Notes

Book isoforms associated with coryza computer virus PA-X and also PB1-F2 shown by computerized annotation.
In HT1080 cells, the IC50 value of PM was 0.16 µM at 24 h and 0.13 µM at 48 h. PM treatment also decreased the levels of phosphorylated AKT, mTOR, NF-κB and phosphorylated ERK in a dose-dependent manner. In the PM injection group, the increase in tumor volume was significantly reduced and the effect on weight loss and liver and renal function were revealed to be insignificant. PM exerted little effect on normal human dermal fibroblasts and was highly effective against human fibrosarcoma cells. The results indicated that PM may be used as a potential therapeutic agent against fibrosarcoma. Copyright © 2020, Spandidos Publications.B-cell acute lymphoblastic leukemia (B-ALL) is a hematopoietic malignancy characterized by overproduction of immature B-lymphoblasts. B-ALL is the most common pediatric tumor and remains the leading cause of mortality in children and adolescents. Molecular and cytogenetic analyses of B-ALL revealed recurrent genetic and structural genomic alterations which are routinely applied for diagnosis, prognosis and choice of treatment regimen. The present case report describes a 4-year-old female diagnosed with B-ALL. GTG-banding at low resolution revealed an abnormal clone with 46,XX,?t(X;19)(q13;q13.3),der(9) besides normal cells. Molecular cytogenetics demonstrated a balanced translocation between chromosomes 16 and 19, and an unbalanced translocation involving chromosomes 5 and 9. A locus-specific probe additionally identified that the FUS gene in 16p11.2 was split and its 5' region was translocated to subband 19q13.33, whereas the 3' region of the FUS gene remained on the derivative chromosome 16. Overall, this complex karyotype included four different chromosomes and five break events. Further analyses, including array-comparative genomic hybridization, additionally revealed biallelic deletion of the tumor suppressor genes CDKN2A/B, and deletion of the NR3C1 and VPREB1 genes. The patient passed away under treatment due to sepsis. Copyright © 2020, Spandidos Publications.Effects of Rapamycin on the proliferation and apoptosis of retinoblastoma cells through the phosphatidylinositol 3-hydroxy kinase (PI3K)/protein kinase B (AKT) signaling pathway were studied. The retinoblastoma Y79 cells were selected and divided into negative control group (NC group), 0.2 µM Rapamycin group and 0.4 µM Rapamycin group. Then the proliferative activity of Y79 cells was detected using Cell Counting Kit-8 (CCK8) assay, the content of reactive oxygen species (ROS), malondialdehyde (MDA) and superoxide dismutase (SOD) in cells in each group was detected using enzyme-linked immunosorbent assay (ELISA), and the apoptosis of Y79 cells was detected via terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay. Moreover, the changes in Y79 cell cycle and apoptosis were determined through flow cytometry, and apoptosis and PI3K/AKT pathway were detected using reverse transcription-polymerase chain reaction (RT-PCR) and western blotting. It was found that the number of cells and the proliferative activity were significantly reduced in 0.2 µM Rapamycin group and 0.4 µM Rapamycin group. In 0.2 µM Rapamycin group and 0.4 µM Rapamycin group, the content of ROS and MDA was significantly decreased, while that of SOD was notably increased. TUNEL assay and flow cytometry showed that in 0.2 µM Rapamycin group and 0.4 µM Rapamycin group, the number of apoptotic cells was obviously increased, and the cell cycle was basically arrested in S phase. The expression levels of Bcl-2, PI3K and AKT declined in 0.2 µM Rapamycin group and 0.4 µM Rapamycin group, whereas the expression of Caspase 8 increased. selleck chemicals Similar results were also obtained in the protein assay. The above results were significantly superior in 0.4 µM Rapamycin group to those in 0.2 µM Rapamycin group. Rapamycin inhibits proliferation and promotes apoptosis of retinoblastoma cells through inhibiting the PI3K/AKT signaling pathway. Copyright © Yao et al.The high expression of metabolic enzymes, including glutaminase (GA) and lactate dehydrogenase A (LDHA), which contribute to bioenergetics and biosynthesis of mammalian cells, has been identified in a variety of cancer types. The current study indicated intratumoral heterogeneity with respect to protein expression of the metabolic enzymes in colorectal cancer (CRC). GA protein expression was determined using immunohistochemistry in 98 cases of surgically resected T3 CRC. A total of 75 cases (74%) exhibited moderate to strong immunopositivity of GA based on whole-section examination. A significant correlation was demonstrated between GA expression and clinicopathological features, including histological type and tumor budding in a patient population. Detailed histological analysis revealed the upregulation of GA protein expression at the invasive margin, including tumor budding of CRC tissues. Semi-quantitative examination revealed a significant difference in immunoexpression level of GA between the invasive margin and central CRC. However, LDHA expression exhibited an opposite pattern, with expression elevated at the center and significantly decreased at the tumors invasive margin. Immunohistochemical expression of another glycolytic enzyme hexokinase II was equivalent in both regions. Furthermore, gene silencing of GLS1, which encodes GA protein, and GA inhibitor treatment significantly inhibited cell growth of CRC cell lines. Therefore, the results of the present study demonstrated that the alteration in GA and LDHA expression is more prominent at the invasive margin, which involves tumor budding in CRC. Copyright © Mizuno et al.The aim of the present study was to examine the association between plasma heavy metals and the metabolome in patients with breast cancer (BC), and the association with cancer development. Nuclear magnetic resonance was used to determine the metabolites involved and an inductively coupled plasma mass spectrometry system was used to quantify the heavy metals in the plasma samples. It was indicated that cadmium was significantly higher in the plasma of patients with BC compared with that in the control population (~15-fold increase). Chromium, arsenic and lead were also elevated in the plasma of patients with BC by ~3.24, 2.14 and 1.52 fold, respectively. A number of small molecules, including amino acids and salts, were altered in the plasma of patients with BC compared with the control population. Another notable finding in this investigation was that plasma lipid levels were elevated in patients with BC compared with those in the control population. The findings of the present study suggest that exposure to heavy metals, including cadmium, arsenic, chromium and lead, may influence blood lipid levels and other small molecule metabolites, which in turn may be involved in BC development.
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