C‐type lectin‐like receptor 2 promotes hematogenous tumor metastasis and prothrombotic state in tumor‐bearing mice
Essentials The role of C‐type lectin‐like receptor‐2 (CLEC‐2) in cancer progression is unclear. CLEC‐2‐depleted mouse model is generated by using a rat anti‐mouse CLEC‐2 monoclonal antibody. CLEC‐2 depletion inhibits hematogenous tumor metastasis of podoplanin‐expressing B16F10 cells. CLEC‐2 depleti...
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| Veröffentlicht in: | Journal of thrombosis and haemostasis 2017-03, Vol.15 (3), p.513-525 |
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| creator | Shirai, T. Inoue, O. Tamura, S. Tsukiji, N. Sasaki, T. Endo, H. Satoh, K. Osada, M. Sato‐Uchida, H. Fujii, H. Ozaki, Y. Suzuki‐Inoue, K. |
| description | Essentials
The role of C‐type lectin‐like receptor‐2 (CLEC‐2) in cancer progression is unclear.
CLEC‐2‐depleted mouse model is generated by using a rat anti‐mouse CLEC‐2 monoclonal antibody.
CLEC‐2 depletion inhibits hematogenous tumor metastasis of podoplanin‐expressing B16F10 cells.
CLEC‐2 depletion prolongs cancer survival by suppressing thrombosis and inflammation.
Summary
Background
C‐type lectin‐like receptor 2 (CLEC‐2) is a platelet activation receptor of sialoglycoprotein podoplanin, which is expressed on the surface of certain types of tumor cells. CLEC‐2–podoplanin interactions facilitate hematogenous tumor metastasis. However, direct evidence of the role of CLEC‐2 in hematogenous metastasis and cancer progression is lacking.
Objective and methods
We generated immunological CLEC‐2‐depleted mice by using anti‐mouse CLEC‐2 monoclonal antibody 2A2B10 and investigated whether CLEC‐2 promoted hematogenous tumor metastasis and tumor growth and exacerbated the prognosis of mice bearing podoplanin‐expressing B16F10 melanoma cells.
Results
Our results showed that hematogenous metastasis was significantly inhibited in CLEC‐2‐depleted mice. B16F10 cells co‐cultured with wild‐type platelets, but not with CLEC‐2‐deficient platelets, showed increased proliferation. However, B16F10 cell proliferation was not inhibited in CLEC‐2‐depleted mice. Histological analysis showed that thrombus formation in tumor vessels was significantly inhibited and functional vessel density was significantly increased in CLEC‐2‐depleted mice. These data suggest that CLEC‐2 deficiency may inhibit thrombus formation in tumor vessels and increase the density of functional vessels, thus improving oxygen and nutrient supply to tumors, indirectly promoting tumor proliferation. Furthermore, the overall survival of CLEC‐2‐depleted mice was significantly prolonged, which may be due to the suppression of thrombus formation in the lungs and subsequent inhibition of systemic inflammation and cachexia.
Conclusions
These data provide a rationale for the targeted inhibition of CLEC‐2 as a new strategy for preventing hematogenous tumor metastasis and for inhibiting cancer‐related thromboembolism. |
| doi_str_mv | 10.1111/jth.13604 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1853743252</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1853743252</sourcerecordid><originalsourceid>FETCH-LOGICAL-c4544-316402bab96df04a8f1bc04a4e6b9ba2a90fc40d0680ef60287a4901e16ba0a53</originalsourceid><addsrcrecordid>eNp1kclqHDEQhkWI8TLxIS8QBLnYh7FLS2_HMHhJMPjinBtJU-3RpJeJpCaZmx_Bz-gncTk9zsFgIagq6uOnqn7GPgs4E_TO12l1JlQO-gM7FJkq50Wp8o-veaXUATuKcQ0gqkzCPjuQJciyguKQ_V08PTym7QZ5iy75nqrW_0Ie0OEmDYFLvglDNySMfIWdScM99sMYeRo76naYTKTvIzf98gVNK8LtkLzj1EjIfT-xpGzRBN_f8847_MT2GtNGPN7FGft5eXG3uJ7f3F59X3y7mTudaT1XItcgrbFVvmxAm7IR1lHUmNvKGmkqaJyGJeQlYJPTWoXRFQgUuTVgMjVjJ5MuzfZ7xJjqzkeHbWt6pD1qUWaq0EpmktCvb9D1MIaepiOqUAqUVCVRpxPlwhBjwKbeBN-ZsK0F1C921GRH_c8OYr_sFEfb4fI_-Xp_As4n4I9vcfu-Uv3j7nqSfAZzgJhu</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1873303238</pqid></control><display><type>article</type><title>C‐type lectin‐like receptor 2 promotes hematogenous tumor metastasis and prothrombotic state in tumor‐bearing mice</title><source>MEDLINE</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>Alma/SFX Local Collection</source><creator>Shirai, T. ; Inoue, O. ; Tamura, S. ; Tsukiji, N. ; Sasaki, T. ; Endo, H. ; Satoh, K. ; Osada, M. ; Sato‐Uchida, H. ; Fujii, H. ; Ozaki, Y. ; Suzuki‐Inoue, K.</creator><creatorcontrib>Shirai, T. ; Inoue, O. ; Tamura, S. ; Tsukiji, N. ; Sasaki, T. ; Endo, H. ; Satoh, K. ; Osada, M. ; Sato‐Uchida, H. ; Fujii, H. ; Ozaki, Y. ; Suzuki‐Inoue, K.</creatorcontrib><description>Essentials
The role of C‐type lectin‐like receptor‐2 (CLEC‐2) in cancer progression is unclear.
