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Polo‐like kinase 1 (PLK1) is overexpressed in primary colorectal cancers
PLK (polo‐like kinase), the human counterpart of polo in Drosophila melanogaster and of CDC5 in Saccharomyces cerevisiae, belongs to a family of serine/threonine kinases. It is intimately involved in spindle formation and chromosome segregation during mitosis. The purpose of this study was to determ...
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Published in: | Cancer science 2003-02, Vol.94 (2), p.148-152 |
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creator | Takahashi, Takao Sano, Bun Nagata, Takayasu Kato, Hiroki Sugiyama, Yasuyuki Kunieda, Katsuyuki Kimura, Masashi Okano, Yukio Saji, Shigetoyo |
description | PLK (polo‐like kinase), the human counterpart of polo in Drosophila melanogaster and of CDC5 in Saccharomyces cerevisiae, belongs to a family of serine/threonine kinases. It is intimately involved in spindle formation and chromosome segregation during mitosis. The purpose of this study was to determine whether PLK1 is overexpressed in primary colorectal cancer specimens as compared with normal colon mucosa and to assess its relation to other kinases as a potential new tumor marker. In the present study, immunohistochemical analyses were performed of PLK1 expression in 78 primary colorectal cancers as well as 15 normal colorectal specimens. Furthermore, we examined the relationship between other kinases, Aurora‐A and Aurora‐C, and PLK1 expression. In normal colon mucosa, some crypt cells showed weakly positive staining for PLK1 in 13 out of 15 cases, the remaining cases being negative. Elevated expression of PLK1 was observed in 57 (73.1%) of the colorectal cancers, statistically significant associations being evident with pT (primary tumor invasion) (P=0.0006, Mann‐Whitney U test), pN (regional lymph nodes) (P=0.008, χ2 test) and the Dukes' classification (P=0.0005, Mann‐Whitney U test). Mean proliferating cell nuclear antigen‐labeling index was 52.3%, with a range of 24.1% to 77.3%. Values for lesions with high and low PLK1 expression were 54.7±10.3% (mean$MpSD) and 45.9$Mp11.9% (P=0.002, Student's t test). PLK1 was significantly associated with Aurora‐A, but PLK1 staining was more diffuse and extensive than for Aurora‐A or Aurora‐C. Interestingly, PLK1 overexpression was significantly associated with p53 accumulation in colorectal cancers. Our results suggest over‐expression of PLK1 might be of pathogenic, prognostic and proliferative importance, so that this kinase might have potential as a new tumor marker for colorectal cancers. (Cancer Sci 2003; 94: 148–152) |
doi_str_mv | 10.1111/j.1349-7006.2003.tb01411.x |
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It is intimately involved in spindle formation and chromosome segregation during mitosis. The purpose of this study was to determine whether PLK1 is overexpressed in primary colorectal cancer specimens as compared with normal colon mucosa and to assess its relation to other kinases as a potential new tumor marker. In the present study, immunohistochemical analyses were performed of PLK1 expression in 78 primary colorectal cancers as well as 15 normal colorectal specimens. Furthermore, we examined the relationship between other kinases, Aurora‐A and Aurora‐C, and PLK1 expression. In normal colon mucosa, some crypt cells showed weakly positive staining for PLK1 in 13 out of 15 cases, the remaining cases being negative. Elevated expression of PLK1 was observed in 57 (73.1%) of the colorectal cancers, statistically significant associations being evident with pT (primary tumor invasion) (P=0.0006, Mann‐Whitney U test), pN (regional lymph nodes) (P=0.008, χ2 test) and the Dukes' classification (P=0.0005, Mann‐Whitney U test). Mean proliferating cell nuclear antigen‐labeling index