Given its role in tumorigenesis and its correlation with various pathologic features of colorectal cancer (CRC), DEK is considered to have the potential to predict CRC prognosis. This review attempts to summarize current knowledge and evidence supporting the potential of DEK as a prognostic biomarker of CRC. We searched meta-analyses, systematic reviews, cohort studies, and cell line studies published in the last 10 years. A literature search was conducted in PubMed, Pubmed Central (PMC), Proquest, EBSCOHost, Scopus, and Cochrane Library using the keywords ‘colorectal/colon/rectal cancer’, ‘DEK’, ‘biomarker’, and ‘prognosis’. Studies that were not published in English, without accessible full text, unrelated to clinical questions, or conducted with a design unsuitable for the eligibility criteria were excluded. Seven included studies reported the potential of DEK as a prognostic biomarker of CRC and its role in cancer cell proliferation, invasion, and metastasis. This role is achieved through the Wnt/β-catenin pathway, prevention of apoptosis through destabilization of p53, and bridging inflammation and tumorigenesis through the nuclear factor (NF)-κB pathway, causing chronic inflammation and activation of tumorigenic genes. DEK overexpression is also associated with CRC clinical and pathological features, such as tumor size, lymph node metastasis, serosal invasion, differentiation, tumor staging, and epithelial-mesenchymal transition. DEK overexpression was found to be associated with lower survival and recovery rates. Its prognostic value was comparable with other prognostic biomarkers of CRC, such as BRAF, topoisomerase-1, and CEA. A cohort study reported that DEK overexpression was associated with a better response to fluoropyrimidine-based chemotherapy, while a cell-line study indicated a correlation between DEK overexpression with a worse response to irinotecan-based chemotherapy. In conclusion, considering its correlation with CRC pathology, its association with worse CRC patient survival, and its possibility to forecast the therapeutic response of various chemotherapeutic regimens, DEK has the potential to be used as a CRC prognostic biomarker.
A deadly and debilitating disease, colorectal cancer (CRC), is rapidly becoming a significant threat to public health. However, current therapeutic approaches are still hampered by various side effects. Due to its benefits and remarkable apoptotic impact on cancer cells, plant-derived flavonoids now garner interest as candidates for cancer therapy. Isoquercitrin, a flavonoid commonly found in fruit plants, especially mangoes, is notable due to its ability to inhibit cancer development through various mechanisms. This review aims to highlight the use of isoquercitrin extracted from mango peels in inhibiting CRC carcinogenesis. A literature search was done on Pubmed, Proquest, and Google Scholar using inclusion and exclusion criteria, and a narrative review was synthesised using the evidence gathered. Validity assessment was done through the the Office of Health Assessment and Translation (OHAT) and Oxford Center for Evidence-Based Medicine (CEBM) critical assessment tools. Evidence suggested that isoquercitrin is promising as adjuvant therapy in CRC. It may inhibit overaccumulation of cytoplasmic β-catenin and its translocation into the nucleus, thus downregulating the expression of target proto-oncogenes leading to carcinogenesis of colon crypts. Isoquercitrin concentration in mango peel is abundant, 557.7 mg/kg in dried mango peel and 31.0 mg/kg in pure extracts. A pharmacology study approved that a daily intake of 5.4 mg/kgBW of isoquercitrin has an effective anticancer effect. This substance has good oral bioavailability and is well-tolerated but inhibits the metabolising enzymes CYP1A1 and CYP1B1. In conclusion, isoquercitrin is a potential adjuvant in inhibiting CRC growth with minimum costs and side effects.
Urinary tract infections (UTIs) are among the most common infections globally, with 150-250 million annual cases. In recent years, there has been an emerging trend of complicated UTIs, partly due to the resistance of uropathogens to commonly used first-line antibiotics. At its worst, antimicrobial resistance increases in-patient time, treatment costs, and the risk of complications and mortality. Resistance also gravely reduces treatment options. The writers review the literature published in 2013-2023 found on Pubmed, EBSCO-Host, and Google Scholar using several combination keywords: "new treatment," "urinary tract infection," "bacteria," "antimicrobial," and "resistance." Thirty-three in-vitro, three animal models (in-vivo), and one multicentre cohort study were found on the composite chitosan, silver nanoparticle, and graphene oxide (Chit-AgNP-GO), and its components. This bioactive material possesses a bactericidal and bacteriostatic effect against Gram-positive and Gram-negative uropathogens. Chit-AgNP-GO has multiple mechanisms of action for each component involved, with literature suggesting good antimicrobial activity for each. Silver destroys bacterial enzymes necessary for electron transfer, disrupts DNA synthesis, and destroys proteins integral to the bacterial structure. Chitosan facilitates adhesion to bacterial cell membranes and can contribute to bacterial cellular leakage. Graphene oxide affects bacterial liposolubility and permeability. The multiple mechanisms of action generated by this antimicrobial make it a promising agent to study in UTI cases, especially those complicated by uropathogenic resistance. However, validating this nanomaterial may be challenging due to the limited number of clinical studies. Therefore further in vivo, and clinical research protocols are highly required to confirm its antimicrobial potential in the clinical setting.
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