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Choi, Eun K,Terai, Kaoru,Ji, In-Mi,Kook, Yeon H,Park, Kyung H,Oh, Eun T,Griffin, Robert J,Lim, Byung U,Kim, Jin-Seok,Lee, Doo S,Boothman, David A,Loren, Melissa,Song, Chang W,Park, Heon Joo Stockton Press 2007 Neoplasia Vol.9 No.8
<P>We found that beta-lapachone (beta-lap), a novel bioreductive drug, caused rapid apoptosis and clonogenic cell death in A549 human lung epithelial cancer cells in vitro in a dose-dependent manner. The clonogenic cell death caused by beta-lap could be significantly inhibited by dicoumarol, an inhibitor of NAD(P)H:quinone oxido-reductase (NQO1), and also by siRNA for NQO1, demonstrating that NQO1-induced bioreduction of beta-lap is an essential step in beta-lap-induced cell death. Irradiation of A549 cells with 4 Gy caused a long-lasting upregulation of NQO1, thereby increasing NQO1-mediated beta-lap-induced cell deaths. Although the direct cause of beta-lap-induced apoptosis is not yet clear, beta-lap treatment reduced the expression of p53 and NF-kappaB, whereas it increased cytochrome C release, caspase-3 activity, and gammaH2AX foci formation. Importantly, beta-lap treatment immediately after irradiation enhanced radiation-induced cell death, indicating that beta-lap sensitizes cancer cells to radiation, in addition to directly killing some of the cells. The growth of A549 tumors induced in immunocompromised mice could be markedly suppressed by local radiation therapy when followed by beta-lap treatment. This is the first study to demonstrate that combined radiotherapy and beta-lap treatment can have a significant effect on human tumor xenografts.</P>
Zhang, Xinyi Cindy,Xu, Chang,Mitchell, Ryan M,Zhang, Bo,Zhao, Derek,Li, Yao,Huang, Xin,Fan, Wenhong,Wang, Hongwei,Lerma, Luisa Angelica,Upton, Melissa P,Hay, Ashley,M?ndez, Eduardo,Zhao, Lue Ping Stockton Press 2013 Neoplasia Vol.15 No.12
<P>Head and neck squamous cell carcinoma (HNSCC) is characterized by significant genomic instability that could lead to clonal diversity. Intratumor clonal heterogeneity has been proposed as a major attribute underlying tumor evolution, progression, and resistance to chemotherapy and radiation. Understanding genetic heterogeneity could lead to treatments specific to resistant and metastatic tumor cells. To characterize the degree of intratumor genetic heterogeneity within a single tumor, we performed whole-genome sequencing on three separate regions of an human papillomavirus (HPV)-positive oropharyngeal squamous cell carcinoma and two separate regions from one corresponding cervical lymph node metastasis. This approach achieved coverage of approximately 97.9% of the genome across all samples. In total, 5701 somatic point mutations (SPMs) and 4347 small somatic insertions and deletions (indels)were detected in at least one sample. Ninety-two percent of SPMs and 77% of indels were validated in a second set of samples adjacent to the discovery set. All five tumor samples shared 41% of SPMs, 57% of the 1805 genes with SPMs, and 34 of 55 cancer genes. The distribution of SPMs allowed phylogenetic reconstruction of this tumor's evolutionary pathway and showed that the metastatic samples arose as a late event. The degree of intratumor heterogeneity showed that a single biopsy may not represent the entire mutational landscape of HNSCC tumors. This approach may be used to further characterize intratumor heterogeneity in more patients, and their sample-to-sample variations could reveal the evolutionary process of cancer cells, facilitate our understanding of tumorigenesis, and enable the development of novel targeted therapies.</P>
Yong, Hae-Young,Hwang, Jin-Sun,Son, Hwajin,Park, Hae-In,Oh, Eok-Soo,Kim, Hyun-Hwi,Kim, Do Kyun,Choi, Wahn Soo,Lee, Bong-Jin,Kim, Hyeong-Reh Choi,Moon, Aree Stockton Press 2011 Neoplasia Vol.13 No.2
<P>Increased expression and/or activation of H-Ras are often associated with tumor aggressiveness in breast cancer. Previously, we showed that H-Ras, but not N-Ras, induces MCF10A human breast epithelial cell invasion and migration, whereas both H-Ras and N-Ras induce cell proliferation and phenotypic transformation. In an attempt to determine the sequence requirement directing the divergent phenotype induced by H-Ras and N-Ras with a focus on the induction of human breast cell invasion, we investigated the structural and functional relationships between H-Ras and N-Ras using domain-swap and site-directed mutagenesis approaches. Here, we report that the hypervariable region (HVR), consisting of amino acids 166 to 189 in H-Ras, determines the invasive/migratory signaling program as shown by the exchange of invasive phenotype by swapping HVR sequences between H-Ras and N-Ras. We also demonstrate that the H-Ras-specific additional palmitoylation site at Cys184 is not responsible for the signaling events that distinguish between H-Ras and N-Ras. Importantly, this work identifies the C-terminal HVR, especially the flexible linker domain with two consecutive proline residues Pro173 and Pro174, as a critical domain that contributes to activation of H-Ras and its invasive potential in human breast epithelial cells. The present study sheds light on the structural basis for the Ras isoform-specific invasive program of breast epithelial cells, providing information for the development of agents that specifically target invasion-related H-Ras pathways in human cancer.</P>
Min, H-J,Lee, M-J,Kim, J-Y,Cho, S-W,Park, H-D,Lee, S-I,Kim, H-J,Jung, H-S Stockton Press 2007 Oral diseases Vol. No.