was 52.3%, with a range of 24.1% to 77.3%. Values for lesions with high and low PLK1 expression were 54.7±10.3% (mean$MpSD) and 45.9$Mp11.9% (P=0.002, Student's t test). PLK1 was significantly associated with Aurora‐A, but PLK1 staining was more diffuse and extensive than for Aurora‐A or Aurora‐C. Interestingly, PLK1 overexpression was significantly associated with p53 accumulation in colorectal cancers. Our results suggest over‐expression of PLK1 might be of pathogenic, prognostic and proliferative importance, so that this kinase might have potential as a new tumor marker for colorectal cancers. (Cancer Sci 2003; 94: 148–152)</description><identifier>ISSN: 1347-9032</identifier><identifier>EISSN: 1349-7006</identifier><identifier>DOI: 10.1111/j.1349-7006.2003.tb01411.x</identifier><identifier>PMID: 12708489</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Adenocarcinoma - enzymology ; Adenocarcinoma - genetics ; Adult ; Aged ; Aged, 80 and over ; Aurora Kinase C ; Aurora Kinases ; Biological and medical sciences ; Biomarkers ; Biomarkers, Tumor - analysis ; Cell Cycle Proteins ; Cell Differentiation ; Colorectal carcinoma ; Colorectal Neoplasms - enzymology ; Colorectal Neoplasms - genetics ; Disease Progression ; Enzyme Induction ; Female ; Gastroenterology. Liver. Pancreas. Abdomen ; Gene Expression Regulation, Neoplastic ; Genes, p53 ; Humans ; Intestinal Mucosa - enzymology ; Lymph nodes ; Lymphatic Metastasis ; Male ; Medical sciences ; Middle Aged ; Mitosis ; Mucosa ; Neoplasm Proteins - biosynthesis ; Neoplasm Proteins - genetics ; p53 Protein ; Polo-Like Kinase 1 ; Prognosis ; Proliferating cell nuclear antigen ; Proliferating Cell Nuclear Antigen - analysis ; Protein Kinases - biosynthesis ; Protein Kinases - genetics ; Protein Serine-Threonine Kinases - biosynthesis ; Protein Serine-Threonine Kinases - genetics ; Proto-Oncogene Proteins ; Serine ; Statistical analysis ; Stomach. Duodenum. Small intestine. Colon. Rectum. Anus ; Threonine ; Tumor markers ; Tumors</subject><ispartof>Cancer science, 2003-02, Vol.94 (2), p.148-152</ispartof><rights>2004 INIST-CNRS</rights><rights>Copyright John Wiley & Sons, Inc. Feb 2003</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c6868-4d09a4b8b5459084f3a1c31b3578bd9101c5764a2ea518dc22cd68288ebfef1b3</citedby><cites>FETCH-LOGICAL-c6868-4d09a4b8b5459084f3a1c31b3578bd9101c5764a2ea518dc22cd68288ebfef1b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/2399350814/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2399350814?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,11543,25733,27903,27904,36991,36992,44569,46030,46454,53769,53771,74872</link.rule.ids><linktorsrc>$$Uhttps://onlinelibrary.wiley.com/doi/abs/10.1111%2Fj.1349-7006.2003.tb01411.x$$EView_record_in_Wiley-Blackwell$$FView_record_in_$$GWiley-Blackwell</linktorsrc><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=15261182$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12708489$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Takahashi, Takao</creatorcontrib><creatorcontrib>Sano, Bun</creatorcontrib><creatorcontrib>Nagata, Takayasu</creatorcontrib><creatorcontrib>Kato, Hiroki</creatorcontrib><creatorcontrib>Sugiyama, Yasuyuki</creatorcontrib><creatorcontrib>Kunieda, Katsuyuki</creatorcontrib><creatorcontrib>Kimura, Masashi</creatorcontrib><creatorcontrib>Okano, Yukio</creatorcontrib><creatorcontrib>Saji, Shigetoyo</creatorcontrib><title>Polo‐like kinase 1 (PLK1) is overexpressed in primary colorectal cancers</title><title>Cancer science</title><addtitle>Cancer Sci</addtitle><description>PLK (polo‐like kinase), the human counterpart of polo in Drosophila melanogaster and of CDC5 in Saccharomyces cerevisiae, belongs to a family of serine/threonine kinases. It is intimately involved in spindle formation and chromosome segregation during mitosis. The