CLEC‐2‐depleted mouse model is generated by using a rat anti‐mouse CLEC‐2 monoclonal antibody.
CLEC‐2 depletion inhibits hematogenous tumor metastasis of podoplanin‐expressing B16F10 cells.
CLEC‐2 depletion prolongs cancer survival by suppressing thrombosis and inflammation.
Summary
Background
C‐type lectin‐like receptor 2 (CLEC‐2) is a platelet activation receptor of sialoglycoprotein podoplanin, which is expressed on the surface of certain types of tumor cells. CLEC‐2–podoplanin interactions facilitate hematogenous tumor metastasis. However, direct evidence of the role of CLEC‐2 in hematogenous metastasis and cancer progression is lacking.
Objective and methods
We generated immunological CLEC‐2‐depleted mice by using anti‐mouse CLEC‐2 monoclonal antibody 2A2B10 and investigated whether CLEC‐2 promoted hematogenous tumor metastasis and tumor growth and exacerbated the prognosis of mice bearing podoplanin‐expressing B16F10 melanoma cells.
Results
Our results showed that hematogenous metastasis was significantly inhibited in CLEC‐2‐depleted mice. B16F10 cells co‐cultured with wild‐type platelets, but not with CLEC‐2‐deficient platelets, showed increased proliferation. However, B16F10 cell proliferation was not inhibited in CLEC‐2‐depleted mice. Histological analysis showed that thrombus formation in tumor vessels was significantly inhibited and functional vessel density was significantly increased in CLEC‐2‐depleted mice. These data suggest that CLEC‐2 deficiency may inhibit thrombus formation in tumor vessels and increase the density of functional vessels, thus improving oxygen and nutrient supply to tumors, indirectly promoting tumor proliferation. Furthermore, the overall survival of CLEC‐2‐depleted mice was significantly prolonged, which may be due to the suppression of thrombus formation in the lungs and subsequent inhibition of systemic inflammation and cachexia.
