Choose an application

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

Dear Colleagues, When Hayflick and Moorhead coined the term “cellular senescence” (CS) almost 60 years ago, this phenomenon was understood as a mechanism, usually induced by activation of the DNA-repair machinery, to prevent uncontrolled proliferation. Meanwhile, additional beneficial roles for CS have been identified, such as embryonic development and wound healing. The senescence associated secretory phenotype (SASP) activated in most senescent cells (SC) signals to the immune system “come here and remove me”. In organisms with young and functional immune systems, occurring SC are usually detected and removed. If SC remain in the tissue expressing the SASP, this will cause not just a damaging local inflammation but can also induce remodeling and regeneration of the surrounding tissue as well as spreading of senescence. Old organisms show reduced regenerative potential and immune function which leads to accumulation of SC. Accordingly, accumulation of SC was observed in tissues of aged individuals, but importantly also in the context of age-related disorders, neurodegenerative, or cardiovascular diseases and others. Because of its detrimental effect of the surrounding tissue, accumulation of SC is not just a consequence, but can rather been understood as a major driver of aging. In line with this, recent studies described that removal of SC showed beneficial effects on healthspan and lifespan. This exciting research led to the discovery of “senolytics”, drugs which can kill SC. Given the heterogeneity of cell types that show senescence-like phenotypes, including heart muscle and post-mitotic neuronal cells, further research is required to unravel the molecular background that renders a cell type vulnerable to senesce. Additionally, it will be important to understand how senescence is cell type-specifically induced and which molecules serve as drug targets to prevent senescence and its spreading, or actively kill SC. This special issue will shed light on the molecular pathways of CS and inflammaging and on possible strategies to interfere with these processes. Dr. Markus Riessland Guest Editor

Research & information: general --- Biology, life sciences --- γH2AX --- Alzheimer's disease --- DNA damage --- mild cognitive impairment --- senescence --- secreted protein acidic and rich in cysteine --- regeneration --- homeostasis --- cellular senescence --- biology of aging --- neurodegeneration --- brain --- geroscience --- senolytics --- tauopathy --- cancer --- stress response --- post-mitotic --- neuronal senescence --- amyotrophic lateral sclerosis --- senescence-associated secretory phenotype (SASP) --- cell-cycle --- melanoma --- pancreatic adenocarcinoma --- tumor infiltration --- chemotherapy resistance --- prostate --- inflammation --- AIM2 inflammasome --- POP3 --- γH2AX --- Alzheimer's disease --- DNA damage --- mild cognitive impairment --- senescence --- secreted protein acidic and rich in cysteine --- regeneration --- homeostasis --- cellular senescence --- biology of aging --- neurodegeneration --- brain --- geroscience --- senolytics --- tauopathy --- cancer --- stress response --- post-mitotic --- neuronal senescence --- amyotrophic lateral sclerosis --- senescence-associated secretory phenotype (SASP) --- cell-cycle --- melanoma --- pancreatic adenocarcinoma --- tumor infiltration --- chemotherapy resistance --- prostate --- inflammation --- AIM2 inflammasome --- POP3

Choose an application

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

Dear Colleagues, When Hayflick and Moorhead coined the term “cellular senescence” (CS) almost 60 years ago, this phenomenon was understood as a mechanism, usually induced by activation of the DNA-repair machinery, to prevent uncontrolled proliferation. Meanwhile, additional beneficial roles for CS have been identified, such as embryonic development and wound healing. The senescence associated secretory phenotype (SASP) activated in most senescent cells (SC) signals to the immune system “come here and remove me”. In organisms with young and functional immune systems, occurring SC are usually detected and removed. If SC remain in the tissue expressing the SASP, this will cause not just a damaging local inflammation but can also induce remodeling and regeneration of the surrounding tissue as well as spreading of senescence. Old organisms show reduced regenerative potential and immune function which leads to accumulation of SC. Accordingly, accumulation of SC was observed in tissues of aged individuals, but importantly also in the context of age-related disorders, neurodegenerative, or cardiovascular diseases and others. Because of its detrimental effect of the surrounding tissue, accumulation of SC is not just a consequence, but can rather been understood as a major driver of aging. In line with this, recent studies described that removal of SC showed beneficial effects on healthspan and lifespan. This exciting research led to the discovery of “senolytics”, drugs which can kill SC. Given the heterogeneity of cell types that show senescence-like phenotypes, including heart muscle and post-mitotic neuronal cells, further research is required to unravel the molecular background that renders a cell type vulnerable to senesce. Additionally, it will be important to understand how senescence is cell type-specifically induced and which molecules serve as drug targets to prevent senescence and its spreading, or actively kill SC. This special issue will shed light on the molecular pathways of CS and inflammaging and on possible strategies to interfere with these processes. Dr. Markus Riessland Guest Editor