purpose of this study was to determine whether PLK1 is overexpressed in primary colorectal cancer specimens as compared with normal colon mucosa and to assess its relation to other kinases as a potential new tumor marker. In the present study, immunohistochemical analyses were performed of PLK1 expression in 78 primary colorectal cancers as well as 15 normal colorectal specimens. Furthermore, we examined the relationship between other kinases, Aurora‐A and Aurora‐C, and PLK1 expression. In normal colon mucosa, some crypt cells showed weakly positive staining for PLK1 in 13 out of 15 cases, the remaining cases being negative. Elevated expression of PLK1 was observed in 57 (73.1%) of the colorectal cancers, statistically significant associations being evident with pT (primary tumor invasion) (P=0.0006, Mann‐Whitney U test), pN (regional lymph nodes) (P=0.008, χ2 test) and the Dukes' classification (P=0.0005, Mann‐Whitney U test). Mean proliferating cell nuclear antigen‐labeling index was 52.3%, with a range of 24.1% to 77.3%. Values for lesions with high and low PLK1 expression were 54.7±10.3% (mean$MpSD) and 45.9$Mp11.9% (P=0.002, Student's t test). PLK1 was significantly associated with Aurora‐A, but PLK1 staining was more diffuse and extensive than for Aurora‐A or Aurora‐C. Interestingly, PLK1 overexpression was significantly associated with p53 accumulation in colorectal cancers. Our results suggest over‐expression of PLK1 might be of pathogenic, prognostic and proliferative importance, so that this kinase might have potential as a new tumor marker for colorectal cancers. (Cancer Sci 2003; 94: 148–152)</description><subject>Adenocarcinoma - enzymology</subject><subject>Adenocarcinoma - genetics</subject><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Aurora Kinase C</subject><subject>Aurora Kinases</subject><subject>Biological and medical sciences</subject><subject>Biomarkers</subject><subject>Biomarkers, Tumor - analysis</subject><subject>Cell Cycle Proteins</subject><subject>Cell Differentiation</subject><subject>Colorectal carcinoma</subject><subject>Colorectal Neoplasms - enzymology</subject><subject>Colorectal Neoplasms - genetics</subject><subject>Disease Progression</subject><subject>Enzyme Induction</subject><subject>Female</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Genes, p53</subject><subject>Humans</subject><subject>Intestinal Mucosa - enzymology</subject><subject>Lymph nodes</subject><subject>Lymphatic Metastasis</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Mitosis</subject><subject>Mucosa</subject><subject>Neoplasm Proteins - biosynthesis</subject><subject>Neoplasm Proteins - genetics</subject><subject>p53 Protein</subject><subject>Polo-Like Kinase 1</subject><subject>Prognosis</subject><subject>Proliferating cell nuclear antigen</subject><subject>Proliferating Cell Nuclear Antigen - analysis</subject><subject>Protein Kinases - biosynthesis</subject><subject>Protein Kinases - genetics</subject><subject>Protein Serine-Threonine Kinases - biosynthesis</subject><subject>Protein Serine-Threonine Kinases - genetics</subject><subject>Proto-Oncogene Proteins</subject><subject>Serine</subject><subject>Statistical analysis</subject><subject>Stomach. Duodenum. Small intestine. Colon. Rectum. Anus</subject><subject>Threonine</subject><subject>Tumor