Conclusions
These data provide a rationale for the targeted inhibition of CLEC‐2 as a new strategy for preventing hematogenous tumor metastasis and for inhibiting cancer‐related thromboembolism.</description><identifier>ISSN: 1538-7933</identifier><identifier>ISSN: 1538-7836</identifier><identifier>EISSN: 1538-7836</identifier><identifier>DOI: 10.1111/jth.13604</identifier><identifier>PMID: 28028907</identifier><language>eng</language><publisher>England: Elsevier Limited</publisher><subject>Animals ; Antibodies, Monoclonal - chemistry ; Blood clots ; Blood Platelets - metabolism ; Blood Platelets - pathology ; Cancer ; Cell Proliferation ; Disease Progression ; Green Fluorescent Proteins - chemistry ; Hemoglobins - chemistry ; inflammation ; Lectins ; Lectins, C-Type - metabolism ; lectins, C‐type ; Medical prognosis ; Melanoma, Experimental ; Metastasis ; Mice ; Mice, Knockout ; Neoplasm Metastasis ; Neoplasms - pathology ; platelet ; Platelet Activation ; Platelet Aggregation ; Prognosis ; Rats ; thrombosis ; Thrombosis - genetics</subject><ispartof>Journal of thrombosis and haemostasis, 2017-03, Vol.15 (3), p.513-525</ispartof><rights>2016 International Society on Thrombosis and Haemostasis</rights><rights>2016 International Society on Thrombosis and Haemostasis.</rights><rights>Copyright © 2017 International Society on Thrombosis and Haemostasis</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4544-316402bab96df04a8f1bc04a4e6b9ba2a90fc40d0680ef60287a4901e16ba0a53</citedby><cites>FETCH-LOGICAL-c4544-316402bab96df04a8f1bc04a4e6b9ba2a90fc40d0680ef60287a4901e16ba0a53</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28028907$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Shirai, T.</creatorcontrib><creatorcontrib>Inoue, O.</creatorcontrib><creatorcontrib>Tamura, S.</creatorcontrib><creatorcontrib>Tsukiji, N.</creatorcontrib><creatorcontrib>Sasaki, T.</creatorcontrib><creatorcontrib>Endo, H.</creatorcontrib><creatorcontrib>Satoh, K.</creatorcontrib><creatorcontrib>Osada, M.</creatorcontrib><creatorcontrib>Sato‐Uchida, H.</creatorcontrib><creatorcontrib>Fujii, H.</creatorcontrib><creatorcontrib>Ozaki, Y.</creatorcontrib><creatorcontrib>Suzuki‐Inoue, K.</creatorcontrib><title>C‐type lectin‐like receptor 2 promotes hematogenous tumor metastasis and prothrombotic state in tumor‐bearing mice</title><title>Journal of thrombosis and haemostasis</title><addtitle>J Thromb Haemost</addtitle><description>Essentials
The role of C‐type lectin‐like receptor‐2 (CLEC‐2) in cancer progression is unclear.
CLEC‐2‐depleted mouse model is generated by using a rat anti‐mouse CLEC‐2 monoclonal antibody.
CLEC‐2 depletion inhibits hematogenous tumor metastasis of podoplanin‐expressing B16F10 cells.
CLEC‐2 depletion prolongs cancer survival by suppressing thrombosis and inflammation.
Summary
Background
C‐type lectin‐like receptor 2 (CLEC‐2) is a platelet activation receptor of sialoglycoprotein podoplanin, which is expressed on the surface of certain types of tumor cells. CLEC‐2–podoplanin interactions facilitate hematogenous tumor metastasis. However, direct evidence of the role of CLEC‐2 in hematogenous metastasis and cancer progression is lacking.
Objective and methods
We generated immunological CLEC‐2‐depleted mice by using anti‐mouse CLEC‐2 monoclonal antibody 2A2B10 and investigated whether CLEC‐2 promoted hematogenous tumor metastasis and tumor growth and exacerbated the prognosis of mice bearing podoplanin‐expressing B16F10 melanoma cells.
Results
Our results showed that hematogenous metastasis was significantly inhibited in CLEC‐2‐depleted mice. B16F10 cells co‐cultured with wild‐type platelets, but not with CLEC‐2‐deficient platelets, showed increased proliferation. However, B16F10 cell proliferation was not inhibited in CLEC‐2‐depleted mice. Histological analysis showed that thrombus formation in tumor vessels was significantly inhibited and functional vessel density was significantly increased in CLEC‐2‐depleted mice. These data suggest that CLEC‐2 deficiency may inhibit thrombus formation in tumor vessels and increase the density of functional vessels, thus improving oxygen and nutrient supply to tumors, indirectly promoting tumor proliferation. Furthermore, the overall survival of CLEC‐2‐depleted mice was significantly prolonged, which may be due to the suppression of thrombus formation in the lungs and subsequent inhibition of systemic inflammation and cachexia.
