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Your search keyword '"Kim, Sun-Jin"' showing total 17 results
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17 results on '"Kim, Sun-Jin"'

1. Gain of Glucose-Independent Growth upon Metastasis of Breast Cancer Cells to the Brain

Author

Chen, Jinyu, primary, Lee, Ho-Jeong, additional, Wu, Xuefeng, additional, Huo, Lei, additional, Kim, Sun-Jin, additional, Xu, Lei, additional, Wang, Yan, additional, He, Junqing, additional, Bollu, Lakshmi R., additional, Gao, Guang, additional, Su, Fei, additional, Briggs, James, additional, Liu, Xiaojing, additional, Melman, Tamar, additional, Asara, John M., additional, Fidler, Isaiah J., additional, Cantley, Lewis C., additional, Locasale, Jason W., additional, and Weihua, Zhang, additional

Published
2015
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2. Abstract 10: Characterization of CD45-/CD31+/CD105+ circulating cells in the peripheral blood of patients with gynecological malignancies

Author

Yu, Hyun-Kyung, primary, Lee, Ho-Jeong, additional, Choi, Ha-Na, additional, Ahn, Jin-Hyung, additional, Choi, Ji-Young, additional, Jeong, Eun-Jeong, additional, Seok, Hyun-Jeong, additional, Song, Haengseok, additional, Lee, Ki-Heon, additional, Yi, Lee S.H., additional, Kim, Sun Jin, additional, Kim, Tae Jin, additional, and Kim, Jang-Seong, additional

Published
2014
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5. Abstract 5481: Therapy of human LN229 glioblastoma growing in the brain of nude mice by Macitentan, a dual endothelin receptor A and B antagonist, combined with Temozolomide.

Author

Kim, Sun Jin, primary, Kim, Seung Wook, additional, Choi, Hyun Jin, additional, Lee, Ho Jeong, additional, Lehembre, Francois, additional, He, Junqin, additional, Regenass, Urs, additional, Conrad, Charles A, additional, Yung, W.K., additional, and Fidler, Isaiah J., additional

Published
2013
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7. Abstract 601: Macitentan (ACT-064992), a tissue-targeting endothelin receptor antagonist enhances therapeutic efficacy of paclitaxel by modulating survival pathways in orthotopic models of metastatic human ovarian cancer

Author

Kim, Sun Jin, primary, Kim, Jang Seong, additional, Kim, Seung Wook, additional, Brantley, Emily C., additional, Yun, Seok Joong, additional, He, Junqin, additional, Marva, Maya K., additional, Zhang, Fahao, additional, Wu, Qiuyu, additional, Lehembre, Francois, additional, Regenass, Urs, additional, and Fidler, Isaiah J., additional

Published
2011
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8. Abstract 3428: Astrocytes upregulate survival genes in tumor cells and induce protection from chemotherapy

Author

Kim, Sun Jin, primary, Kim, Jang-Seong, additional, Park, Eun Sung, additional, Lee, Ju-Seog, additional, Lin, Qintang, additional, Langley, Robert R., additional, Maya, Marva, additional, He, Junqin, additional, Kim, Seung Wook, additional, Weihua, Zhang, additional, Balasubramanian, Krishnakumar, additional, Fan, Dominc, additional, Mills, Gordon B., additional, Hung, Mien-Chie, additional, and Fidler, Isaiah J., additional

Published
2010
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11. Antivascular Therapy of Human Follicular Thyroid Cancer Experimental Bone Metastasis by Blockade of Epidermal Growth Factor Receptor and Vascular Growth Factor Receptor Phosphorylation

Author

Younes, Maher Nabil, primary, Yigitbasi, Orhan Gazi, additional, Park, Young Wook, additional, Kim, Sun-Jin, additional, Jasser, Samar A., additional, Hawthorne, Valerie Stone, additional, Yazici, Yasemin Dakak, additional, Mandal, Mahitosh, additional, Bekele, Benjamin Nebiyou, additional, Bucana, Corazon D., additional, Fidler, Isaiah J., additional, and Myers, Jeffrey N., additional