markers</subject><subject>Tumors</subject><issn>1347-9032</issn><issn>1349-7006</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><recordid>eNqVkc9u1DAQxiNERUvhFVAEAsEhwWM7jt1Dq2rF_5WoBJwtx5mAt9l4sXfL9sYj8Iw8SR02aoELwhdbmt8383m-LHsIpIR0ni9KYFwVNSGipISwct0Q4ADl9lZ2cF26_etdF4owup_djXGRUMEVv5PtA62J5FIdZG_PfO9_fv_Ru3PMz91gIuaQPz2bv4NnuYu5v8CA21XAGLHN3ZCvgluacJnbpAto16bPrRkshngv2-tMH_H-dB9mn16--Dh7Xczfv3ozO50XVkghC94SZXgjm4pXKrnomAHLoGFVLZtWAQFb1YIbiqYC2VpKbSsklRKbDrvEHWYnu76rTbPE1uKwDqbXkzHtjdN_Vgb3RX_2FzrtThAqeerwZOoQ_NcNxrVeumix782AfhN1zSjwWql_gqAoU1SIBD76C1z4TRjSGnQiFKuIhHHu0Y6ywccYsLs2DWR0B3qhx_z0mJ8eo9VTtHqbxA9-__aNdMoyAY8nwERr-i6kWFy84SoqACRN3PGO--Z6vPwPC3p2-gG4ZFfAUcBV</recordid><startdate>200302</startdate><enddate>200302</enddate><creator>Takahashi, Takao</creator><creator>Sano, Bun</creator><creator>Nagata, Takayasu</creator><creator>Kato, Hiroki</creator><creator>Sugiyama, Yasuyuki</creator><creator>Kunieda, Katsuyuki</creator><creator>Kimura, Masashi</creator><creator>Okano, Yukio</creator><creator>Saji, Shigetoyo</creator><general>Blackwell Publishing Ltd</general><general>Blackwell</general><general>John Wiley & Sons, Inc</general><scope>IQODW</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>8FE</scope><scope>8FH</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>LK8</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7TO</scope><scope>H94</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>200302</creationdate><title>Polo‐like kinase 1 (PLK1) is overexpressed in primary colorectal cancers</title><author>Takahashi, Takao ; Sano, Bun ; Nagata, Takayasu ; Kato, Hiroki ; Sugiyama, Yasuyuki ; Kunieda, Katsuyuki ; Kimura, Masashi ; Okano, Yukio ; Saji, Shigetoyo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c6868-4d09a4b8b5459084f3a1c31b3578bd9101c5764a2ea518dc22cd68288ebfef1b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Adenocarcinoma - enzymology</topic><topic>Adenocarcinoma - genetics</topic><topic>Adult</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Aurora Kinase C</topic><topic>Aurora Kinases</topic><topic>Biological and medical sciences</topic><topic>Biomarkers</topic><topic>Biomarkers, Tumor - analysis</topic><topic>Cell Cycle Proteins</topic><topic>Cell Differentiation</topic><topic>Colorectal carcinoma</topic><topic>Colorectal Neoplasms - enzymology</topic><topic>Colorectal Neoplasms - genetics</topic><topic>Disease Progression</topic><topic>Enzyme Induction</topic><topic>Female</topic><topic>Gastroenterology. Liver. Pancreas. Abdomen</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Genes, p53</topic><topic>Humans</topic><topic>Intestinal Mucosa - enzymology</topic><topic>Lymph nodes</topic><topic>Lymphatic Metastasis</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Mitosis</topic><topic>Mucosa</topic><topic>Neoplasm Proteins - biosynthesis</topic><topic>Neoplasm Proteins - genetics</topic><topic>p53 Protein</topic><topic>Polo-Like Kinase 1</topic><topic>Prognosis</topic><topic>Proliferating cell nuclear antigen</topic><topic>Proliferating Cell Nuclear Antigen - analysis</topic><topic>Protein Kinases - biosynthesis</topic><topic>Protein Kinases - genetics</topic><topic>Protein Serine-Threonine Kinases - biosynthesis</topic><topic>Protein Serine-Threonine Kinases - genetics</topic><topic>Proto-Oncogene Proteins</topic><topic>Serine</topic><topic>Statistical analysis</topic><topic>Stomach. Duodenum. Small intestine. Colon. Rectum. Anus</topic><topic>Threonine</topic><topic>Tumor markers</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Takahashi, Takao</creatorcontrib><creatorcontrib>Sano, Bun</creatorcontrib><creatorcontrib>Nagata, Takayasu</creatorcontrib><creatorcontrib>Kato, Hiroki</creatorcontrib><creatorcontrib>Sugiyama, Yasuyuki</creatorcontrib><creatorcontrib>Kunieda, Katsuyuki</creatorcontrib><creatorcontrib>Kimura, Masashi</creatorcontrib><creatorcontrib>Okano, Yukio</creatorcontrib><creatorcontrib>Saji, Shigetoyo</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>Biological Sciences</collection><collection>Biological Science Database</collection><collection>Publicly Available Content Database</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>Oncogenes and Growth Factors Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cancer