorks)

In Belgium, one woman at an 11 has to deal with breast cancer during her life. In 20 to 25 % of the cases, the cancer is due to a protein overexpression at the cell’s surface: protein HER2. HER2 overexpression can be detected by immunohistochemistry or by fluorescent in situ hybridization. On the market since 2000, trastuzumab 15 a monoclonal antibody able to target and inhibit this protein. It is indicated to treat an early or metastatic breast cancer either associated with chemotherapy (docetaxel or paclitaxel) or as a monotherapy after chemotherapy. Trastuzumab efficiency relies on different mechanisms of action such as ADCC induction, HER2 cleavage inhibition, inhibition of signaling pathways below the receptor, protein P27modulation, DNA repair inhibition and angiogenesis inhibition. Even though Herceptin remains relatively safe, cardiotoxicity can occur during the treatment, especially when associated with anthracyclines, which should be avoided. Moreover, polymorphism at level of coding genes for protein HER2 could promote risk of cardiac toxicity. Despite clearly demonstrated high efficiency, a high resistance rate was observed during treatment with Herceptin. This resistance 15 ruled by different mechanisms. Otherwise, oncogene HER2 identification has pushed researchers to develop new anti-HER2 agents such as, for example, Iapatinib. At the pharmacoeconomy level, given the results from different studies, the question is to know whether a one year treatment is necessary or if a shorter treatment, therefore less expensive wouldn’t be enough En Belgique, le cancer du sein touche 1 femme sur 11 au cours de sa vie. Dans 20 à 25% des cas, le cancer surexprime une protéine a la surface de ses cellules, la protéine HER2. La surexpression de HER2 chez les patientes peut être détectée par immunohistochimie ou par hybridation par florescence in situ Mis sur le marche en Europe en 2000, le trastuzumab (Herceptin9 est un anticorps monoclonal capable de cibler et d’inhiber cette protéine. Il est indiqué dans le traitement du cancer du sein précoce ou métastasique en association avec une chimiothérapie (docetaxel ou paclitaxel) ou en monothérapie après une chimiothérapie. L’efficacité du trastuzumab repose sur différents mécanismes d’action tels que l’induction de la cytotoxicité cellulaire dépendante de l’anticorps (ADCC), l’inhibition du clivage de HER2, l’inhibition des voies de signalisation en aval du récepteur, la modulation de la protéine p27k1p1 l’inhibition de la réparation de l’ADN et l’inhibition de l’angiogenèse Bien que l’Herceptin® reste relativement sûr, une cardiotoxicité est parfois mise en évidence lors du traitement, surtout lors d’une association avec des anthracyclines, celle-ci sera dès lors évitée. En outre, un polymorphisme au niveau du gène codant pour la protéine HER2 pourrait favoriser le risque de toxicité cardiaque. Malgré une très bonne efficacité clairement démontrée, un haut taux de résistance a été observé lors du traitement par Herceptin®. Cette résistance est régie par différents mécanismes. Par ailleurs, l’identification de l’oncogène HER2 a poussé les chercheurs à développer des nouveaux agents anti-HER2, comme, entre autres, le lapatinib. Au niveau pharmacoéconomie, au vu des résultats des différentes études, la question se pose de savoir si un traitement d’un an est vraiment nécessaire et si un traitement plus court, et donc moins cher ne pourrait pas suffire

Breast Neoplasms --- HER2 protein, human --- Antibodies, Monoclonal --- trastuzumab

Choose an application

• Reference Manager
• EndNote
• RefWorks (Direct export to RefWorks)

Identification and development of cancer biomarkers and targets have greatly accelerated progress towards precision medicine in oncology. Studies of tumor biology have not only provided insights into the mechanisms underlying carcinogenesis, but also led to discovery of molecules that have been developed into cancer biomarkers and targets. Multi-platforms for molecular characterization of tumors using next-generation genomic sequencing, immunohistochemistry, in situ hybridization, and blood-based biopsies have greatly expanded the portfolio of potential biomarkers and targets. These cancer biomarkers have been developed for diagnosis, early detection, prognosis, and prediction of treatment response. The molecular targets have been exploited for anti-cancer therapy and delivery of therapeutic agents. This Special Issue of Biomedicines focuses on recent advances in the discovery, characterization, translation, and clinical application of cancer biomarkers and targets in malignant diseases of the digestive system. The goal is to stimulate basic and translational research and clinical collaboration in this exciting field with the hope of developing strategies for prevention and early detection/diagnosis of cancer in digestive organs, and improving therapeutic and psychosocial outcomes in patients with these malignant diseases.

