Left lateral decubitus sleeping position is associated with improved gastroesophageal reflux disease symptoms: A systematic review and meta-analysis.

BACKGROUND: A limited number of studies have demonstrated that sleeping in the left lateral decubitus (LLD) decreases nocturnal reflux in patients with gastroesophageal reflux disease (GERD) compared to right lateral decubitus (RLD) and supine. AIM: This systematic review summarizes the association between sleeping in the LLD position and nocturnal reflux in patients with GERD. METHODS: Studies published up to July 17, 2023, in MEDLINE, EMBASE, and CENTRAL were searched. Eligible studies were randomized and nonrandomized studies assessing the effect of sleeping in LLD compared to RLD and supine in reducing nocturnal reflux in GERD patients. Outcomes include the acid exposure time (AET) (% time in pH<4), acid clearance time (ACT) (in sec/episode), number of reflux episodes, and improvement in N-GSSIQ scores. RESULTS: Two nonrandomized studies showed decreased AET and ACT in LLD sleep position in comparison to RLD (mean difference [MD] -2.03 [95%CI: -3.62 to -0.45]; -81.84 [95%CI: -127.48 to -36.20], respectively) and supine position (MD -2.71 [95%CI: -4.34 to -1.09]; -74.47 [95%CI: -116.26 to -32.69], respectively). There was no difference in AET and ACT between RLD sleep position and supine. Furthermore, one randomized controlled trial investigating the use of electronic sleep positional therapy, which increased the duration of LLD sleep and decreased the duration of RLD sleep compared to sham, showed nocturnal symptoms improvement (improved N-GSSIQ score, increased reflux-free nights, and resolution of nocturnal reflux symptoms). CONCLUSION: Current evidence suggests that sleeping on the left side could reduce nocturnal reflux and improve GERD-related quality of life, therefore warranting interventions that promote LLD sleep position.

Role of DEK in carcinogenesis, diagnosis, prognosis, and therapeutic outcome of breast cancer: An evidence-based clinical review.

Breast cancer is a significantly burdening women's cancer with limited diagnostic modalities. DEK is a novel biomarker overexpressed in breast cancers, currently exhaustively researched for its diagnosis and prognosis. Search for relevant meta-analyses, cohorts, and experimental studies in the last fifteen years was done in five large scientific databases. Non-English, non-full text articles or unrelated studies were excluded. Thirteen articles discussed the potential of DEK to estimate breast cancer characteristics, treatment outcomes, and prognosis. This proto-oncogene plays a role in breast carcinogenesis, increasing tumour proliferation and invasion, preventing apoptosis, and creating an immunodeficient tumour milieu with M2 tumour-associated macrophages. DEK is also associated with worse clinicopathological features and survival in breast cancer patients. Using a Kaplan-Meier plotter data analysis, DEK expression predicts worse overall survival (HR 1.24, 95%CI: 1.01-1.52, p = 0.039), comparable to other biomarkers. DEK is a promising novel biomarker requiring further research to determine its bedside applications.

Potential of DEK proto-oncogene as a prognostic biomarker for colorectal cancer: An evidence-based review.

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/ß-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.