A novel bisphosphonate minodronate (YM529) specifically inhibits osteolytic bone metastasis produced by human small-cell lung cancer cells in NK-cell depleted SCID mice
In the present study, we examined the effects of a newly developed bisphosphonate, minodronate (YM529), on osteolytic bone metastasis caused by lung cancer. Human small-cell lung cancer (SBC-5) cells, injected intravenously into natural killer cell-depleted SCID mice, produced radiologically detecta...
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| Veröffentlicht in: | Clinical & experimental metastasis 2003-01, Vol.20 (2), p.153-159 |
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| creator | Zhang, Helong Yano, Seiji Miki, Toyokazu Goto, Hisatsugu Kanematsu, Takanori Muguruma, Hiroaki Uehara, Hisanori Sone, Saburo |
| description | In the present study, we examined the effects of a newly developed bisphosphonate, minodronate (YM529), on osteolytic bone metastasis caused by lung cancer. Human small-cell lung cancer (SBC-5) cells, injected intravenously into natural killer cell-depleted SCID mice, produced radiologically detectable bone metastasis by day 18 and macroscopically visible visceral metastases (lung, liver, kidney, systemic lymph node) by day 35. Prophylactic treatment with YM529 on day 1 significantly inhibited the formation of osteolytic bone metastasis evaluated on X-ray photographs in a dose-dependent manner. In addition, treatment with YM529 after establishment of bone metastasis (on day 21) also inhibited bone metastasis, although the treatment was more effective when started earlier. Single administration was as effective as repeated treatment, suggesting a sustained inhibitory effect of YM529 on bone metastasis. YM529 reduced the number of osteoclasts in the bone metastatic lesions in vivo, but had no effect on the proliferation or cytokine production of SBC-5 cells in vitro. These results suggest that YM529 is a potent inhibitor of bone metastasis of human lung cancer, probably by suppressing osteoclastic bone resorption. In contrast, treatment with YM529 had no effect on visceral metastasis, even if started on day 1, and did not prolong the survival of the mice. Therefore, development of a combined modality is necessary for prolonging the survival of small-cell lung cancer patients with multiple-organ metastasis. |
| doi_str_mv | 10.1023/A:1022621622063 |
| format | Article |
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Human small-cell lung cancer (SBC-5) cells, injected intravenously into natural killer cell-depleted SCID mice, produced radiologically detectable bone metastasis by day 18 and macroscopically visible visceral metastases (lung, liver, kidney, systemic lymph node) by day 35. Prophylactic treatment with YM529 on day 1 significantly inhibited the formation of osteolytic bone metastasis evaluated on X-ray photographs in a dose-dependent manner. In addition, treatment with YM529 after establishment of bone metastasis (on day 21) also inhibited bone metastasis, although the treatment was more effective when started earlier. Single administration was as effective as repeated treatment, suggesting a sustained inhibitory effect of YM529 on bone metastasis. YM529 reduced the number of osteoclasts in the bone metastatic lesions in vivo, but had no effect on the proliferation or cytokine production of SBC-5 cells in vitro. These results suggest that YM529 is a potent inhibitor of bone metastasis of human lung cancer, probably by suppressing osteoclastic bone resorption. In contrast, treatment with YM529 had no effect on visceral metastasis, even if started on day 1, and did not prolong the survival of the mice. Therefore, development of a combined modality is necessary for prolonging the survival of small-cell lung cancer patients with multiple-organ metastasis.