Published
2005
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13. Dual Inhibition of Epidermal Growth Factor Receptor and Vascular Endothelial Growth Factor Receptor Phosphorylation by AEE788 Reduces Growth and Metastasis of Human Colon Carcinoma in an Orthotopic Nude Mouse Model

Author

Yokoi, Kenji, primary, Thaker, Premal H., additional, Yazici, Sertac, additional, Rebhun, Robert R., additional, Nam, Do-Hyun, additional, He, Junqin, additional, Kim, Sun-Jin, additional, Abbruzzese, James L., additional, Hamilton, Stanley R., additional, and Fidler, Isaiah J., additional

Published
2005
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14. Simultaneous Blockade of Platelet-Derived Growth Factor-Receptor and Epidermal Growth Factor-Receptor Signaling and Systemic Administration of Paclitaxel as Therapy for Human Prostate Cancer Metastasis in Bone of Nude Mice

Author

Kim, Sun Jin, primary, Uehara, Hisanori, additional, Yazici, Sertac, additional, Langley, Robert R., additional, He, Junqin, additional, Tsan, Rachel, additional, Fan, Dominic, additional, Killion, Jerald J., additional, and Fidler, Isaiah J., additional

Published
2004
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16. Blockade of epidermal growth factor receptor signaling leads to inhibition of renal cell carcinoma growth in the bone of nude mice.

Author

Weber KL, Doucet M, Price JE, Baker C, Kim SJ, and Fidler IJ

Subjects
Animals, Antineoplastic Combined Chemotherapy Protocols pharmacology, Apoptosis drug effects, Bone Neoplasms drug therapy, Carcinoma, Renal Cell blood supply, Carcinoma, Renal Cell drug therapy, Cell Division drug effects, Cell Division physiology, Epidermal Growth Factor pharmacology, ErbB Receptors metabolism, ErbB Receptors physiology, Humans, Kidney Neoplasms blood supply, Male, Mice, Mice, Nude, Paclitaxel administration & dosage, Phosphorylation drug effects, Pyrimidines administration & dosage, Pyrroles administration & dosage, Recombinant Proteins pharmacology, Signal Transduction drug effects, Transforming Growth Factor alpha pharmacology, Tumor Cells, Cultured, Xenograft Model Antitumor Assays, Bone Neoplasms prevention & control, Bone Neoplasms secondary, Carcinoma, Renal Cell prevention & control, Carcinoma, Renal Cell secondary, ErbB Receptors antagonists & inhibitors, Kidney Neoplasms drug therapy, Kidney Neoplasms pathology, Pyrimidines pharmacology, Pyrroles pharmacology
Abstract

Renal cell carcinoma (RCC) frequently produces metastases to the musculoskeletal system that are a major source of morbidity in the form of pain, immobilization, fractures, neurological compromise, and a decreased ability to perform activities of daily living. Patients with metastatic RCC therefore have a dismal prognosis because there is no effective adjuvant treatment for this disease. Because the epidermal growth factor receptor (EGF-R) signaling cascade is important in the growth and metastasis of RCC, its blockade has been hypothesized to inhibit tumor growth and hence prevent resultant bone destruction. We determined whether blockade of EGF-R by the tyrosine kinase inhibitor PKI 166 inhibited the growth of RCC in bone. We use a novel cell line, RBM1-IT4, established from a human RCC bone metastasis. Protein and mRNA expression of the ligands and receptors was assessed by Western and Northern blots. The stimulation of RBM1-IT4 cells with epidermal growth factor or transforming growth factor alpha resulted in increased cellular proliferation and tyrosine kinase autophosphorylation. PKI 166 prevented these effects. First, RBM1-IT4 cells were implanted into the tibia of nude mice, where they established lytic, progressively growing lesions, after which the mice were treated with PKI 166 alone or in combination with paclitaxel (Taxol). Immunohistochemical analysis revealed that tumor cells and tumor-associated endothelial cells in control mice expressed activated EGF-R. Treatment of mice with PKI 166 alone or in combination with Taxol produced a significant decrease in the incidence and size of bone lesions as compared with the results in control or Taxol-treated mice (P < 0.001). Treatment with PKI 166 also decreased the expression of phosphorylated EGF-R by tumor cells and tumor-associated endothelial cells, and this was even more pronounced with PKI 166 plus Taxol treatment. The PKI 166 plus Taxol combination produced apoptosis of tumor cells and tumor-associated endothelial cells. Tumor cell proliferation, shown by proliferating cell nuclear antigen positivity, was decreased in all treatment groups. In addition, the integrity of the bone was maintained in mice treated with PKI 166 or PKI 166 plus Taxol, whereas massive bone destruction was seen in control and Taxol-treated mice. These results suggest that blockade of EGF-R signaling inhibits growth of RCC in the bone by its effect on tumor cells and tumor-associated endothelial cells.