Conclusions
These data provide a rationale for the targeted inhibition of CLEC‐2 as a new strategy for preventing hematogenous tumor metastasis and for inhibiting cancer‐related thromboembolism.</description><subject>Animals</subject><subject>Antibodies, Monoclonal - chemistry</subject><subject>Blood clots</subject><subject>Blood Platelets - metabolism</subject><subject>Blood Platelets - pathology</subject><subject>Cancer</subject><subject>Cell Proliferation</subject><subject>Disease Progression</subject><subject>Green Fluorescent Proteins - chemistry</subject><subject>Hemoglobins - chemistry</subject><subject>inflammation</subject><subject>Lectins</subject><subject>Lectins, C-Type - metabolism</subject><subject>lectins, C‐type</subject><subject>Medical prognosis</subject><subject>Melanoma, Experimental</subject><subject>Metastasis</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Neoplasm Metastasis</subject><subject>Neoplasms - pathology</subject><subject>platelet</subject><subject>Platelet Activation</subject><subject>Platelet Aggregation</subject><subject>Prognosis</subject><subject>Rats</subject><subject>thrombosis</subject><subject>Thrombosis - genetics</subject><issn>1538-7933</issn><issn>1538-7836</issn><issn>1538-7836</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kclqHDEQhkWI8TLxIS8QBLnYh7FLS2_HMHhJMPjinBtJU-3RpJeJpCaZmx_Bz-gncTk9zsFgIagq6uOnqn7GPgs4E_TO12l1JlQO-gM7FJkq50Wp8o-veaXUATuKcQ0gqkzCPjuQJciyguKQ_V08PTym7QZ5iy75nqrW_0Ie0OEmDYFLvglDNySMfIWdScM99sMYeRo76naYTKTvIzf98gVNK8LtkLzj1EjIfT-xpGzRBN_f8847_MT2GtNGPN7FGft5eXG3uJ7f3F59X3y7mTudaT1XItcgrbFVvmxAm7IR1lHUmNvKGmkqaJyGJeQlYJPTWoXRFQgUuTVgMjVjJ5MuzfZ7xJjqzkeHbWt6pD1qUWaq0EpmktCvb9D1MIaepiOqUAqUVCVRpxPlwhBjwKbeBN-ZsK0F1C921GRH_c8OYr_sFEfb4fI_-Xp_As4n4I9vcfu-Uv3j7nqSfAZzgJhu</recordid><startdate>201703</startdate><enddate>201703</enddate><creator>Shirai, T.</creator><creator>Inoue, O.</creator><creator>Tamura, S.</creator><creator>Tsukiji, N.</creator><creator>Sasaki, T.</creator><creator>Endo, H.</creator><creator>Satoh, K.</creator><creator>Osada, M.</creator><creator>Sato‐Uchida, H.</creator><creator>Fujii, H.</creator><creator>Ozaki, Y.</creator><creator>Suzuki‐Inoue, K.</creator><general>Elsevier Limited</general><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>7T5</scope><scope>H94</scope><scope>K9.</scope><scope>7X8</scope></search><sort><creationdate>201703</creationdate><title>C‐type lectin‐like receptor 2 promotes hematogenous tumor metastasis and prothrombotic state in tumor‐bearing mice</title><author>Shirai, T. ; Inoue, O. ; Tamura, S. ; Tsukiji, N. ; Sasaki, T. ; Endo, H. ; Satoh, K. ; Osada, M. ; Sato‐Uchida, H. ; Fujii, H. ; Ozaki, Y. ; Suzuki‐Inoue, K.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4544-316402bab96df04a8f1bc04a4e6b9ba2a90fc40d0680ef60287a4901e16ba0a53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Animals</topic><topic>Antibodies, Monoclonal - chemistry</topic><topic>Blood clots</topic><topic>Blood Platelets - metabolism</topic><topic>Blood Platelets - pathology</topic><topic>Cancer</topic><topic>Cell Proliferation</topic><topic>Disease Progression</topic><topic>Green Fluorescent Proteins - chemistry</topic><topic>Hemoglobins - chemistry</topic><topic>inflammation</topic><topic>Lectins</topic><topic>Lectins, C-Type - metabolism</topic><topic>lectins, C‐type</topic><topic>Medical prognosis</topic><topic>Melanoma, Experimental</topic><topic>Metastasis</topic><topic>Mice</topic><topic>Mice, Knockout</topic><topic>Neoplasm Metastasis</topic><topic>Neoplasms - pathology</topic><topic>platelet</topic><topic>Platelet Activation</topic><topic>Platelet Aggregation</topic><topic>Prognosis</topic><topic>Rats</topic><topic>thrombosis</topic><topic>Thrombosis - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Shirai, T.</creatorcontrib><creatorcontrib>Inoue, O.</creatorcontrib><creatorcontrib>Tamura, S.</creatorcontrib><creatorcontrib>Tsukiji, N.</creatorcontrib><creatorcontrib>Sasaki, T.</creatorcontrib><creatorcontrib>Endo, H.</creatorcontrib><creatorcontrib>Satoh, K.</creatorcontrib><creatorcontrib>Osada, M.</creatorcontrib><creatorcontrib>Sato‐Uchida, H.</creatorcontrib><creatorcontrib>Fujii, H.</creatorcontrib><creatorcontrib>Ozaki, Y.</creatorcontrib><creatorcontrib>Suzuki‐Inoue, K.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of thrombosis and haemostasis</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Shirai, T.</au><au>Inoue, O.</au><au>Tamura, S.</au><au>Tsukiji, N.</au><au>Sasaki, T.</au><au>Endo, H.</au><au>Satoh, K.</au><au>Osada, M.</au><au>Sato‐Uchida, H.</au><au>Fujii, H.</au><au>Ozaki, Y.</au><au>Suzuki‐Inoue, K.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>C‐type lectin‐like receptor 2 promotes hematogenous tumor metastasis and prothrombotic state in tumor‐bearing mice</atitle><jtitle>Journal of thrombosis and haemostasis</jtitle><addtitle>J Thromb Haemost</addtitle><date>2017-03</date><risdate>2017</risdate><volume>15</volume><issue>3</issue><spage>513</spage><epage>525</epage><pages>513-525</pages><issn>1538-7933</issn><issn>1538-7836</issn><eissn>1538-7836</eissn><abstract>Essentials
The role of C‐type lectin‐like receptor‐2 (CLEC‐2) in cancer progression is unclear.
