Disruption of Id1 reveals major differences in angiogenesis between transplanted and autochthonous tumors
Id genes regulate tumor angiogenesis and loss of Id1 inhibits tumor xenograft growth in mice. Here we evaluate the role of Id1 in a more clinically relevant tumor model system using a two-step chemical carcinogenesis protocol. Remarkably, we find that Id1 −/− mice are more susceptible to skin tumori...
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| Veröffentlicht in: | Cancer cell 2003-10, Vol.4 (4), p.291-299 |
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| creator | Sikder, Hashmat Huso, David L. Zhang, Hong Wang, Binghe Ryu, Byungwoo Hwang, Sam T. Powell, Jonathan D. Alani, Rhoda M. |
| description | Id genes regulate tumor angiogenesis and loss of
Id1 inhibits tumor xenograft growth in mice. Here we evaluate the role of Id1 in a more clinically relevant tumor model system using a two-step chemical carcinogenesis protocol. Remarkably, we find that
Id1
−/− mice are
more susceptible to skin tumorigenesis compared to their wild-type counterparts. Cutaneous neoplasms in
Id1
−/− mice show increased proliferation without alterations in tumor angiogenesis; however,
Id1
−/− mice possess 50% fewer cutaneous γδ T cells than their wild-type counterparts due to an intrinsic migration defect associated with loss of expression of the chemokine receptor, CXCR4. We suggest that there are important differences between the mechanisms of angiogenesis in transplanted and autochthonous tumors and that these findings will have significant implications for the potential utility of antiangiogenic therapies in cancer. |
| doi_str_mv | 10.1016/S1535-6108(03)00245-9 |
| format | Article |
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Id1 inhibits tumor xenograft growth in mice. Here we evaluate the role of Id1 in a more clinically relevant tumor model system using a two-step chemical carcinogenesis protocol. Remarkably, we find that
Id1
−/− mice are
more susceptible to skin tumorigenesis compared to their wild-type counterparts. Cutaneous neoplasms in
Id1
−/− mice show increased proliferation without alterations in tumor angiogenesis; however,
Id1
−/− mice possess 50% fewer cutaneous γδ T cells than their wild-type counterparts due to an intrinsic migration defect associated with loss of expression of the chemokine receptor, CXCR4. We suggest that there are important differences between the mechanisms of angiogenesis in transplanted and autochthonous tumors and that these findings will have significant implications for the potential utility of antiangiogenic therapies in cancer.</description><identifier>ISSN: 1535-6108</identifier><identifier>EISSN: 1878-3686</identifier><identifier>DOI: 10.1016/S1535-6108(03)00245-9</identifier><identifier>PMID: 14585356</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Animals ; Carcinogens - toxicity ; Endothelium, Vascular - physiopathology ; Flow Cytometry ; Inhibitor of Differentiation Protein 1 ; Melanoma - chemically induced ; Melanoma - metabolism ; Mice ; Mice, Knockout ; Microscopy, Fluorescence ; Neoplasms, Experimental - chemically induced ; Neoplasms, Experimental - physiopathology ; Neovascularization, Pathologic - physiopathology ; Receptors, CXCR4 - metabolism ; Repressor Proteins ; Skin Neoplasms - chemically induced ; Skin Neoplasms - physiopathology ; T-Lymphocytes - immunology ; T-Lymphocytes - metabolism ; Transcription Factors - genetics ; Transcription Factors - metabolism ; Transplantation, Heterologous</subject><ispartof>Cancer cell, 2003-10, Vol.4 (4), p.291-299</ispartof><rights>2003 Cell Press</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c505t-b38a98485d9136c9adf5228389e24d2c20c2bba06b94f1dd45e7ce22c6b317e93</citedby><cites>FETCH-LOGICAL-c505t-b38a98485d9136c9adf5228389e24d2c20c2bba06b94f1dd45e7ce22c6b317e93</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S1535610803002459$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/14585356$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sikder, Hashmat</creatorcontrib><creatorcontrib>Huso, David L.</creatorcontrib><creatorcontrib>Zhang, Hong</creatorcontrib><creatorcontrib>Wang, Binghe</creatorcontrib><creatorcontrib>Ryu, Byungwoo</creatorcontrib><creatorcontrib>Hwang, Sam T.</creatorcontrib><creatorcontrib>Powell, Jonathan D.</creatorcontrib><creatorcontrib>Alani, Rhoda M.</creatorcontrib><title>Disruption of Id1 reveals major differences in angiogenesis between transplanted and autochthonous tumors</title><title>Cancer cell</title><addtitle>Cancer Cell</addtitle><description>Id genes regulate tumor angiogenesis and loss of