Published
2003

17. Inhibition of growth and metastasis of orthotopic human prostate cancer in athymic mice by combination therapy with pegylated interferon-alpha-2b and docetaxel.

Author

Huang SF, Kim SJ, Lee AT, Karashima T, Bucana C, Kedar D, Sweeney P, Mian B, Fan D, Shepherd D, Fidler IJ, Dinney CP, and Killion JJ

Subjects
Angiogenesis Inhibitors administration & dosage, Animals, Antineoplastic Agents, Phytogenic administration & dosage, Cadherins biosynthesis, Cell Division drug effects, Docetaxel, Dose-Response Relationship, Drug, Drug Synergism, Fibroblast Growth Factor 2 biosynthesis, Humans, Immunohistochemistry, Interferon alpha-2, Interferon-alpha administration & dosage, Male, Matrix Metalloproteinase 2 biosynthesis, Matrix Metalloproteinase 9 biosynthesis, Mice, Mice, Nude, Neoplasm Metastasis prevention & control, Paclitaxel administration & dosage, Polyethylene Glycols administration & dosage, Prostatic Neoplasms blood supply, Prostatic Neoplasms metabolism, Prostatic Neoplasms pathology, Random Allocation, Recombinant Proteins, Xenograft Model Antitumor Assays, Angiogenesis Inhibitors pharmacology, Antineoplastic Agents, Phytogenic pharmacology, Antineoplastic Combined Chemotherapy Protocols pharmacology, Interferon-alpha pharmacology, Paclitaxel analogs & derivatives, Paclitaxel pharmacology, Polyethylene Glycols pharmacology, Prostatic Neoplasms drug therapy, Taxoids
Abstract

We evaluated whether treatment of orthotopic human prostate cancer in nude mice with pegylated IFN-alpha-2b (PEG-IFN-alpha-2b) and docetaxel could represent a two-compartment targeting of primary tumor (tumor cells and tumor-associated endothelial cells) and inhibition of regional lymph node metastasis. The antiangiogenic properties of IFN were combined with the cytotoxic properties of docetaxel, resulting in apoptosis of both tumor cells and endothelium and hence significant inhibition of primary tumor growth. We first determined the optimal biological dose of PEG-IFN-alpha-2b (70,000 IU/week) necessary to down-regulate the expression of basic fibroblast growth factor, matrix metalloprotease-9, and matrix metalloprotease-2. The therapeutic dose of docetaxel (10 mg/kg/week) was determined by efficacy and minimal body weight loss. Therapy beginning 3 days after orthotopic implantation of PC3-MM2 prostate cancer cells reduced tumor weight by 37% in mice treated with PEG-IFN-alpha-2b, by 60% in mice treated with docetaxel, and by 83% in those given both drugs. PEG-IFN-alpha-2b also induced apoptosis of tumor-associated endothelial cells and hence a significant decrease in microvessel density. Our data indicate that the combination of PEG-IFN-alpha and docetaxel inhibits neoplastic angiogenesis by inducing a decrease in the local production of proangiogenic molecules by tumor cells, resulting in increased apoptosis of tumor-associated endothelial cells.

Published
2002

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