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This reference book compiles together different animal models in cancer research. It provides knowledge and a better understanding of the advancement of the molecular and cellular mechanisms associated with the progression, formation, and clinical results of various types of cancer from the evidence collected from animal models utilized for cancer research. It discusses animal models for screening anti-cancer drugs and exploration of gene therapy. It presents different methods used to construct cancer animal models and the progress of each animal model in tumor research. The book also highlights the applications of genetic engineering, including CRISP/Cas9, in designing and developing animal models for cancer research. Further, it discusses strategies for modeling animals for investigating growth, metastasis, tumor-associated inflammation and microenvironment, cancer stem cells, tumor heterogeneity, and therapeutic resistance. This book is s a valuable resource for basic and translational cancer researchers, clinicians, and health care.

Cancer—Animal models. --- Tumors—Classification. --- Tumors—Immunological aspects. --- Cancer Models. --- Cancer Staging. --- Tumour Immunology.

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Advances in cancer genomics are transforming our understanding of cancer, and have profound implications for its prevention, diagnosis, and treatment. Evolutionary dynamics suggests that as few as two mutations can cause transformation of normal cells into cancer stem cells. A process of Darwinian selection, involving a further three or more mutations, taking place over a period of years, can then result in progression to a life-threatening tumour. In many cases the immune response can recognise and eliminate the mutant cells, but most advanced tumours have mutations that activate immune checkpoints and enable the tumour to hide from the immune system. For the most hard-to-treat tumours, future progress will require molecular diagnostics to detect cancer-causing mutations in healthy subjects, and new drugs or vaccines that prevent the progression process. Chapters of this book deal with the signalling pathways that control cell division, and changes in these pathways in cancer cells. Three cell cycle checkpoints that are often mutated in cancer are analysed in detail. A discussion of chronic myeloid leukaemia illustrates the role of reactive oxygen species in driving progression from a chronic to an acute condition. A single drug that suppresses reactive oxygen can prevent disease progression and turn an otherwise deadly disease into a condition that can be managed to enable many years of normal life. Another chapter discusses chronic myelomonocytic leukaemia, a disease that involves both genetic and epigenetic change. Tumour progression is discussed as a multi-stage process in which cancer stem cells evolve into genetically unstable, invasive, metastatic, drug-resistant growths. Each of these stages can act as targets for drugs or immunomodulators, but the future of cancer treatment lies in understanding tumour dynamics, and arresting malignancy at the earliest possible stage. Evolutionary dynamics is a primarily mathematical technique, but the target readership will be tumour biologists, clinicians, and drug developers. Computational detail is provided in an online supplement, but the main text emphasises the implications of the dynamics for an understanding of tumour biology and does not require mathematical expertise.

Cancer. --- Cancer—Animal models. --- Cancer—Treatment. --- Cancer—Genetic aspects. --- Cancer Biology. --- Cancer Models. --- Cancer Therapy. --- Cancer Genetics and Genomics. --- Cancer Microenvironment. --- Cancers --- Carcinoma --- Malignancy (Cancer) --- Malignant tumors --- Tumors

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The Special Issue "In Vitro and In Vivo Models of Colorectal Cancer for Clinical Application", edited by Marta Baiocchi and Ann Zeuner for Cancers, collects original research papers and reviews, depicting the current state and the perspectives of CRC models for preclinical and translational research. Original research papers published in this issue focus on some of the hottest topics in CRC research, such as circulating tumor cells, epigenetic regulation of stemness states, new therapeutic targets, molecular CRC classification and experimental CRC models such as organoids and PDXs. Additionally, four reviews on CRC stem cells, immunotherapy and drug discovery provide an updated viewpoint on key topics linking benchtop to bedside research in CRC.

colorectal cancer --- organoids --- 3D bioprinting --- patient-derived xenograft --- cancer-on-chip --- drug combination --- cancer stem cells --- drug resistance --- clinical trials --- tumor-initiating cells --- tumor heterogeneity --- patient-derived cancer models --- single-cell RNA-sequencing --- tumor metabolism --- transcriptional programs --- tumor cell differentiation --- immunotherapy --- methods --- chromosomal instability --- DNA damage --- targeted therapy --- decitabine --- colon cancer --- DNA methylation --- clinical translation study --- machine learning --- patient-derived tumor organoid --- precision medicine --- radiation response --- rectal cancer --- PDX model --- CRC --- mutation analysis --- histological examination --- animal models --- in vitro culture --- cancer stem cell methods --- SATB2 --- colorectal carcinoma --- prognosis --- CDX2 --- circulating tumor cells --- CTC cluster --- size-based method --- ScreenCell® --- epithelial mesenchymal transition --- hypoxia --- HIF-1α --- immunofluorescence analysis --- sequential filtration

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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