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Your search keyword '"Jeng, Y. M."' showing total 128 results
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128 results on '"Jeng, Y. M."'

9. Immune classification of soft tissue sarcoma predicts clinical outcome

Author

Petitprez, F., primary, de Reyniès, A., additional, Keung, E.Z., additional, Chen, T W-W, additional, Sun, C.-M., additional, Jeng, Y.-M., additional, Hsiao, L.-P., additional, Lacroix, L., additional, Lucchesi, C., additional, Toulmonde, M., additional, Burgess, M.A., additional, Bolejack, V., additional, Reinke, D., additional, Lazar, A.J., additional, Roland, C.L., additional, Wargo, J., additional, Italiano, A., additional, Sautès-Fridman, C., additional, Tawbi, H.A., additional, and Fridman, W.H., additional

Published
2019
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19. TGF-β1 secreted by Tregs in lymph nodes promotes breast cancer malignancy via up-regulation of IL-17RB

Author

Huang, S-C, Wei, P-C, Hwang-Verslues, WW, Kuo, W-H, Jeng, Y-M, Hu, C-M, Shew, J-Y, Huang, C-S, Chang, K-J, Lee, EY-H, and Lee, W-H

Subjects
Mice, Inbred BALB C, Receptors, Interleukin-17, Breast Neoplasms, Mammary Neoplasms, Animal, Mice, SCID, T-Lymphocytes, Regulatory, Up-Regulation, Transforming Growth Factor beta1, Mice, Mice, Inbred NOD, Lymphatic Metastasis, Tumor Cells, Cultured, Animals, Humans, Transplantation, Homologous, Female, Lymph Nodes, RNA, Small Interfering, Signal Transduction
Abstract

Lymph node (LN) metastasis is commonly associated with systemic distant organ metastasis in human breast cancer and is an important prognostic predictor for survival of breast cancer patients. However, whether tumor-draining LNs (TDLNs) play a significant role in modulating the malignancy of cancer cells for distant metastasis remains controversial. Using a syngeneic mouse mammary tumor model, we found that breast tumor cells derived from TDLN have higher malignancy and removal of TDLNs significantly reduced distant metastasis. Up-regulation of oncogenic Il-17rb in cancer cells derived from TDLNs contributes to their malignancy. TGF-β1 secreted from regulatory T cells (Tregs) in the TDLNs mediated the up-regulation of Il-17rb through downstream Smad2/3/4 signaling. These phenotypes can be abolished by TGF-β1 neutralization or depletion of Tregs. Consistently, clinical data showed that the up-regulation of IL-17RB in cancer cells from LN metastases correlated with the increased prevalence of Tregs as well as the aggressive growth of tumors in mouse xenograft assay. Together, these results indicate that Tregs in TDLNs play an important role in modulating the malignancy of breast cancer cells for distant metastasis. Blocking IL-17RB expression could therefore be a potential approach to curb the process.

Published
2017

29. MiR-520h-mediated FOXC2 regulation is critical for inhibition of lung cancer progression by resveratrol

Author

Yu, Y-H, primary, Chen, H-A, additional, Chen, P-S, additional, Cheng, Y-J, additional, Hsu, W-H, additional, Chang, Y-W, additional, Chen, Y-H, additional, Jan, Y, additional, Hsiao, M, additional, Chang, T-Y, additional, Liu, Y-H, additional, Jeng, Y-M, additional, Wu, C-H, additional, Huang, M-T, additional, Su, Y-H, additional, Hung, M-C, additional, Chien, M-H, additional, Chen, C-Y, additional, Kuo, M-L, additional, and Su, J-L, additional

Published
2012
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32. 16 ANALYSIS OF HBsAg LEVELS IN PATIENTS COINFECTED WITH HEPATITIS B VIRUS AND HEPATITIS C VIRUS TREATED WITH PEGINTERFERON ALFA-2A AND RIBAVIRIN

Author

Liu, C.-J., primary, Chuang, W.-L., additional, Lee, C.-M., additional, Yu, M.-L., additional, Lu, S.-N., additional, Wu, S.-S., additional, Liao, L.-Y., additional, Chen, C.-L., additional, Kuo, H.-T., additional, Chao, Y.-C., additional, Tung, S.-Y., additional, Yang, S.-S., additional, Kao, J.-H., additional, Liu, C.-H., additional, Su, W.-W., additional, Lin, C.-L., additional, Jeng, Y.-M., additional, Chen, P.-J., additional, and Chen, D.-S., additional

Published
2009
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36. CCN2 inhibits lung cancer metastasis through promoting DAPK-dependent anoikis and inducing EGFR degradation.

