Here, we review several established chemical carcinogenesis protocols based on DEN injection into mice and discuss their advantages as well as potential limitations.Long-standing inflammatory bowel diseases (IBD) increase the risk for the development of colorectal cancer (CRC). This increase is due in large part to chronic intestinal inflammation which exposes the epithelium to pro-carcinogenic factors. Moreover, enhanced mucosal proliferation associated with repetitive wound healing events following an inflammatory episode, further enhance this pro-tumorigenic environment. Although multiple factors involved in IBD pathogenesis and its associated neoplasia have been identified, more work is needed to develop and improve therapies to ameliorate disease and thus reduce CRC risk. https://www.selleckchem.com/products/furimazine.html Murine models have served as useful tools to identify factors involved in the pathogenesis of colitis-associated neoplasia and test therapies. These include both chemically-induced and genetic engineering approaches, resulting in chronic inflammation and tumor development. Here, we present a step-by-step method of inducing inflammation-associated colon neoplasia by combining administration of azoxymethane and dextran sodium sulfate in mice. A detailed description of this methodology will facilitate its use in the scientific community with the goals of further elucidating the mechanisms underlying colitis-associated tumorigenesis and developing risk reducing interventions.Mice are the most important animals to model tumor formation and malignant progression in humans. Chemical induction of skin tumors in mice by treatment with DMBA and TPA is a well-studied tumor induction model that is easy to use and directly applicable to genetically modified mice without any mandatory crossing with mice carrying mutations in oncogenes and tumorsuppressors. This article describes the basic protocol for DMBA/TPA induced skin tumor formation and discusses the advantages and limitations of this model, in particular the translatability of results obtained in this system to human cancer patients.The polycyclic aromatic hydrocarbon 7,12-dimethylbenz[a]anthracene (DMBA, D) administered per os to wild-type female mice bearing slow-release medroxyprogesterone (MPA, M) pellets s.c. drives the formation of mammary carcinomas that recapitulate numerous immunobiological features of human luminal B breast cancer. In particular, M/D-driven mammary carcinomas established in immunocompetent C57BL/6 female mice (1) express hormone receptors, (2) emerge by evading natural immunosurveillance and hence display a scarce immune infiltrate largely polarized toward immunosuppression, (3) exhibit exquisite sensitivity to CDK4/CDK6 inhibitors, and (4) are largely resistant to immunotherapy with immune checkpoint blockers targeting PD-1. Thus, M/D-driven mammary carcinomas evolving in immunocompetent female mice stand out as a privileged preclinical platform for the study of luminal B breast cancer. Here, we provide a detailed protocol for the establishment of M/D-driven mammary carcinomas in wild-type C57BL/6 female mice. This protocol can be easily adapted to generate M/D-driven mammary carcinomas in female mice with most genetic backgrounds (including genetically-engineered mice).Dynamic decision making requires an intact medial frontal cortex. Recent work has combined theory and single-neuron measurements in frontal cortex to advance models of decision making. We review behavioral tasks that have been used to study dynamic decision making and algorithmic models of these tasks using reinforcement learning theory. We discuss studies linking neurophysiology and quantitative decision variables. We conclude with hypotheses about the role of other cortical and subcortical structures in dynamic decision making, including ascending neuromodulatory systems.The rodent medial prefrontal cortex (mPFC) plays a key role in regulating cognition, emotion, and behavior. mPFC neurons are activated in diverse experimental paradigms, raising the questions of whether there are specific task elements or dimensions encoded by mPFC neurons, and whether these encoded parameters are selective to neurons in particular mPFC subregions or networks. Here, we consider the role of mPFC neurons in processing appetitive and aversive cues, outcomes, and related behaviors. mPFC neurons are strongly activated in tasks probing value and outcome-associated actions, but these responses vary across experimental paradigms. Can we identify specific categories of responses (e.g., positive or negative value), or do mPFC neurons exhibit response properties that are too heterogeneous/complex to cluster into distinct conceptual groups? Based on a review of relevant studies, we consider what has been done and what needs to be further explored in order to address these questions.Medial secondary motor cortex (MOs or M2) constitutes the dorsal aspect of the rodent medial frontal cortex. We previously proposed that the function of MOs is to link antecedent conditions, including sensory stimuli and prior choices, to impending actions. In this review, we focus on the long-range pathways between MOs and other cortical and subcortical regions. We highlight three circuits (1) connections with visual and auditory cortices that are essential for predictive coding of perceptual inputs; (2) connections with motor cortex and brainstem that are responsible for top-down, context-dependent modulation of movements; (3) connections with retrosplenial cortex, orbitofrontal cortex, and basal ganglia that facilitate reward-based learning. Together, these long-range circuits allow MOs to broadcast choice signals for feedback and to bias decision-making processes.Across species, the medial prefrontal cortex guides actions in time. This process can be studied using behavioral paradigms such as simple reaction-time and interval-timing tasks. Temporal control of action can be influenced by prefrontal neurotransmitters such as dopamine and acetylcholine and is highly relevant to human diseases such as Parkinson's disease, schizophrenia, and attention-deficit hyperactivity disorder (ADHD). We review evidence that across species, medial prefrontal lesions impair the temporal control of action. We then consider neurophysiological correlates in humans, primates, and rodents that might encode temporal processing and relate to cognitive-control mechanisms. These data have informed brain-stimulation studies in rodents and humans that can compensate for timing deficits. This line of work illuminates basic mechanisms of temporal control of action in the medial prefrontal cortex, which underlies a range of high-level cognitive processing and could contribute to new biomarkers and therapies for human brain diseases.