n/a --- liver graft injury --- HFE --- neurokinin --- chemotherapy --- intestinal tumors --- therapeutic targets --- biliary tract carcinoma --- hepatocellular carcinoma --- clinical trial --- cell adhesion molecules --- colorectal cancer --- biomarkers --- phenotypic mosaics --- gastrointestinal oncology --- Asian Cancer Research Group (ACRG) --- biomarker --- psychosocial support --- precision therapy --- pancreatic carcinoma --- precision medicine --- Liver transplantation --- predictive biomarkers --- CD274 --- cholecystokinin --- The Cancer Genome Atlas (TCGA) --- gastrin --- pembrolizumab --- immunotherapy --- gastrin-releasing peptide --- stereotactic body radiation therapy --- immunohistochemistry --- gastric carcinoma --- liver transplant --- CAM invasion assay --- intragraft gene expression profiles --- molecular profiling --- targeted therapy --- neurotensin --- intestinal disorder --- ramucirumab --- next-generation sequencing --- colorectal carcinoma --- tumor progenitor --- circulating tumor cells --- gastrointestinal malignancies --- bombesin --- trastuzumab --- somatostatin --- zebrafish --- G protein–coupled receptors --- G protein-coupled receptors

Choose an application

• Reference Manager
• EndNote
• RefWorks (Direct export to RefWorks)

Treatment strategies for breast cancer are wide-ranging and often based on a multi-modality approach, depending on the stage and biology of the tumour and the acceptance and tolerance of the patient. They may include surgery, radiotherapy, and systemic therapy (endocrine therapy, chemotherapy, and targeted therapy). Advances in technologies such as oncoplastic surgery, radiation planning and delivery, and genomics, and the development of novel systemic therapy agents alongside their evaluation in ongoing clinical trials continue to strive for improvements in outcomes. In this Special Issue, we publish a collection of studies looking at all forms of therapeutic strategies for early and advanced breast cancer, focusing on their outcomes, notably survival.

relative survival --- young women --- cancer treatment --- n/a --- fulvestrant --- lapatinib --- tumor biology --- antihormone therapy --- mastectomy --- aromatase inhibitors --- chemotherapy --- serum biomarker --- cyclin E --- anthracycline resistance --- zero-inflated Poisson regression model --- lymph-node ratio --- CHEK2 --- comparative effectiveness --- breast-conserving therapy --- taxane sensitivity --- liquid biopsy --- HER2 c-erbB2 --- colorectal cancer --- infiltrating breast cancer --- survival --- exercise characteristics --- lactate dehydrogenase --- biomarker --- breast cancer survivors --- BRCA --- disease-free survival --- PIK3CA --- metastatic breast cancer --- cell-free DNA --- invasive breast cancer --- radiotherapy --- Metformin --- social well-being --- gene expression --- contralateral breast cancer --- basal-like breast cancer --- LMK-235 --- Src kinase --- HER2/neu --- LKB1 --- Older women --- LDH --- mutation carriers --- stage IV --- mammography screening --- NCDB --- cMet --- SEER --- pertuzumab --- physical function --- outcome --- ribociclib --- older patients --- geriatric oncology --- metastatic --- overdiagnosis --- next-generation sequencing --- abemaciclib --- Endocrine therapy --- monitoring metastatic breast cancer --- breast cancer --- circulating tumor cells --- Breast Cancer --- PALB2 --- histone deacetylase --- prognosis --- physical activity --- trastuzumab --- ductal carcinoma in situ --- contralateral prophylactic mastectomy --- ERCC1 --- family history --- T-DM1 --- ATM --- advanced breast cancer --- incidence --- palbociclib --- HDAC5 inhibitors --- APOBEC3B

Choose an application

• Reference Manager
• EndNote
• RefWorks (Direct export to RefWorks)

The cooperation of highly specialized cell types maintains the homeostasis of multicellular organisms. The disturbance of that harmony contributes to the development of several diseases. Most of the cellular functions are executed by proteins, so it is essential to investigate biological processes at the protein level. Antibodies, complex biomolecules with high specificity, are used to recognize our protein of interest in a process known as “immunophenotyping”. One of the routinely used methods to study cellular proteins is flow cytometry, which detects cell surface or intracellular proteins at single-cell resolution. The other most frequent technique is the traditional immunohistochemical investigation of microscopic sections of human tissues. We called authors to publish their latest data studying cancer or autoimmune diseases by immunophenotyping.