Id1 inhibits tumor xenograft growth in mice. Here we evaluate the role of Id1 in a more clinically relevant tumor model system using a two-step chemical carcinogenesis protocol. Remarkably, we find that
Id1
−/− mice are
more susceptible to skin tumorigenesis compared to their wild-type counterparts. Cutaneous neoplasms in
Id1
−/− mice show increased proliferation without alterations in tumor angiogenesis; however,
Id1
−/− mice possess 50% fewer cutaneous γδ T cells than their wild-type counterparts due to an intrinsic migration defect associated with loss of expression of the chemokine receptor, CXCR4. We suggest that there are important differences between the mechanisms of angiogenesis in transplanted and autochthonous tumors and that these findings will have significant implications for the potential utility of antiangiogenic therapies in cancer.</description><subject>Animals</subject><subject>Carcinogens - toxicity</subject><subject>Endothelium, Vascular - physiopathology</subject><subject>Flow Cytometry</subject><subject>Inhibitor of Differentiation Protein 1</subject><subject>Melanoma - chemically induced</subject><subject>Melanoma - metabolism</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Microscopy, Fluorescence</subject><subject>Neoplasms, Experimental - chemically induced</subject><subject>Neoplasms, Experimental - physiopathology</subject><subject>Neovascularization, Pathologic - physiopathology</subject><subject>Receptors, CXCR4 - metabolism</subject><subject>Repressor Proteins</subject><subject>Skin Neoplasms - chemically induced</subject><subject>Skin Neoplasms - physiopathology</subject><subject>T-Lymphocytes - immunology</subject><subject>T-Lymphocytes - metabolism</subject><subject>Transcription Factors - genetics</subject><subject>Transcription Factors - metabolism</subject><subject>Transplantation, Heterologous</subject><issn>1535-6108</issn><issn>1878-3686</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkE1PHSEUhkmj8av-hBpWxi5G-RhmYNU0WluTm7jQrgkDZxRzB67A2Pjv5X40XXZBIDnPOe_hQegLJZeU0O7qgQoumo4SeUH4V0JYKxr1CR1R2cuGd7Lbq--_yCE6zvmF1D7aqwN0SFsha607Qv7G5zSvio8BxxHfOYoTvIFZZjyZl5iw8-MICYKFjH3AJjz5-AQBss94gPIHIOCSTMirpQkFXCXqmUu0z-U5hjhnXOYppvwZ7Y91LJzu7hP0-_bH4_WvZnH_8-76-6KxgojSDFwaJVspnKK8s8q4UTAmuVTAWscsI5YNgyHdoNqROtcK6C0wZruB0x4UP0Hn27mrFF9nyEVPPltY1vWgbqNp37eKCFpBsQVtijknGPUq-cmkd02JXjvWG8d6LVATrjeO9TrgbBcwDxO4f107qRX4tgWgfvPNQ9LZ-rVB5xPYol30_4n4AIx5jbU</recordid><startdate>20031001</startdate><enddate>20031001</enddate><creator>Sikder, Hashmat</creator><creator>Huso, David L.</creator><creator>Zhang, Hong</creator><creator>Wang, Binghe</creator><creator>Ryu, Byungwoo</creator><creator>Hwang, Sam T.</creator><creator>Powell, Jonathan D.</creator><creator>Alani, Rhoda M.</creator><general>Elsevier Inc</general><scope>6I.</scope><scope>AAFTH</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7TO</scope><scope>8FD</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>RC3</scope></search><sort><creationdate>20031001</creationdate><title>Disruption of Id1 reveals major differences in angiogenesis between transplanted and autochthonous tumors</title><author>Sikder, Hashmat ; Huso, David L. ; Zhang, Hong ; Wang, Binghe ; Ryu, Byungwoo ; Hwang, Sam T. ; Powell, Jonathan D. ; Alani, Rhoda M.