Author

Chang, C-C, Yang, M-H, Lin, B-R, Chen, S-T, Pan, S-H, Hsiao, M, Lai, T-C, Lin, S-K, Jeng, Y-M, Chu, C-Y, Chen, R-H, Yang, P-C, Eugene Chin, Y, and Kuo, M-L

Subjects
METASTASIS, LUNG cancer, LUNG diseases, EPIDERMAL growth factor receptors, PHOSPHORYLATION, GENE expression, ANOIKIS
Abstract

CCN family protein 2 (CCN2), also known as connective tissue growth factor, is a secreting protein that modulates multiple cellular events. We previously demonstrated the metastasis-suppressive effect of CCN2 in lung cancer cells. In this study, we investigate the role of CCN2 in anoikis, a form of programmed cell death that is critical in suppressing cancer metastasis. CCN2 binds to the epidermal growth factor receptor (EGFR) and triggers ubiquitination by inhibiting the formation of the β-pix/Cbl complex, resulting in the degradation of EGFR. Binding of CCN2 to EGFR suppresses the phosphorylation of c-Src and extracellular signal-regulated kinase but increases the expression of death-associated protein kinase, which leads to anoikis. Overall, our findings provide evidence validating the use of CCN2 as an anti-metastatic therapy in lung cancer patients, and prospect a potential therapeutic synergy between CCN2 and the anti-EGFR antibody for the treatment of lung cancer. [ABSTRACT FROM AUTHOR]

Published
2013
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37. Intravasation-Related Metastatic Factors in Colorectal Cancer

Author

Tien, Y.-W., Jeng, Y.-M., Hu, R.-H., Chang, K.-J., Hsu, S.-M., and Lee, P.-H.

Abstract

AbstractAlterations in adhesion molecules, angiogenesis, and matrix metalloproteinases have been associated with metastasis and intravasation. The present study investigated the role of these metastatic factors in the context of primary colorectal tumor. Intravasated colorectal epithelial cells were detected by an RT-PCR assay, and the expression of E-cadherin, α-catenin, or β-catenin as well as the vascularity of tumor were assessed by immunohistochemical staining. Activity of matrix metalloproteinase was assessed by gelatin zymography. The tumor venous blood was positive for guanylyl cyclase C (GCC) mRNA expression in 40 of 68 patients, but alteration in expression of E-cadherin, α-catenin, or β-catenin was not significantly associated with the presence of colorectal epithelial cells in paired portal venous blood. Further, matrix metalloproteinase activity did not correlate with the presence of intravasated colorectal epithelial cells. Multivariate analysis demonstrated that the only factor associated with intravasated colorectal tumor cells was the vascularity of the tumor. Thus, metastasis of colon cancer may result from passive entry into the circulation secondary to angiogenic factors and does not appear to involve other metastatic factors studied in our experiments.Copyright © 2004 S. Karger AG, Basel

Published
2004

38. Expression of mutant nuclear β-catenin correlates with non-invasive hepatocellular carcinoma, absence of portal vein spread, and good prognosis

Author

Mao, T-L., Chu, J-S., Jeng, Y-M., Lai, P-L., and Hsu, H-C.

Abstract

β-catenin has functions both in the cadherin-mediated cell adhesion system and in the signalling pathway that mediates dorsal axis patterning in the embryo; it has been shown to be aberrantly expressed or mutated in diverse types of human tumour, but the biological significance of this remains to be clarified. To elucidate the clinical implications of aberrant β-catenin expression and the potential differences between mutant and wild-type β-catenin protein expression in hepatocellular carcinoma (HCC), the protein expression was analysed by immunohistochemical staining, supplemented by the analysis of gene mutation. Among 372 unifocal primary HCCs, β-catenin was detected in the tumour cell membrane alone in 272 tumours (group A) and also in the nuclei in 100 (group B). In group A, 148 tumours had decreased β-catenin expression, but the reduction did not correlate with invasion or prognosis. When compared with group A, however, group B had significantly lower frequencies of hepatitis B surface antigen carrier (p=0.015), and α-fetoprotein elevation (p=0.0003), but more often had non-invasive HCC (p<0.001) and better survival (p=0.01). Nuclear β-catenin expression strongly correlated with mutation of the gene (p<0.00001). In group B, HCC with mutant nuclear β-catenin correlated positively with non-invasive (stage 1) tumour and inversely with portal vein tumour thrombi (stage 3 HCC), and had significantly better 5-year survival, p<0.001 and p<0.0003, respectively. These results suggest that β-catenin mutation plays an important role in the tumourigenesis of a subset of HCC of good prognosis, and that mutant and wild-type nuclear β-catenin proteins are not functionally equivalent. Copyright © 2000 John Wiley & Sons, Ltd.

Published
2001

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