전윤근 동문 축하
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- 작성자 : sgskim
- 작성일 : 2006-12-08
- 조회 : 1,282회
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Penn State University 의과대학 내분비내과 (Endocrinology)에서 임상 fellow를 하고 있는 전 윤근 동문의 논문이 출판되었습니다. 그곳 과장님이신 Dr. Andrea Manni 선생님께서 지난 암심포지움 시 우리 학교에 방문하셔서 전 윤근 선생님에 대해서 많은 칭찬을 하셨습니다. 특히 경희의대에서 기초의학 석사를 하면서 출판한 두 편의 논문 (Hepatology, BBRC)이 전 윤근 선생님을 fellow로 선발하는데 많은 도움을 주었다고 합니다. 당시에 전 윤근 선생님은 Penn State University 의과대학을 졸업하고 그곳 대학 병원에서 레지던트를 마친 2명을 물리치고 fellow로 선발되었다고 합니다. 아래 논문은 fellow 하면서 6개월 간 간간히 실험을 하여 출판하였다고 합니다. 임상, 연구 양면 모두에 매우 우수하다고 전 윤근 선생님을 많이 칭찬하였습니다. Dr. Manni께서 교수 요원으로 육성하고 싶다는 강력한 희망의 말씀도 하셨습니다. 전 윤근 선생님이 훌륭한 학자로 성장할 수 있도록 많은 성원 바랍니다. 전 윤근 선생님처럼 경희의대 기초의학 교실에서 튼튼한 소양을 쌓아 훌륭한 의학자가 될 수 있는 초석을 마련하는 경희의대, 의학전문대학원 학생들이 많이 나오기를 기원합니다.
아래는 최근 출판된 논문입니다.
Effects of polyamine depletion by α-difluoromethylornithine on in vitro and in vivo biological properties of 4T1 murine mammary cancer cells
Journal Breast Cancer Research and Treatment
Publisher Springer Netherlands
ISSN 0167-6806 (Print) 1573-7217 (Online)
Subject Medicine
Status
Category Clinical Study
DOI 10.1007/s10549-006-9432-4
Online Date Saturday, December 02, 2006
Clinical Study
Effects of polyamine depletion by α-difluoromethylornithine on in vitro and in vivo biological properties of 4T1 murine mammary cancer cells
John Yoonkeun Jun1, James W. Griffith2, Richard Bruggeman3, Sharlene Washington1, Laurence M. Demers1, 3, Michael F. Verderame1, 4 and Andrea Manni1
(1) Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, Pennsylvania State University College of Medicine, 500 University Drive, Hershey, PA 17033, USA
(2) Department of Comparative Medicine, Pennsylvania State University College of Medicine, Hershey, PA, USA
(3) Department of Pathology, Pennsylvania State University College of Medicine, Hershey, PA, USA
(4) Department of Microbiology and Immunology, Pennsylvania State University College of Medicine, Hershey, PA, USA
Received: 5 October 2006 Accepted: 11 October 2006 Published online: 2 December 2006
Abstract Increased polyamine synthesis has been associated with proliferation and progression of breast cancer, and thus, is a potential target for anti-cancer therapy. Polyamine depletion by DFMO has been shown to decrease pulmonary and bone metastasis from human breast cancer cell xenografts. Following these observations, this study was designed to test the effects of DFMO on in vitro and in vivo features of the highly invasive and metastatic 4T1 murine mammary cancer cells. DFMO inhibited proliferation, caused G1-S arrest, and suppressed in vitro invasiveness of 4T1 cells. In contrast to our previous findings with MDA-MB-435 cells, DFMO did not affect the activation of STAT3, JNK, and ERK, but decreased phosphorylation of p38. DFMO did not alter the expression of Twist. DFMO delayed the orthotopic growth of 4T1 xenografts in association with suppressed putrescine and spermidine levels but increased levels of spermine. DFMO did not affect pulmonary metastasis when primary tumors of control and DFMO-treated mice were matched for size. Interestingly, DFMO reduced Ki-67 expression only in the primary tumors but did not affect its expression in the metastatic tumors in the lung. Cleaved caspase-3 expression was not affected by DFMO in either the primary tumors or pulmonary metastasis. In summary, DFMO treatment markedly inhibited in vitro proliferation and invasiveness of 4T1 cells and retarded the growth of orthotopic xenografts in mice. The failure of DFMO to inhibit pulmonary metastasis in this system appears to be due, at least in part, to its lack of anti-proliferative effect at the metastatic sites.
아래는 최근 출판된 논문입니다.
Effects of polyamine depletion by α-difluoromethylornithine on in vitro and in vivo biological properties of 4T1 murine mammary cancer cells
Journal Breast Cancer Research and Treatment
Publisher Springer Netherlands
ISSN 0167-6806 (Print) 1573-7217 (Online)
Subject Medicine
Status
Category Clinical Study
DOI 10.1007/s10549-006-9432-4
Online Date Saturday, December 02, 2006
Clinical Study
Effects of polyamine depletion by α-difluoromethylornithine on in vitro and in vivo biological properties of 4T1 murine mammary cancer cells
John Yoonkeun Jun1, James W. Griffith2, Richard Bruggeman3, Sharlene Washington1, Laurence M. Demers1, 3, Michael F. Verderame1, 4 and Andrea Manni1
(1) Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, Pennsylvania State University College of Medicine, 500 University Drive, Hershey, PA 17033, USA
(2) Department of Comparative Medicine, Pennsylvania State University College of Medicine, Hershey, PA, USA
(3) Department of Pathology, Pennsylvania State University College of Medicine, Hershey, PA, USA
(4) Department of Microbiology and Immunology, Pennsylvania State University College of Medicine, Hershey, PA, USA
Received: 5 October 2006 Accepted: 11 October 2006 Published online: 2 December 2006
Abstract Increased polyamine synthesis has been associated with proliferation and progression of breast cancer, and thus, is a potential target for anti-cancer therapy. Polyamine depletion by DFMO has been shown to decrease pulmonary and bone metastasis from human breast cancer cell xenografts. Following these observations, this study was designed to test the effects of DFMO on in vitro and in vivo features of the highly invasive and metastatic 4T1 murine mammary cancer cells. DFMO inhibited proliferation, caused G1-S arrest, and suppressed in vitro invasiveness of 4T1 cells. In contrast to our previous findings with MDA-MB-435 cells, DFMO did not affect the activation of STAT3, JNK, and ERK, but decreased phosphorylation of p38. DFMO did not alter the expression of Twist. DFMO delayed the orthotopic growth of 4T1 xenografts in association with suppressed putrescine and spermidine levels but increased levels of spermine. DFMO did not affect pulmonary metastasis when primary tumors of control and DFMO-treated mice were matched for size. Interestingly, DFMO reduced Ki-67 expression only in the primary tumors but did not affect its expression in the metastatic tumors in the lung. Cleaved caspase-3 expression was not affected by DFMO in either the primary tumors or pulmonary metastasis. In summary, DFMO treatment markedly inhibited in vitro proliferation and invasiveness of 4T1 cells and retarded the growth of orthotopic xenografts in mice. The failure of DFMO to inhibit pulmonary metastasis in this system appears to be due, at least in part, to its lack of anti-proliferative effect at the metastatic sites.