science</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext_linktorsrc</fulltext></delivery><addata><au>Takahashi, Takao</au><au>Sano, Bun</au><au>Nagata, Takayasu</au><au>Kato, Hiroki</au><au>Sugiyama, Yasuyuki</au><au>Kunieda, Katsuyuki</au><au>Kimura, Masashi</au><au>Okano, Yukio</au><au>Saji, Shigetoyo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Polo‐like kinase 1 (PLK1) is overexpressed in primary colorectal cancers</atitle><jtitle>Cancer science</jtitle><addtitle>Cancer Sci</addtitle><date>2003-02</date><risdate>2003</risdate><volume>94</volume><issue>2</issue><spage>148</spage><epage>152</epage><pages>148-152</pages><issn>1347-9032</issn><eissn>1349-7006</eissn><abstract>PLK (polo‐like kinase), the human counterpart of polo in Drosophila melanogaster and of CDC5 in Saccharomyces cerevisiae, belongs to a family of serine/threonine kinases. It is intimately involved in spindle formation and chromosome segregation during mitosis. The purpose of this study was to determine whether PLK1 is overexpressed in primary colorectal cancer specimens as compared with normal colon mucosa and to assess its relation to other kinases as a potential new tumor marker. In the present study, immunohistochemical analyses were performed of PLK1 expression in 78 primary colorectal cancers as well as 15 normal colorectal specimens. Furthermore, we examined the relationship between other kinases, Aurora‐A and Aurora‐C, and PLK1 expression. In normal colon mucosa, some crypt cells showed weakly positive staining for PLK1 in 13 out of 15 cases, the remaining cases being negative. Elevated expression of PLK1 was observed in 57 (73.1%) of the colorectal cancers, statistically significant associations being evident with pT (primary tumor invasion) (P=0.0006, Mann‐Whitney U test), pN (regional lymph nodes) (P=0.008, χ2 test) and the Dukes' classification (P=0.0005, Mann‐Whitney U test). Mean proliferating cell nuclear antigen‐labeling index was 52.3%, with a range of 24.1% to 77.3%. Values for lesions with high and low PLK1 expression were 54.7±10.3% (mean$MpSD) and 45.9$Mp11.9% (P=0.002, Student's t test). PLK1 was significantly associated with Aurora‐A, but PLK1 staining was more diffuse and extensive than for Aurora‐A or Aurora‐C. Interestingly, PLK1 overexpression was significantly associated with p53 accumulation in colorectal cancers. Our results suggest over‐expression of PLK1 might be of pathogenic, prognostic and proliferative importance, so that this kinase might have potential as a new tumor marker for colorectal cancers. (Cancer Sci 2003; 94: 148–152)</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>12708489</pmid><doi>10.1111/j.1349-7006.2003.tb01411.x</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Adenocarcinoma - enzymology Adenocarcinoma - genetics Adult Aged Aged, 80 and over Aurora Kinase C Aurora Kinases Biological and medical sciences Biomarkers Biomarkers, Tumor - analysis Cell Cycle Proteins Cell Differentiation Colorectal carcinoma Colorectal Neoplasms - enzymology Colorectal Neoplasms - genetics Disease Progression Enzyme Induction Female Gastroenterology. Liver. Pancreas. Abdomen Gene Expression Regulation, Neoplastic Genes, p53 Humans Intestinal Mucosa - enzymology Lymph nodes Lymphatic Metastasis Male Medical sciences Middle Aged Mitosis Mucosa Neoplasm Proteins - biosynthesis Neoplasm Proteins - genetics p53 Protein Polo-Like Kinase 1 Prognosis Proliferating cell nuclear antigen Proliferating Cell Nuclear Antigen - analysis Protein Kinases - biosynthesis Protein Kinases - genetics Protein Serine-Threonine Kinases - biosynthesis Protein Serine-Threonine Kinases - genetics Proto-Oncogene Proteins Serine Statistical analysis Stomach. Duodenum. Small intestine. Colon. Rectum. Anus Threonine Tumor markers Tumors |
title | Polo‐like kinase 1 (PLK1) is overexpressed in primary colorectal cancers |
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