</description><identifier>ISSN: 0262-0898</identifier><identifier>EISSN: 1573-7276</identifier><identifier>DOI: 10.1023/A:1022621622063</identifier><identifier>PMID: 12705636</identifier><identifier>CODEN: CEXMD2</identifier><language>eng</language><publisher>Netherlands: Springer Nature B.V</publisher><subject>Animals ; Antineoplastic Agents - therapeutic use ; Bone Neoplasms - drug therapy ; Bone Neoplasms - immunology ; Bone Neoplasms - secondary ; Bone Resorption - drug therapy ; Carcinoma, Small Cell - drug therapy ; Carcinoma, Small Cell - immunology ; Carcinoma, Small Cell - secondary ; Cell Division - drug effects ; Cytokines - metabolism ; Diphosphonates - therapeutic use ; Disease Models, Animal ; Dose-Response Relationship, Drug ; Endothelial Growth Factors - metabolism ; Humans ; Imidazoles - therapeutic use ; Immunoenzyme Techniques ; Intercellular Signaling Peptides and Proteins - metabolism ; Kidney Neoplasms - drug therapy ; Kidney Neoplasms - secondary ; Killer Cells, Natural - physiology ; Liver Neoplasms - drug therapy ; Liver Neoplasms - secondary ; Lung Neoplasms - drug therapy ; Lung Neoplasms - immunology ; Lung Neoplasms - pathology ; Lymphatic Metastasis - prevention & control ; Lymphocyte Depletion ; Lymphokines - metabolism ; Male ; Mice ; Mice, SCID ; Osteolysis ; Parathyroid Hormone-Related Protein ; Peptide Hormones - metabolism ; Severe Combined Immunodeficiency - immunology ; Tumor Cells, Cultured ; Vascular Endothelial Growth Factor A ; Vascular Endothelial Growth Factors</subject><ispartof>Clinical & experimental metastasis, 2003-01, Vol.20 (2), p.153-159</ispartof><rights>Copyright Kluwer Academic Publishers 2003</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c311t-c1cb8f8848742b224073b8f2fc71f8a56c768655cbaf97959b0c628dff1a5b9c3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12705636$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhang, Helong</creatorcontrib><creatorcontrib>Yano, Seiji</creatorcontrib><creatorcontrib>Miki, Toyokazu</creatorcontrib><creatorcontrib>Goto, Hisatsugu</creatorcontrib><creatorcontrib>Kanematsu, Takanori</creatorcontrib><creatorcontrib>Muguruma, Hiroaki</creatorcontrib><creatorcontrib>Uehara, Hisanori</creatorcontrib><creatorcontrib>Sone, Saburo</creatorcontrib><title>A novel bisphosphonate minodronate (YM529) specifically inhibits osteolytic bone metastasis produced by human small-cell lung cancer cells in NK-cell depleted SCID mice</title><title>Clinical & experimental metastasis</title><addtitle>Clin Exp Metastasis</addtitle><description>In the present study, we examined the effects of a newly developed bisphosphonate, minodronate (YM529), on osteolytic bone metastasis caused by lung cancer. Human small-cell lung cancer (SBC-5) cells, injected intravenously into natural killer cell-depleted SCID mice, produced radiologically detectable bone metastasis by day 18 and macroscopically visible visceral metastases (lung, liver, kidney, systemic lymph node) by day 35. Prophylactic treatment with YM529 on day 1 significantly inhibited the formation of osteolytic bone metastasis evaluated on X-ray photographs in a dose-dependent manner. In addition, treatment with YM529 after establishment of bone metastasis (on day 21) also inhibited bone metastasis, although the treatment was more effective when started earlier. Single administration was as effective as repeated treatment, suggesting a sustained inhibitory effect of YM529 on bone metastasis. YM529 reduced the number of osteoclasts in the bone metastatic lesions in vivo, but had no effect on the proliferation or cytokine production of SBC-5 cells in vitro. These results suggest that YM529 is a potent inhibitor of bone metastasis of human lung cancer, probably by suppressing osteoclastic bone resorption. In contrast, treatment with YM529 had no effect on visceral metastasis, even if started on day 1, and did not prolong the survival of the mice. Therefore, development of a combined modality is necessary for prolonging the survival of small-cell lung cancer patients with multiple-organ metastasis.