<P>Objective: </P><P>Temporomandibular disorder (TMD) includes a number of clinical conditions involving the masticatory musculature or the temporomandibular joint (TMJ) and associated structures. Previous studies have shown the presence of high-affinity estrogen receptors in the TMJ articular cartilage. The aim of this study was to evaluate the developmental changes in mouse TMJ under estrogen deficiency.</P><P>Materials and methods: </P><P>Four-month-old ovariectomized mice were killed after certain weeks. We examined the significant alterations of the expression patterns of bone morphogenetic protein (BMP)-4, <I>Runx2</I>, and bone sialoprotein (BSP) after ovariectomy.</P><P>Results: </P><P>In the control group, BMP-4, <I>Runx2</I>, and BSP expressions showed no definite difference at any stage. In the ovariectomy group, the intensity of BMP-4 and <I>Runx2</I> expression increased after ovariectomy. BSP immunoreactivity, however, increased slightly at 2 weeks but then decreased gradually.</P><P>Conclusions: </P><P>Estrogen plays important roles in the metabolism and maintenance of TMJ via regulations of signaling molecules such as BMP-4, <I>Runx2</I>, and BSP. Our results suggest that estrogen deficiency is a candidate cause of TMD. This study revealed further osteogenetic properties of estrogen that may be useful in the clinical treatment and prevention of TMD.</P>
Factors for time to trastuzumab-induced cardiotoxicity in breast cancer patients
Lee, Mi Hyung,Yee, Jeong,Kim, Young Ju,Moon, Jin Young,Kim, Joo Hee,Rhie, Sandy Jeong,Gwak, Hye Sun STOCKTON 2017 MEDICAL ONCOLOGY -NORTHWOOD THEN BASINGSTOKE THEN Vol.34 No.12
<P>Trastuzumab is a drug used for the treatment of metastatic breast cancer patients. Due to blockage of the human epidermal growth factor receptor 2 signaling in cardiac myocytes, cardiotoxicity has been observed. There are many studies that investigated risk factors for trastuzumab-induced cardiotoxicity, but no study has been published for factors on the time to cardiotoxicity. This study aimed to investigate the factors for the time to occur trastuzumab-induced cardiotoxicity. From January 2014 to December 2015, a retrospective study was performed with breast cancer patients who were treated with trastuzumab. Associations between presence of and time to cardiotoxicity and various factors were analyzed. Based on multi-variate models, it was found that baseline left ventricular ejection fraction (LVEF) < 62.5% (AHR 5.96, 95% CI 2543-13.95) and anthracycline-based chemotherapy (AHR 7.90, 95% CI 1.05-59.71) were significant factors for time to cardiotoxicity after adjusting other confounding factors. Multivariate analysis also showed that BMI = 23 kg/m(2) and baseline LVEF value < 62.5% increased cardiotoxicity 3.0 and 6.6 times, respectively. Our study showed that BMI = 23 kg/m(2), LVEF < 62.5%, and anthracycline-based chemotherapy were associated with time to trastuzumab-induced cardiotoxicity. Thus, close monitoring of cardiac function is recommended especially for patients using the above risk factors.</P>
The effect of cortical activation on orthodontic tooth movement
Cho, K-W,Cho, S-W,Oh, C-O,Ryu, Y-K,Ohshima, H,Jung, H-S Stockton Press 2007 Oral Diseases Vol. No.
<P>Objective: </P><P>Cortical activation is one of the procedures to accelerate tooth movement by manipulating the cortical bone. In this study, the effect of cortical activation on orthodontic tooth movement was investigated clinically and histologically in the surrounding bony tissue.</P><P>Materials and methods: </P><P>In the lower and upper jaws of two beagle dogs, cortical activation was applied to the buccal and lingual side of the alveolar bone in the right jaw where 12 holes were made on each cortical plate 4 weeks after the extraction of all the second bicuspids while under deep anesthesia. All third bicuspids on both jaws were forced to move forward by a 150-g force using NiTi coil spring with/without guiding wire. The tooth movement was measured and the animals were killed after tooth movement.</P><P>Results: </P><P>Rapid initial tooth movement was apparent after cortical activation. However, after 6 months of cortical activation, the cell number and cellular activity of the surrounding periodontal tissue were decreased.</P><P>Conclusions: </P><P>This experiment showed that rapid initial tooth movement was apparent following the application of orthodontic force after cortical activation but the cellular activity and fibroblast structure were abnormal in the surrounding periodontal tissue.</P>