Research & information: general --- Biology, life sciences --- γH2AX --- Alzheimer’s disease --- DNA damage --- mild cognitive impairment --- senescence --- secreted protein acidic and rich in cysteine --- regeneration --- homeostasis --- cellular senescence --- biology of aging --- neurodegeneration --- brain --- geroscience --- senolytics --- tauopathy --- cancer --- stress response --- post-mitotic --- neuronal senescence --- amyotrophic lateral sclerosis --- senescence-associated secretory phenotype (SASP) --- cell-cycle --- melanoma --- pancreatic adenocarcinoma --- tumor infiltration --- chemotherapy resistance --- prostate --- inflammation --- AIM2 inflammasome --- POP3 --- n/a --- Alzheimer's disease

Choose an application

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

Metastasis is the dissemination of neoplastic cells from the primary tumor, and their colonization and growth in another part of the body. The process of metastasis is orchestrated by a complex network of biological events, and our understanding of the processes that regulate metastasis has significantly improved. This open access book provides an in-depth analysis of our understanding of the molecular mechanisms, detection, and clinical management of metastatic cancer. Updates are given on molecular imaging of brain metastasis and recurrence, management of pulmonary nodules for the early diagnosis of lung cancer, surgical management of both primary and metastatic lung cancers, genomic landscapes and tumor evolution of metastatic gynecological cancers, epigenetic changes in metastatic ovarian cancer, microRNAs in metastasis of prostate cancer, hematological toxicity of radiation therapy for bone metastasis, DNA damage response in cancer metastasis, tumor endothelial cells and angiogenesis in cancer metastasis, apoptosis-induced compensatory proliferation in cancer, the potential of targeting apoptosis to overcome chemotherapy resistance, and features of metastatic Ewing sarcoma. This open access book is aimed primarily at clinicians and scientists, but many areas will also be of interest to the layperson.

Molecular Imaging of Brain Metastases; Imaging Tests for the Diagnosis of Lung Nodules; Thoracic Surgery for Lung Cancer; Pulmonary Metastases; Surgery for Pulmonary Metastasis; Metastatic Gynecological Cancers; Epigenetic Changes in Ovarian Cancer Metastasis; Tumor Microenvironment in Ovarian Cancer Metastasis; MetastamiRs; MicroRNAs in Metastatic Prostate Cancer; Hematological Toxicity; Bone Metastasis Radiation Therapy; DNA Damage Response; Cancer Metastasis; Tumor Endothelial Cells in Cancer Metastasis; Apoptosis-Induced Compensatory Proliferation; Targeting Apoptosis to Overcome Chemotherapy Resistance; Metastatic Ewing Sarcoma

Choose an application

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

The cancer stem cell (CSC) paradigm represents one of the most prominent breakthroughs of the last decades in tumor biology. CSCs are that subpopulation within a tumor that can survive conventional therapies and as a consequence are able to fuel tumor recurrence. Nevertheless, the biological characteristics of CSCs and even their existence, remain the main topic among tumor biologists debates. The difficulty in achieving a better definition of CSC biology may actually be explained by the plasticity of such a cell subpopulation. Indeed, the emerging view is that CSCs represent a dynamic “state” of tumor cells that can acquire stemness-related properties under specific circumstances, rather than referring to a well-defined group of cells. Regardless of their origin, it is clear that designing novel antitumor treatments based on the eradication of CSCs will only be possible upon unraveling the biological mechanisms that underlie their pathogenic role in tumor progression and therapy resistance. The Special Issue on “New aspects of cancer stem cell biology: implications for innovative therapies” aims at highlighting recent insights into CSC features that can make them an attractive target for novel therapeutic strategies.

Research & information: general --- Biology, life sciences --- Cadherin 11 --- WNT signaling --- β-catenin --- cancer stem cells --- TNBC --- early breast cancer --- bevacizumab --- neoadjuvant chemotherapy --- ALDH1 --- solid cancer --- chemo-resistance --- HDAC inhibitors --- head and neck squamous cell carcinoma --- SRC --- dasatinib --- saracatinib --- EC-8042 --- Ovarian cancer --- Wnt signaling --- tumor progression --- therapy resistance --- exosomes --- oral cancer risk --- oral epithelial dysplasia --- SOX2 --- immunohistochemistry --- oral squamous cell carcinoma --- genome-wide --- transcriptome --- lung cancer --- ATAC-seq --- RNA-seq --- CSCs --- NSCLC --- B4GALT1 --- LUAD --- breast cancer --- lipid --- metabolism --- therapeutic resistance --- bowel cancer --- organoid --- tumoroid --- colorectal --- colon --- stem cell --- chemotherapy resistance --- ovarian cancer --- cancer stem cell --- genetic heterogeneity --- SNP array --- L1CAM --- chemoresistance --- epithelial-mesenchymal transition --- cancer therapy --- cell adhesion molecule --- Cadherin 11 --- WNT signaling --- β-catenin --- cancer stem cells --- TNBC --- early breast cancer --- bevacizumab --- neoadjuvant chemotherapy --- ALDH1 --- solid cancer --- chemo-resistance --- HDAC inhibitors --- head and neck squamous cell carcinoma --- SRC --- dasatinib --- saracatinib --- EC-8042 --- Ovarian cancer --- Wnt signaling --- tumor progression --- therapy resistance --- exosomes --- oral cancer risk --- oral epithelial dysplasia --- SOX2 --- immunohistochemistry --- oral squamous cell carcinoma --- genome-wide --- transcriptome --- lung cancer --- ATAC-seq --- RNA-seq --- CSCs --- NSCLC --- B4GALT1 --- LUAD --- breast cancer --- lipid --- metabolism --- therapeutic resistance --- bowel cancer --- organoid --- tumoroid --- colorectal --- colon --- stem cell --- chemotherapy resistance --- ovarian cancer --- cancer stem cell --- genetic heterogeneity --- SNP array --- L1CAM --- chemoresistance --- epithelial-mesenchymal transition --- cancer therapy --- cell adhesion molecule