</description><subject>Animals</subject><subject>Antineoplastic Agents - therapeutic use</subject><subject>Bone Neoplasms - drug therapy</subject><subject>Bone Neoplasms - immunology</subject><subject>Bone Neoplasms - secondary</subject><subject>Bone Resorption - drug therapy</subject><subject>Carcinoma, Small Cell - drug therapy</subject><subject>Carcinoma, Small Cell - immunology</subject><subject>Carcinoma, Small Cell - secondary</subject><subject>Cell Division - drug effects</subject><subject>Cytokines - metabolism</subject><subject>Diphosphonates - therapeutic use</subject><subject>Disease Models, Animal</subject><subject>Dose-Response Relationship, Drug</subject><subject>Endothelial Growth Factors - metabolism</subject><subject>Humans</subject><subject>Imidazoles - therapeutic use</subject><subject>Immunoenzyme Techniques</subject><subject>Intercellular Signaling Peptides and Proteins - metabolism</subject><subject>Kidney Neoplasms - drug therapy</subject><subject>Kidney Neoplasms - secondary</subject><subject>Killer Cells, Natural - physiology</subject><subject>Liver Neoplasms - drug therapy</subject><subject>Liver Neoplasms - secondary</subject><subject>Lung Neoplasms - drug therapy</subject><subject>Lung Neoplasms - immunology</subject><subject>Lung Neoplasms - pathology</subject><subject>Lymphatic Metastasis - prevention & control</subject><subject>Lymphocyte Depletion</subject><subject>Lymphokines - metabolism</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, SCID</subject><subject>Osteolysis</subject><subject>Parathyroid Hormone-Related Protein</subject><subject>Peptide Hormones - metabolism</subject><subject>Severe Combined Immunodeficiency - immunology</subject><subject>Tumor Cells, Cultured</subject><subject>Vascular Endothelial Growth Factor A</subject><subject>Vascular Endothelial Growth Factors</subject><issn>0262-0898</issn><issn>1573-7276</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqFkT1PHDEQhi2UCA5CnS6yUqCkWPC3vXSnC0lQ-CiAgmple705I6-9rHeR7h_lZ-LTkSZNpLFmNPO8o9caAD5idIoRoWfL85KIIFgQggTdAwvMJa0kkeIdWKAyqZCq1QE4zPkJIcSkVPvgABOJuKBiAf4sYUwvLkDj87BO2xf15GDvY2rHXf3l8ZqT-ivMg7O-81aHsIE-rr3xU4YpTy6FzeQtNCkWpZt0LuEzHMbUzta10Gzgeu51hLkv4sq6EGCY429odbRuhNtGLivhza_dsHVDcFNR3q0uvxUz1n0A7zsdsjt-y0fg4fvF_epndXX743K1vKosxXiqLLZGdUoxJRkxhDAkaWmQzkrcKc2FlUIJzq3RXS1rXhtkBVFt12HNTW3pETjZ7S3mn2eXp6b3eetJR5fm3EhKcM2x_C-Ia8YQY7SAn_8Bn9I8xvKJhmCGBWKEF-jTGzSb3rXNMPpej5vm76XoK-M_loY</recordid><startdate>20030101</startdate><enddate>20030101</enddate><creator>Zhang, Helong</creator><creator>Yano, Seiji</creator><creator>Miki, Toyokazu</creator><creator>Goto, Hisatsugu</creator><creator>Kanematsu, Takanori</creator><creator>Muguruma, Hiroaki</creator><creator>Uehara, Hisanori</creator><creator>Sone, Saburo</creator><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>3V.</scope><scope>7TO</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8FE</scope><scope>8FG</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>P5Z</scope><scope>P62</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7QP</scope><scope>7X8</scope></search><sort><creationdate>20030101</creationdate><title>A novel bisphosphonate minodronate (YM529) specifically inhibits osteolytic bone metastasis produced by human small-cell lung cancer cells in NK-cell depleted SCID mice</title><author>Zhang, Helong ; Yano, Seiji ; Miki, Toyokazu ; Goto, Hisatsugu ; Kanematsu, Takanori ; Muguruma, Hiroaki ; Uehara, Hisanori ; Sone, Saburo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c311t-c1cb8f8848742b224073b8f2fc71f8a56c768655cbaf97959b0c628dff1a5b9c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Animals</topic><topic>Antineoplastic Agents - 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drug therapy</topic><topic>Lung Neoplasms - immunology</topic><topic>Lung Neoplasms - pathology</topic><topic>Lymphatic Metastasis - prevention & control</topic><topic>Lymphocyte Depletion</topic><topic>Lymphokines - metabolism</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, SCID</topic><topic>Osteolysis</topic><topic>Parathyroid Hormone-Related Protein</topic><topic>Peptide Hormones - metabolism</topic><topic>Severe Combined Immunodeficiency - immunology</topic><topic>Tumor Cells, Cultured</topic><topic>Vascular Endothelial Growth Factor A</topic><topic>Vascular Endothelial Growth Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhang, Helong</creatorcontrib><creatorcontrib>Yano, Seiji</creatorcontrib><creatorcontrib>Miki, Toyokazu</creatorcontrib><creatorcontrib>Goto, Hisatsugu</creatorcontrib><creatorcontrib>Kanematsu, Takanori</creatorcontrib><creatorcontrib>Muguruma, Hiroaki</creatorcontrib><creatorcontrib>Uehara, Hisanori</creatorcontrib><creatorcontrib>Sone, Saburo</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>ProQuest Central (Corporate)</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>Advanced