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in patients with AJCC stage III, while there was no significant difference in OS between the CRT, SCT and CRT-SCT groups in patients with AJCC stage I/II. Different adjuvant therapy according to AJCC stage can be applied in patients with PC.

SCT and CRT-SCT showed significantly longer OS and recurrence-free survival than CRT in patients with AJCC stage III, while there was no significant difference in OS between the CRT, SCT and CRT-SCT groups in patients with AJCC stage I/II. Different adjuvant therapy according to AJCC stage can be applied in patients with PC.

Inflammation is a well-established enabling factor for cancer development and provides a framework for the high prevalence of colon cancer in inflammatory bowel disease. In accordance, chronic inflammation has recently been implicated in the development of cancer stem cells (CSCs). However, the mechanism whereby anti-inflammatory drugs act in the prevention of colitis-associated cancer (CAC) is only partially understood.

To evaluate the role of diacerein (DAR), an anti-inflammatory drug that mainly acts through the inhibition of interleukin (IL)-1β expression in the development of CSCs and CAC.

The effects of DAR on colon inflammation in mice with CAC were evaluated by inflammatory index, reverse real-time transcription polymerase chain reaction and western blot. Cytokine levels were measured by enzyme-linked immunosorbent assay. AD-5584 Cells assays evaluated the effects of DAR on CSCs. Immunohistochemistry and apoptosis assays were also used to evaluate the effects of DAR on tumorigenesis associated with inflammation.

DAR treatment reduced colon inflammation as well as the number and size of tumors in azoxymethane plus dextran sulphate sodium-treated animals. Accordingly, DAR treatment was associated with reduced intracellular signals of inflammation (inhibitor of nuclear factor kappa B kinase and c-Jun N-terminal kinase phosphorylation) in the colon. In addition, DAR treatment was associated with a decrease in colon CSC formation, suggesting that besides reducing colonic inflammation, DAR has a direct effect on the inhibition of colon carcinogenesis.

Together, these data indicate that DAR-mediated IL-1β suppression attenuates inflammation-induced colon cancer and CSC formation, highlighting DAR as a potential candidate for the chemoprevention of CAC.

Together, these data indicate that DAR-mediated IL-1β suppression attenuates inflammation-induced colon cancer and CSC formation, highlighting DAR as a potential candidate for the chemoprevention of CAC.For many years tissue biopsy has been the primary procedure to establish cancer diagnosis and determine further treatment and prognosis. However, this method has multiple drawbacks, including, to mention some, being an invasive procedure carrying significant risk for fragile patients and allowing only for a "snapshot" of the tumor biology in time. The process of liquid biopsy allows for a minimally invasive procedure that provides molecular information about underlying cancer by analyzing circulating tumor DNA (ctDNA) via next-generation sequencing technology and circulating tumor cells. This paper focuses on describing the basis of ctDNA and its current utilities.Globally, cancer care delivery is marked by inequalities, where some economic, demographic, and sociocultural groups have worse outcomes than others. In this review, we sought to identify patient-facing interventions designed to reduce disparities in cancer care in both high- and low-income countries. We found two broad categories of interventions that have been studied in the current literature Patient navigation and telehealth. Navigation has the strongest evidence base for reducing disparities, primarily in cancer screening. Improved outcomes with navigation interventions have been seen in both high- and low-income countries. Telehealth interventions remain an active area of exploration, primarily in high income countries, with the best evidence being for the remote delivery of palliative care. Ongoing research is needed to identify the most efficacious, cost-effective, and scalable interventions to reduce barriers to the receipt of cancer care globally.Every day, investigators find a new link between a form of cancer and a particular alteration in the sequence or/and expression level of a key gene, awarding this gene the title of "biomarker". The clinician may choose from numerous available panels to assess the type of cancer based on the mutation or expression regulation ("transcriptomic signature") of "driver" genes. However, cancer is not a "one-gene show" and, together with the alleged biomarker, hundreds other genes are found as mutated or/and regulated in cancer samples. Regardless of the platform, a well-designed transcriptomic study produces three independent features for each gene Average expression level, expression variability and coordination with expression of each other gene. While the average expression level is used in all studies to identify what genes were up-/down-regulated or turn on/off, the other two features are unfairly ignored. We use all three features to quantify the transcriptomic change during the progression of the disease and recovery in response to a treatment. Data from our published microarray experiments on cancer nodules and surrounding normal tissue from surgically removed tumors prove that the transcriptomic topologies are not only different in histopathologically distinct regions of a tumor but also dynamic and unique for each human being. We show also that the most influential genes in cancer nodules [the Gene Master Regulators (GMRs)] are significantly less influential in the normal tissue. As such, "smart" manipulation of the cancer GMRs expression may selectively kill cancer cells with little consequences on the normal ones. Therefore, we strongly recommend a really personalized approach of cancer medicine and present the experimental procedure and the mathematical algorithm to identify the most legitimate targets (GMRs) for gene therapy.Mass spectrometry (MS) is an emerging method to determine the accurate concentration of immunogenic gluten peptides. It is of interest to quantify specific peptides within the gluten peptidome due to the role they play in the activation of the celiac immune cascade. Celiac disease is an autoimmune disorder triggered in genetically susceptible individuals by the presence of specific gluten peptides that resist digestion in the gastrointestinal tract. The protocol detailed within this paper can accurately quantify (label-free) the concentration of six immunogenic gluten peptides (including the 33mer) released from a food matrix using the INFOGEST in vitro digestion protocol. This method can be used to monitor small changes in the concentration of these marker peptides in response to exogenous factors such as plant-breeding, fermentation or food processing.