CLEC‐2‐depleted mouse model is generated by using a rat anti‐mouse CLEC‐2 monoclonal antibody.
CLEC‐2 depletion inhibits hematogenous tumor metastasis of podoplanin‐expressing B16F10 cells.
CLEC‐2 depletion prolongs cancer survival by suppressing thrombosis and inflammation.
Summary
Background
C‐type lectin‐like receptor 2 (CLEC‐2) is a platelet activation receptor of sialoglycoprotein podoplanin, which is expressed on the surface of certain types of tumor cells. CLEC‐2–podoplanin interactions facilitate hematogenous tumor metastasis. However, direct evidence of the role of CLEC‐2 in hematogenous metastasis and cancer progression is lacking.
Objective and methods
We generated immunological CLEC‐2‐depleted mice by using anti‐mouse CLEC‐2 monoclonal antibody 2A2B10 and investigated whether CLEC‐2 promoted hematogenous tumor metastasis and tumor growth and exacerbated the prognosis of mice bearing podoplanin‐expressing B16F10 melanoma cells.
Results
Our results showed that hematogenous metastasis was significantly inhibited in CLEC‐2‐depleted mice. B16F10 cells co‐cultured with wild‐type platelets, but not with CLEC‐2‐deficient platelets, showed increased proliferation. However, B16F10 cell proliferation was not inhibited in CLEC‐2‐depleted mice. Histological analysis showed that thrombus formation in tumor vessels was significantly inhibited and functional vessel density was significantly increased in CLEC‐2‐depleted mice. These data suggest that CLEC‐2 deficiency may inhibit thrombus formation in tumor vessels and increase the density of functional vessels, thus improving oxygen and nutrient supply to tumors, indirectly promoting tumor proliferation. Furthermore, the overall survival of CLEC‐2‐depleted mice was significantly prolonged, which may be due to the suppression of thrombus formation in the lungs and subsequent inhibition of systemic inflammation and cachexia.
Conclusions
These data provide a rationale for the targeted inhibition of CLEC‐2 as a new strategy for preventing hematogenous tumor metastasis and for inhibiting cancer‐related thromboembolism.</abstract><cop>England</cop><pub>Elsevier Limited</pub><pmid>28028907</pmid><doi>10.1111/jth.13604</doi><tpages>13</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Journal of thrombosis and haemostasis, 2017-03, Vol.15 (3), p.513-525 |
| issn | 1538-7933 1538-7836 1538-7836 |
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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
| subjects | Animals Antibodies, Monoclonal - chemistry Blood clots Blood Platelets - metabolism Blood Platelets - pathology Cancer Cell Proliferation Disease Progression Green Fluorescent Proteins - chemistry Hemoglobins - chemistry inflammation Lectins Lectins, C-Type - metabolism lectins, C‐type Medical prognosis Melanoma, Experimental Metastasis Mice Mice, Knockout Neoplasm Metastasis Neoplasms - pathology platelet Platelet Activation Platelet Aggregation Prognosis Rats thrombosis Thrombosis - genetics |
| title | C‐type lectin‐like receptor 2 promotes hematogenous tumor metastasis and prothrombotic state in tumor‐bearing mice |
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