Technologies & Aerospace Database</collection><collection>ProQuest Advanced Technologies & Aerospace Collection</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Clinical & experimental metastasis</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhang, Helong</au><au>Yano, Seiji</au><au>Miki, Toyokazu</au><au>Goto, Hisatsugu</au><au>Kanematsu, Takanori</au><au>Muguruma, Hiroaki</au><au>Uehara, Hisanori</au><au>Sone, Saburo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A novel bisphosphonate minodronate (YM529) specifically inhibits osteolytic bone metastasis produced by human small-cell lung cancer cells in NK-cell depleted SCID mice</atitle><jtitle>Clinical & experimental metastasis</jtitle><addtitle>Clin Exp Metastasis</addtitle><date>2003-01-01</date><risdate>2003</risdate><volume>20</volume><issue>2</issue><spage>153</spage><epage>159</epage><pages>153-159</pages><issn>0262-0898</issn><eissn>1573-7276</eissn><coden>CEXMD2</coden><abstract>In the present study, we examined the effects of a newly developed bisphosphonate, minodronate (YM529), on osteolytic bone metastasis caused by lung cancer. Human small-cell lung cancer (SBC-5) cells, injected intravenously into natural killer cell-depleted SCID mice, produced radiologically detectable bone metastasis by day 18 and macroscopically visible visceral metastases (lung, liver, kidney, systemic lymph node) by day 35. Prophylactic treatment with YM529 on day 1 significantly inhibited the formation of osteolytic bone metastasis evaluated on X-ray photographs in a dose-dependent manner. In addition, treatment with YM529 after establishment of bone metastasis (on day 21) also inhibited bone metastasis, although the treatment was more effective when started earlier. Single administration was as effective as repeated treatment, suggesting a sustained inhibitory effect of YM529 on bone metastasis. YM529 reduced the number of osteoclasts in the bone metastatic lesions in vivo, but had no effect on the proliferation or cytokine production of SBC-5 cells in vitro. These results suggest that YM529 is a potent inhibitor of bone metastasis of human lung cancer, probably by suppressing osteoclastic bone resorption. In contrast, treatment with YM529 had no effect on visceral metastasis, even if started on day 1, and did not prolong the survival of the mice. Therefore, development of a combined modality is necessary for prolonging the survival of small-cell lung cancer patients with multiple-organ metastasis.</abstract><cop>Netherlands</cop><pub>Springer Nature B.V</pub><pmid>12705636</pmid><doi>10.1023/A:1022621622063</doi><tpages>7</tpages></addata></record> |
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| ispartof | Clinical & experimental metastasis, 2003-01, Vol.20 (2), p.153-159 |
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| subjects | Animals Antineoplastic Agents - therapeutic use Bone Neoplasms - drug therapy Bone Neoplasms - immunology Bone Neoplasms - secondary Bone Resorption - drug therapy Carcinoma, Small Cell - drug therapy Carcinoma, Small Cell - immunology Carcinoma, Small Cell - secondary Cell Division - drug effects Cytokines - metabolism Diphosphonates - therapeutic use Disease Models, Animal Dose-Response Relationship, Drug Endothelial Growth Factors - metabolism Humans Imidazoles - therapeutic use Immunoenzyme Techniques Intercellular Signaling Peptides and Proteins - metabolism Kidney Neoplasms - drug therapy Kidney Neoplasms - secondary Killer Cells, Natural - physiology Liver Neoplasms - drug therapy Liver Neoplasms - secondary Lung Neoplasms - drug therapy Lung Neoplasms - immunology Lung Neoplasms - pathology Lymphatic Metastasis - prevention & control Lymphocyte Depletion Lymphokines - metabolism Male Mice Mice, SCID Osteolysis Parathyroid Hormone-Related Protein Peptide Hormones - metabolism Severe Combined Immunodeficiency - immunology Tumor Cells, Cultured Vascular Endothelial Growth Factor A Vascular Endothelial Growth Factors |
| title | A novel bisphosphonate minodronate (YM529) specifically inhibits osteolytic bone metastasis produced by human small-cell lung cancer cells in NK-cell depleted SCID mice |
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