Anti-cancer drugs

Biosensors consist of a biocatalyst that can detect a biological element and a transducer which can convert the combination event of the biocatalyst and the biological element into a detectable parameter. The biocatalyst can be biomolecules like, enzyme, DNA, RNA, metabolites, cells, oligonucleotides etc., and the transducers can be electrochemical, optical, piezoelectric, acoustics, calorimetric etc. In disease diagnostics biosensors utilizing immobilized cells, enzymes, nucleic acids have come into the field in recent years. Nanobiosensors exploiting the ultrasmall size and unique properties have also been used for engineering disease diagnostic biosensors. The use of biosensors can rapidly assess the health status, onset of the disease and its progression and can help to plan treatment for many diseases with the aid of multidisciplinary combination of chemistry, medical science and nanotechnology. The devices are cost effective, highly sensitive, rapid, user friendly and can be produced in bulk for human use. This review focuses on the different biosensors for the diagnosis of three major diseases like diabetes, cardiovascular disease and cancer.

Diagnostic biosensors in medicine – A review

Gastric and esophageal cancers are as main cancers of the gastrointestinal (GI) tract, which are associated with poor diagnosis and survival. Several efforts were made in the past few decades to finding effective therapeutic approaches, but these approaches had several problems. Finding new biomarkers is a critical step in finding new approaches for the treatment of these cancers. Finding new biomarkers that cover various aspects of the diseases could provide a choice of suitable therapies and better monitoring of patients with these cancers. Among several biomarkers tissue specific and circulating microRNAs (miRNAs) have emerged as powerful candidates in the diagnosis of gastric and esophageal cancers. MiRNAs are small noncoding single-stranded RNA molecules that are found in the blood and regulate gene expression. These have numerous characteristics that make them suitable for being used as ideal biomarkers in cancer diagnosis. Research has indicated that the level and profile of miRNA in serum and plasma are very high. They are potentially noninvasive and sensitive enough to detect tumors in their primary stages of infection. Multiple lines of evidence indicate that the presence, absence, or deregulation of several circulating miRNAs (i.e., let-7a, miR-21, miR-93, miR-192a, miR-18a, and miR-10b for gastric cancer, and miR-21, miR-375, miR-25-3p, miR-151a-3p, and miR-100-3p for esophageal cancer) are associated with initiation and progression of gastric and esophageal cancers. The aim of this review is to highlight the recent advances in the roles of miRNAs in diagnosis and treatment of gastric and esophageal cancers.

Circulating microRNAs as diagnostic and therapeutic biomarkers in gastric and esophageal cancers

Simple Summary Over 500,000 individuals died due to esophageal cancer (EC) worldwide in 2020. More than four decades of etiological research have predominantly focused on the esophageal squamous cell carcinoma (ESCC) subtype, which accounts for 80% of EC cases, while less etiologic research has been done on the esophageal adenocarcinoma (EAC) subtype whose incidence rates are rapidly increasing in some high-income countries. Recent advances in genomics and microbiome studies, and the establishment of high-quality research infrastructure in high-risk regions, including Africa and Iran, have advanced our understanding of the causes and potential risk factors of these diseases in different regions. For therapy and early detection, topical studies that have used chemoprevention methods, such as using aspirin and proton pump inhibitors, and early detection methods, such as using Cytosponge™ and biomarker assays among symptomatic or high-risk individuals, have shown promising results. However, there are still challenges in each field that need to be addressed in future studies. Abstract Esophageal cancer (EC) is the ninth most common cancer and the sixth leading cause of cancer deaths worldwide. Esophageal squamous cell carcinoma (ESCC) and esophageal adenocarcinoma (EAC) are the two main histological subtypes with distinct epidemiological and clinical features. While the global incidence of ESCC is declining, the incidence of EAC is increasing in many countries. Decades of epidemiologic research have identified distinct environmental exposures for ESCC and EAC subtypes. Recent advances in understanding the genomic aspects of EC have advanced our understanding of EC causes and led to using specific genomic alterations in EC tumors as biomarkers for early diagnosis, treatment, and prognosis of this cancer. Nevertheless, the prognosis of EC is still poor, with a five-year survival rate of less than 20%. Currently, there are significant challenges for early detection and secondary prevention for both ESCC and EAC subtypes, but Cytosponge™ is shifting this position for EAC. Primary prevention remains the preferred strategy for reducing the global burden of EC. In this review, we will summarize recent advances, current status, and future prospects of the studies related to epidemiology, time trends, environmental risk factors, prevention, early diagnosis, and treatment for both EC subtypes.