Medicine --- CD8+CD28− T cells --- cancer immunology --- glioblastoma --- immunotherapy --- malignant glioma --- cancer --- accidental cell death --- oncosis --- DDR --- parthanatos --- flow cytometry --- systemic lupus erythematosus --- T cells --- glycosylation --- sialylation --- lectin binding --- glycosylation enzymes --- galectin 1 --- choriocarcinoma --- hydatidiform mole --- galectin --- gestational trophoblastic disease --- placental-specific gene --- systems biology --- trophoblast differentiation --- B cells --- non-switched B cells --- systemic sclerosis --- dcSSc --- TLR --- CD180 --- RP105 --- CpG --- IL-6 --- IL-10 --- natural autoantibodies --- IgM --- citrate synthase --- DNA topoisomerase I --- unfolded protein response --- Inositol-requiring enzyme 1 (IRE1) --- PKR-like endoplasmic reticulum kinase (PERK) --- Glucose-regulated protein 78 (GRP78) --- Activating transcription factor 6 (ATF6) --- immune cells --- T cell --- macrophage --- tumor microenvironment --- single cell mass cytometry --- metastatic breast cancer --- myeloid-derived suppressor cells --- immunophenotyping --- breast cancer --- trastuzumab --- chimeric antigen receptor --- cell therapy --- neuroendocrine neoplasia --- neuroendocrine tumor --- neuroendocrine carcinoma --- immunohistochemistry --- syntaxin 1 --- CD8+CD28− T cells --- cancer immunology --- glioblastoma --- immunotherapy --- malignant glioma --- cancer --- accidental cell death --- oncosis --- DDR --- parthanatos --- flow cytometry --- systemic lupus erythematosus --- T cells --- glycosylation --- sialylation --- lectin binding --- glycosylation enzymes --- galectin 1 --- choriocarcinoma --- hydatidiform mole --- galectin --- gestational trophoblastic disease --- placental-specific gene --- systems biology --- trophoblast differentiation --- B cells --- non-switched B cells --- systemic sclerosis --- dcSSc --- TLR --- CD180 --- RP105 --- CpG --- IL-6 --- IL-10 --- natural autoantibodies --- IgM --- citrate synthase --- DNA topoisomerase I --- unfolded protein response --- Inositol-requiring enzyme 1 (IRE1) --- PKR-like endoplasmic reticulum kinase (PERK) --- Glucose-regulated protein 78 (GRP78) --- Activating transcription factor 6 (ATF6) --- immune cells --- T cell --- macrophage --- tumor microenvironment --- single cell mass cytometry --- metastatic breast cancer --- myeloid-derived suppressor cells --- immunophenotyping --- breast cancer --- trastuzumab --- chimeric antigen receptor --- cell therapy --- neuroendocrine neoplasia --- neuroendocrine tumor --- neuroendocrine carcinoma --- immunohistochemistry --- syntaxin 1

Choose an application

• Reference Manager
• EndNote
• RefWorks (Direct export to RefWorks)

This book includes some recent works providing the readers with novel relevant findings about the main signaling pathways that govern the molecular pathogenesis of some of the highest prevalent human tumors, which are the basis for developing alternative therapeutic strategies to improve patient outcomes.

Medicine --- Oncology --- actin cytoskeletal reorganization --- breast cancer --- CD99 agonist --- EGFR dimerization --- endocytosis --- FAK dephosphorylation --- PTPN12 --- Rac1 --- RhoA --- tripeptide --- OMD --- PRELP --- tumor suppression gene --- bladder cancer initiation --- tight junction --- partial EMT --- tousled-like kinase (TLK) --- NIMA-related kinase 1 (NEK1) --- yes-associated protein 1 (YAP1) --- thioridazine (THD) --- MS-determined phosphopeptides --- human immunodeficiency virus type 1 --- epithelial cells --- carcinogenicity --- oxidative stress --- reactive oxygen species --- gp120 --- Tat --- Nef --- matrix protein p17 --- reverse transcriptase --- mitochondria --- metastasis --- OXPHOS --- cancer --- Warburg effect --- cancer therapeutics --- myeloproliferative neoplasms --- signaling pathways --- JAK2 --- CALR --- MPL --- TPOR --- DUSP1 --- MAPK --- Snail --- prostate cancer --- migration and invasion --- patient survival --- biomarkers --- pBRD4 --- SET --- PP2A --- prognosis --- triple negative breast cancer --- resistance --- anti-receptor therapy --- trastuzumab --- PI3K --- mTOR --- TAK-228 --- epigenetic --- methylation --- acetylation --- non-coding RNA --- small-cell lung cancer --- triple-negative breast cancer --- pancreatic ductal adenocarcinoma --- glioblastoma --- metastatic melanoma --- advanced ovarian cancer --- hepatocellular carcinoma --- immune evasion --- immunotherapy --- immune checkpoint inhibitors --- oncogenic signaling pathway --- molecular targeted agents --- genome --- epigenome --- tumor immune microenvironment --- ovarian cancer --- adaptive immunity --- innate immunity --- complement system --- cancer immunology --- tumor microenvironment --- splicing pathway --- luminal breast cancer --- BET inhibitors --- n/a