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c505t-b38a98485d9136c9adf5228389e24d2c20c2bba06b94f1dd45e7ce22c6b317e93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Animals</topic><topic>Carcinogens - toxicity</topic><topic>Endothelium, Vascular - physiopathology</topic><topic>Flow Cytometry</topic><topic>Inhibitor of Differentiation Protein 1</topic><topic>Melanoma - chemically induced</topic><topic>Melanoma - metabolism</topic><topic>Mice</topic><topic>Mice, Knockout</topic><topic>Microscopy, Fluorescence</topic><topic>Neoplasms, Experimental - chemically induced</topic><topic>Neoplasms, Experimental - physiopathology</topic><topic>Neovascularization, Pathologic - physiopathology</topic><topic>Receptors, CXCR4 - metabolism</topic><topic>Repressor Proteins</topic><topic>Skin Neoplasms - chemically induced</topic><topic>Skin Neoplasms - physiopathology</topic><topic>T-Lymphocytes - immunology</topic><topic>T-Lymphocytes - metabolism</topic><topic>Transcription Factors - genetics</topic><topic>Transcription Factors - metabolism</topic><topic>Transplantation, Heterologous</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sikder, Hashmat</creatorcontrib><creatorcontrib>Huso, David L.</creatorcontrib><creatorcontrib>Zhang, Hong</creatorcontrib><creatorcontrib>Wang, Binghe</creatorcontrib><creatorcontrib>Ryu, Byungwoo</creatorcontrib><creatorcontrib>Hwang, Sam T.</creatorcontrib><creatorcontrib>Powell, Jonathan D.</creatorcontrib><creatorcontrib>Alani, Rhoda M.</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><jtitle>Cancer cell</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sikder, Hashmat</au><au>Huso, David L.</au><au>Zhang, Hong</au><au>Wang, Binghe</au><au>Ryu, Byungwoo</au><au>Hwang, Sam T.</au><au>Powell, Jonathan D.</au><au>Alani, Rhoda M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Disruption of Id1 reveals major differences in angiogenesis between transplanted and autochthonous tumors</atitle><jtitle>Cancer cell</jtitle><addtitle>Cancer Cell</addtitle><date>2003-10-01</date><risdate>2003</risdate><volume>4</volume><issue>4</issue><spage>291</spage><epage>299</epage><pages>291-299</pages><issn>1535-6108</issn><eissn>1878-3686</eissn><abstract>Id genes regulate tumor angiogenesis and loss of
Id1 inhibits tumor xenograft growth in mice. Here we evaluate the role of Id1 in a more clinically relevant tumor model system using a two-step chemical carcinogenesis protocol. Remarkably, we find that
Id1
−/− mice are
more susceptible to skin tumorigenesis compared to their wild-type counterparts. Cutaneous neoplasms in
Id1
−/− mice show increased proliferation without alterations in tumor angiogenesis; however,
Id1
−/− mice possess 50% fewer cutaneous γδ T cells than their wild-type counterparts due to an intrinsic migration defect associated with loss of expression of the chemokine receptor, CXCR4. We suggest that there are important differences between the mechanisms of angiogenesis in transplanted and autochthonous tumors and that these findings will have significant implications for the potential utility of antiangiogenic therapies in cancer.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>14585356</pmid><doi>10.1016/S1535-6108(03)00245-9</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Cancer cell, 2003-10, Vol.4 (4), p.291-299 |
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| source | MEDLINE; Cell Press Free Archives; Elsevier ScienceDirect Journals; EZB-FREE-00999 freely available EZB journals |
| subjects | Animals Carcinogens - toxicity Endothelium, Vascular - physiopathology Flow Cytometry Inhibitor of Differentiation Protein 1 Melanoma - chemically induced Melanoma - metabolism Mice Mice, Knockout Microscopy, Fluorescence Neoplasms, Experimental - chemically induced Neoplasms, Experimental - physiopathology Neovascularization, Pathologic - physiopathology Receptors, CXCR4 - metabolism Repressor Proteins Skin Neoplasms - chemically induced Skin Neoplasms - physiopathology T-Lymphocytes - immunology T-Lymphocytes - metabolism Transcription Factors - genetics Transcription Factors - metabolism Transplantation, Heterologous |
| title | Disruption of Id1 reveals major differences in angiogenesis between transplanted and autochthonous tumors |
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