/pdf/current-status-and-future-prospects-for-esophageal-cancer-3fixuiau.pdf

Current Status and Future Prospects for Esophageal Cancer

Esophageal cancer (EC) is a disease often marked by aggressive growth and poor prognosis. Lack of targeted therapies, resistance to chemoradiation therapy, and distant metastases among patients with advanced disease account for the high mortality rate. The tumor microenvironment (TME) contains several cell types, including fibroblasts, immune cells, adipocytes, stromal proteins, and growth factors, which play a significant role in supporting the growth and aggressive behavior of cancer cells. The complex and dynamic interactions of the secreted cytokines, chemokines, growth factors, and their receptors mediate chronic inflammation and immunosuppressive TME favoring tumor progression, metastasis, and decreased response to therapy. The molecular changes in the TME are used as biological markers for diagnosis, prognosis, and response to treatment in patients. This review highlighted the novel insights into the understanding and functional impact of deregulated cytokines and chemokines in imparting aggressive EC, stressing the nature and therapeutic consequences of the cytokine-chemokine network. We also discuss cytokine-chemokine oncogenic potential by contributing to the Epithelial-Mesenchymal Transition (EMT), angiogenesis, immunosuppression, metastatic niche, and therapeutic resistance development. In addition, it discusses the wide range of changes and intracellular signaling pathways that occur in the TME. Overall, this is a relatively unexplored field that could provide crucial insights into tumor immunology and encourage the effective application of modulatory cytokine-chemokine therapy to EC.

/pdf/cytokine-chemokine-network-driven-metastasis-in-esophageal-4evuqkumw5.pdf

Cytokine-chemokine network driven metastasis in esophageal cancer; promising avenue for targeted therapy

Esophageal cancer, which consist of esophageal adenocarcinoma and esophageal squamous cell carcinoma, is one of the most common malignant tumors in the world, especially in the south of Iran and China. To find and investigate the biomarkers in the initiation, development and progression of esophageal cancer will help us predict the prognosis of esophageal cancer patients and improve the curative effect and survival rate. Here, we reviewed the potential biomarkers of esophageal cancer in three aspects: Immunohistochemical markers, blood-based markers, miRNA markers and Gene expression profiling. All these biomarkers provided promising therapeutic targets for the diagnosis, treatment, and prognosis of esophageal cancer.

/pdf/potential-biomarkers-for-esophageal-cancer-2cw5uiw4pq.pdf

Potential biomarkers for esophageal cancer

Esophageal carcinoma (EC) is a lethal disease with high morbidity and mortality worldwide, and the incidence has been increasing in recent years. Although the diagnosis and treatment of EC have improved considerably, EC has rapidly progressed in the clinical setting and has a poor prognosis for its metastasis and recurrence. The general idea of cancer stem cells (CSCs) is primarily based on clinical and experimental observations, indicating the existence of a subpopulation of cells that can self-renew and differentiate. The EC stem cells, which can be isolated from normal pluripotent stem cells by applying similar biomarkers, may participate in promoting esophageal tumorigenesis through renewal and repair. In this review, major emphasis is given to CSC markers, altered CSC-specific pathways, and molecular targeting agents currently available to target CSCs of esophageal cancer. The roles of numerous markers (CD44, aldehyde dehydrogenase, CD133, and ATP-binding cassette subfamily G member 2) and developmental signaling pathways (Wnt/β-catenin, Notch, hedgehog, and Hippo) in isolating esophageal CSCs are discussed in detail. Targeting CSCs can be a logical strategy to treat EC, as these cells are responsible for carcinoma recurrence and chemoradiation resistance.