Choose an application

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

Every minute, 34 new patients are diagnosed with cancer globally. Although over the past 50 years treatments have improved and survival rates have increased dramatically for several types of cancers, many remain incurable. Several aggressive types of blood and solid cancers form when mutations occur in a critical cellular signaling pathway, the JAK-STAT pathway; (Janus Kinase-Signal Transducer and Activator of Transcription). Currently, there are no clinically available drugs that target the oncogenic STAT3/5 proteins in particular or their Gain of Function hyperactive mutant products. Here, we summarize targeting approaches on STAT3/5, as the field moves towards clinical applications as well as we illuminate on upstream or downstream JAK-STAT pathway interference with kinase inhibitors, heat shock protein blockers or changing nuclear import/export processes. We cover the design paradigms and medicinal chemistry approaches to illuminate progress and challenges in understanding the pleiotropic role of STAT3 and STAT5 in oncogenesis, the microenvironment, the immune system in particular, all culminating in a complex interplay towards cancer progression.

multiple myeloma --- STAT3 --- S3I-1757 --- nanoparticle --- CD38 --- siRNA/RNAi --- polyethylenimine --- PEI --- lipopolyplex --- siRNA delivery --- glioma --- glioblastoma --- STAT5 --- AKT --- ERK1/2 --- prolactin --- androgens --- prostate cancer --- knockout --- escape mechanisms --- stem/progenitor cells --- cell hierarchy --- cancer --- CD4+ T cells --- CD8+ T cells --- myeloid cells --- immune check point --- hepatitis C virus (HCV) --- cirrhosis --- hepatocellular carcinoma (HCC) --- endoplasmic reticulum (ER) stress --- oxidative stress (OS) --- unfolded protein response (UPR) --- microRNA-122 (miR-122) --- nuclear factor erythroid 2-related factor 2 (NRF2) --- signal transducer and activator of transcription 3 (STAT3) --- hepatocyte nuclear factor 4 alpha (HNF4A) --- solid cancers --- cell cycle --- apoptosis --- inflammation --- mitochondria --- stemness --- tumor suppression --- melanoma --- autoimmune disease --- immunotherapy --- tumor–immune cell interactions --- breast cancer --- PD-L1 --- M2 macrophages --- NK cells --- STAT3 inhibitor XIII --- hedging --- transaction costs --- dynamic programming --- risk management --- post-decision state variable --- cancer progression --- cancer-stem cell --- cytokine --- therapy resistance --- metastasis --- immunosuppression --- tumor microenvironment --- proliferation --- tyrosine kinase 2 --- JAK family of protein tyrosine kinases --- signal transducer and activator of transcription --- cytokine receptor signaling --- gain-of-function mutation --- tumorigenesis --- ADAM17 --- interleukin-6 --- trans-signaling --- epidermal growth factor receptor (EGF-R) --- shedding --- metalloprotease --- tumor necrosis factor alpha (TNFα) --- inflammation associated cancer --- colon cancer --- lung cancer --- SH2 domain --- mutations --- autosomal-dominant hyper IgE syndrome --- inflammatory hepatocellular adenomas --- T-cell large granular lymphocytic leukemia --- T-cell prolymphocytic leukemia --- growth hormone insensitivity syndrome --- nuclear pore complex --- nuclear transport receptors --- nucleocytoplasmic shuttling --- targeting --- tumor-associated macrophages --- adoptive T cell therapy --- immune suppression --- STAT transcription factors --- JAK --- STAT --- T-PLL --- T-cell leukemia --- meta-analysis --- STAT5B signaling --- small-molecule inhibitors --- cancer models --- companion animals --- comparative oncology --- pharmacological inhibitor --- STAT5 signaling --- chemotherapy resistance --- myeloid leukemia --- heat shock proteins --- chaperones --- stabilization --- targeted therapy --- ovarian cancer --- hematopoietic cancers --- therapeutic targeting --- pharmacological inhibitors --- mTOR --- Bone Marrow Failure Syndromes --- lymphocytes --- lymphoma --- T-cells --- RHOA --- NGS --- MPN --- JAK2 V617F --- neoplastic stem cells --- n/a --- tumor-immune cell interactions