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Comparability of Health-Promoting Behaviors associated with Student nurses From various Racial/Ethnic Organizations.
005). The 5-year overall survival rate was worse in the high-expression group as compared with that in the low-expression group (51.6% vs. 74.4%, p=0.008). High GPR56 expression was a significant prognostic factor for overall survival of CRC patients in the univariate (p=0.001) and multivariate (p less then 0.001) analyses. The expression level of GPR56 plays an important role in tumor progression in CRC, and it may serve as a prognostic indicator in CRC patients.As a core scaffold protein, Cullin 7 (Cul7) forms Skp1-Cullin-F-box (SCF) E3 ubiquitin ligase complexes with the regulator of cullins-1 (ROC1), S-phase kinase associated protein 1 (Skp1) and F-Box, and WD repeat domain containing 8 (Fbxw8). Alternatively, Cul7 can form a CRL7SMU1 complex with suppressor of Mec-8 and Unc-52 protein homolog (SMU1), damage-specific DNA binding protein 1 (DDB1), and ring finger protein 40 (RNF40), to promote cell growth. The mutations of Cul7 cause the 3-M dwarf syndrome, indicating Cul7 plays an important role in growth and development in humans and mice. Moreover, Cul7 regulates cell transformation, tumor protein p53 activity, cell senescence, and apoptosis, mutations in Cul7 are also involved in the development of tumors, indicating the characteristics of an oncogene. Cul7 is highly expressed in breast cancer, lung cancer, hepatocellular carcinoma, pancreatic cancer, ovarian cancer, and other malignant tumors where Cul7 promotes tumor development, cell transformation, and cell survival by regulating complex signaling pathways associated with protein degradation. In this review, we discuss the roles of Cul7 in malignant tumor development and its involvement in oncogenic signaling. We finally discuss the potential of Cul7 as a potential significant anti-cancer target.Chromosome 7 plays an important role in lung tumorigenesis. Chromosome 7 copy number changes might be an early event of lung cancer tumorigenesis. Here we investigate whether chromosome 7p copy number gain is a detectable genetic event with plasma cell-free DNA for early lung cancer detection. Eighteen surgical eligible lung cancer patients and eighteen non-cancer controls were recruited. Peripheral blood was collected before surgery. Cell-free DNA was profiled with low coverage whole-genome sequencing. Chromosome 7 copy number gains were defined as chr7 normalized coverage ≥1.0005 and p-value less then 0.05. Plasma cell-free DNA chr7 copy gains were then compared to pathological examinations on surgical tissues. 83.3% of patients were confirmed as malignancy post-operation, 12 patients with adenocarcinoma, and 3 with squamous-carcinoma. The other 16.7% were benign lesions. Cell-free DNA was successfully extracted from pre-surgical plasma samples, with a concentration range from 0.18 to 0.49 ng/µl. Chromosome 7 short arm copy gains were found in 66.7% (10/15) patients, including 66.7% (4/6) T1aN0M0 and 50.0% (1/2) Tis patients, otherwise, chr7p gain was found in 0% (0/3) benign lesions. The specificity was further examined in 18 volunteers who undergoing routine body examinations. Meanwhile, positive carcinoembryonic antigen (CEA) and cytokeratin-19-fragment (CYFRA21-1) were only found in 1/18 (5.7%) and 4/18 (22.2%), respectively. Taking together, Ultrasensitive- Chromosomal Aneuploidy Detector (UCAD) chr7p or UCAD chr7p and tumor biomarker positivity can predict 12/15 (80%, 95% CI 49.0-94.3%) early lung cancers. Further analyses showed that chr7p copy number gains tend to be enriched in normal EGFR/KRAS patients (Fisher's test, p-value = 0.077). Chromosome 7p copy gain is a useful peripheral blood tumor biomarker from lung cancer detection.Hepatocellular carcinoma (HCC) is one of the most aggressive types of cancer and currently lacks effective treatment strategies. The present study revealed that deoxyribonuclease 1 like 3 (DNase1L3) expression levels were significantly downregulated in numerous types of gastrointestinal cancer, and especially in HCC. Tissue microarrays were further used to illustrate that DNase1L3 expression levels were frequently downregulated in HCC tissues compared with normal liver tissues. In addition, DNase1L3 expression levels were identified to be significantly associated with tumor size (p=0.0028), tumor thrombus formation (p less then 0.01), and a poorer overall survival (p=0.005) and disease-free survival (p=0.006) of HCC. Gene Ontology functional term enrichment analysis of biological processes discovered that DNase1L3 was significantly associated with complement activation. Further studies demonstrated that the ectopic expression of DNase1L3 suppressed cell growth and inhibited the PI3K/AKT signaling pathway activation following C3a receptor agonist treatment. In conclusion, the findings of the present study suggested, for the first time, that DNase1L3 may serve as a biomarker for the prognosis of patients with HCC, and may suppress HCC growth via inhibiting the PI3K/AKT signaling pathway.Despite the high efficacy of current induction regimens, most multiple myeloma (MM) patients relapse over time. The link between changes in the immune system and the prognosis of the disease is still not entirely clear. Therefore, we analyzed whether the pattern of bone marrow (BM) lymphocytes during routine BM examination after autologous stem cell transplant (ASCT) is related to disease prognosis or MRD negative complete remission. From 2009 to 2018, 98 MM patients underwent routine BM testing after the first ASCT. Using multi-parametric flow cytometry, twelve BM lymphocyte subtypes were analyzed. In 60% of patients who achieved a complete response (CR), MRD by flow cytometric analysis (sensitivity threshold 10-6) was evaluated. 680C91 We found an association of relative proportion of BM lymphocyte subtypes with treatment response, progression-free survival (PFS), overall survival (OS), and minimal residual disease (MRD) negativity. Higher relative proportion of memory B cells was associated with inferior median PFS [HR 1.089 (95% CI 1.023-1.160), p=0.008] and median OS [HR 1.170 (95% CI 1.074-1.274), p less then 0.001]. In non-responding patients (minimal response and worse), higher proportion of memory B cells was found when compared to patients achieving CR [3.8% (range 0.5-35.0) vs. 1.0% (range 0.1-12.5); p=0.001]. No significant association of BM lymphocyte subtypes proportion with MRD negative CR was found. Our results show that changes in BM lymphocyte subsets including memory B cells may have prognostic value in MM patients after ASCT.
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