/pdf/esophageal-cancer-stem-cells-and-implications-for-future-1it54q3hx8.pdf

Esophageal cancer stem cells and implications for future therapeutics.

Radiation therapy is widely used in esophageal squamous cell carcinoma (ESCC). Promoting radiation sensitivity is important. Recent studies have shown that fenofibrate can inhibit the growth of several cancer lines and hypoxia-inducible factor-1α (HIF-1α) expression in MCF-7 cells. However, few studies on the radiosensitive effect of fenofibrate on ESCCs under hypoxic condition have been conducted. In this study, we assessed the radiosensitive effects of fenofibrate on human ESCC cells. In vitro experiments showed the inhibition of cytotoxic effects after ionizing irradiation. We measured cell viability and clonogenic survival rate. Flow cytometry showed that fenofibrate pretreatment promoted apoptosis. The in vivo data also suggest that fenofibrate had radiosensitizing effects in ECA-109 cells xenografted into nude mice. Western blot and immunohistochemical analyses revealed that the HIF-1α and vascular endothelial growth factor (VEGF) protein content decreased by fenofibrate. Thus, the inhibition of HIF-1α and VEGF expression in ESCC cells contributed to the radiosensitive effect. These data suggest that fenofibrate may be a potential radiosensitive drug.

Fenofibrate enhances radiosensitivity of esophageal squamous cell carcinoma by suppressing hypoxia-inducible factor-1α expression.

In this study, the expression of neural precursor cell expressed developmentally downregulated 9 (NEDD9) in benign and malignant gastric tissues was investigated, and the significance of NEDD9 in gastric cancer prognosis was explored. Immunohistochemistry was used to detect NEDD9 expression in gastric cancer, nontumor gastric, and normal gastric tissues. The relationship between NEDD9 expression in gastric cancer tissues and the clinicopathologic factors was examined using the Mann-Whitney U test. The two factors between NEDD9 expression and tumor node metastasis (TNM) stage in gastric cancer patients were analyzed by Spearman rank correlation analysis. The Kaplan-Meier method and log-rank test were used to compare the overall survival of NEDD9 negative, weak positive expression, and strong positive expression group. NEDD9 expression rates were significantly higher (P < 0.001) in gastric cancer tissues (162 out of 187, 86.6 %) compared with normal (2 out of 11, 18.2 %) and nontumor (11 out of 58, 19.0 %) gastric tissues. The upregulated NEDD9 expression in gastric cancer tissue was significantly correlated with high preoperative CEA level (P = 0.044), poor differentiation (P = 0.007), tissue invasion (P = 0.015), present lymph node metastasis (P < 0.001), and high TNM stage (P < 0.001). NEDD9 expression was positively correlated with clinical TNM stage. Advancing clinical TNM stage corresponded with higher NEDD9 expression (r s = 0.289, P < 0.001). The overall 5-year survival of gastric cancer patients with strong positive NEDD9 expression was significantly shorter compared with the survival of NEDD9 negative and weakly positive expression group. NEDD9 may be used as a biomarker in the clinical setting to predict the prognosis of gastric cancer patients.

NEDD9 overexpression correlates with poor prognosis in gastric cancer

The utility model discloses a manual oral cavity gag, including upper shed subassembly and under shed subassembly, the upper shed subassembly with it is articulated that the under shed subassembly passes through the connecting axle, the upper shed subassembly includes upper shed board (1) and first handle (3), the under shed subassembly includes under shed board (2) and second handle (4), be provided with between first handle (3) and second handle (4) elastomeric element (5), be equipped with bolt (6) on second handle (4), it wears to be equipped with the through -hole on the first handle bolt (6) are gone up and are spacing through nut (7). The utility model provides a manual oral cavity gag carries out the patient and independently opens one's mouth to train in the oral cavity when can be used to carry out oral cavity observation or radiation therapy to the patient.

Manual oral cavity gag

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