Expression of Aurora B and alternative variant forms in hepatocellular carcinoma and adjacent tissue
Surgical resection is the effective treatment modality for hepatocellular carcinoma (HCC); however, rapid recurrence of the tumors are frequently observed even after apparently curative resection. The recurrence and prognostic assessment of patients with HCC after resection is an important clinical...
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| Veröffentlicht in: | Cancer science 2009-03, Vol.100 (3), p.472-480 |
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| creator | Yasen, Mahmut Mizushima, Hiroshi Mogushi, Kaoru Obulhasim, Gulanbar Miyaguchi, Ken Inoue, Kazuhiko Nakahara, Izumi Ohta, Tsutomu Aihara, Arihiro Tanaka, Shinji Arii, Shigeki Tanaka, Hiroshi |
| description | Surgical resection is the effective treatment modality for hepatocellular carcinoma (HCC); however, rapid recurrence of the tumors are frequently observed even after apparently curative resection. The recurrence and prognostic assessment of patients with HCC after resection is an important clinical issue. We recently reported that aberrant expression of Aurora B is observed in primary HCC, and that it can be a predictive factor for HCC recurrence exceeding Milan criteria after curative hepatectomy. In this study we investigated the expression of the newly observed Aurora B splicing variant forms in HCC, and their roles in hepatocarcinogenisis. The expression of Aurora B and splicing variant forms were screened in 125 HCC patients (94 chronic hepatitis with cirrhosis background liver specimens), 18 metastatic liver cancer patients and 16 normal liver specimens by cDNA microarray, reverse transcription – polymerase chain reaction (RT–PCR) and Real time quentitative Reverse Transcription PCR (qRT‐PCR). The results showed that expression of Aurora B splicing variant 2 (AURKB‐Sv2) variant form was absent in normal liver and was higher in metastatic liver cancer than HCC. This aberrant expression was associated with the advanced stages of HCC (P |
| doi_str_mv | 10.1111/j.1349-7006.2008.01068.x |
| format | Article |
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The recurrence and prognostic assessment of patients with HCC after resection is an important clinical issue. We recently reported that aberrant expression of Aurora B is observed in primary HCC, and that it can be a predictive factor for HCC recurrence exceeding Milan criteria after curative hepatectomy. In this study we investigated the expression of the newly observed Aurora B splicing variant forms in HCC, and their roles in hepatocarcinogenisis. The expression of Aurora B and splicing variant forms were screened in 125 HCC patients (94 chronic hepatitis with cirrhosis background liver specimens), 18 metastatic liver cancer patients and 16 normal liver specimens by cDNA microarray, reverse transcription – polymerase chain reaction (RT–PCR) and Real time quentitative Reverse Transcription PCR (qRT‐PCR). The results showed that expression of Aurora B splicing variant 2 (AURKB‐Sv2) variant form was absent in normal liver and was higher in metastatic liver cancer than HCC. This aberrant expression was associated with the advanced stages of HCC (P < 0.01), correlated with a poor outcome (P = 0.008) and short disease‐free period (P = 0.018). Furthermore, AURKB‐Sv2 variant form is associated with a higher level of serum α‐fetoprotein, protein induced by vitamin K absence or antagonist‐II (PIVKAII), tumor capsular invasion, multiple tumor formation and at an age younger than those with other variant forms (P < 0.05). The results thus suggest that AURKB‐Sv2 variant form is more significantly associated with the advanced stages of HCC than others and is a marker of poor prognosis. Founded in the tumor capsular invasion and multiple tumor regions, suggests that this might play a role in enhancing multiple malignant tumor formation and recurrence of HCC in hepatocarcinogenesis. This is the first study to report clinicopathological significance of aberrant expression of AURKB‐Sv2 variant form in hepatocellular carcinoma. (Cancer Sci 2009; 100: 472–480)</description><identifier>ISSN: 1347-9032</identifier><identifier>ISSN: 1349-7006</identifier><identifier>EISSN: 1349-7006</identifier><identifier>DOI: 10.1111/j.1349-7006.2008.01068.x</identifier><identifier>PMID: 19134008</identifier><language>eng</language><publisher>Melbourne, Australia: Blackwell Publishing Asia</publisher><subject>Aged ; Aurora Kinase B ; Aurora Kinases ; Biological and medical sciences ; Biomarkers, Tumor - analysis ; Blotting, Western ; Carcinoma, Hepatocellular - enzymology ; Carcinoma, Hepatocellular - genetics ; Carcinoma, Hepatocellular - pathology ; Female ; Gastroenterology. Liver. Pancreas. Abdomen ; Humans ; Isoenzymes - biosynthesis ; Kaplan-Meier Estimate ; Liver Neoplasms - enzymology ; Liver Neoplasms - genetics ; Liver Neoplasms - pathology ; Liver. Biliary tract. Portal circulation. Exocrine pancreas ; Male ; Medical sciences ; Neoplasm Recurrence, Local - enzymology ; Neoplasm Recurrence, Local - genetics ; Neoplasm Recurrence, Local - pathology ; Oligonucleotide Array Sequence Analysis ; Original ; Prognosis ; Protein Serine-Threonine Kinases - biosynthesis ; Reverse Transcriptase Polymerase Chain Reaction ; Tumors</subject><ispartof>Cancer science, 2009-03, Vol.100 (3), p.472-480</ispartof><rights>2009 Japanese Cancer Association</rights><rights>2009 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c6538-a4f04c043d5458754f1679eab3c99aff12d0fc684f9036c67f7d606a07ea22693</citedby><cites>FETCH-LOGICAL-c6538-a4f04c043d5458754f1679eab3c99aff12d0fc684f9036c67f7d606a07ea22693</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC11158790/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC11158790/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,723,776,780,881,1411,11541,27901,27902,45550,45551,46027,46451,53766,53768</link.rule.ids><linktorsrc>$$Uhttps://onlinelibrary.wiley.com/doi/abs/10.1111%2Fj.1349-7006.2008.01068.x$$EView_record_in_Wiley-Blackwell$$FView_record_in_$$GWiley-Blackwell</linktorsrc><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=21180665$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19134008$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yasen, Mahmut</creatorcontrib><creatorcontrib>Mizushima, Hiroshi</creatorcontrib><creatorcontrib>Mogushi, Kaoru</creatorcontrib><creatorcontrib>Obulhasim, Gulanbar</creatorcontrib><creatorcontrib>Miyaguchi, Ken</creatorcontrib><creatorcontrib>Inoue, Kazuhiko</creatorcontrib><creatorcontrib>Nakahara, Izumi</creatorcontrib><creatorcontrib>Ohta, Tsutomu</creatorcontrib><creatorcontrib>Aihara, Arihiro</creatorcontrib><creatorcontrib>Tanaka, Shinji</creatorcontrib><creatorcontrib>Arii, Shigeki</creatorcontrib><creatorcontrib>Tanaka, Hiroshi</creatorcontrib><title>Expression of Aurora B and alternative variant forms in hepatocellular carcinoma and adjacent tissue</title><title>Cancer science</title><addtitle>Cancer Sci</addtitle><description>Surgical resection is the effective treatment modality for hepatocellular carcinoma (HCC); however, rapid recurrence of the tumors are frequently observed even after apparently curative resection. The recurrence and prognostic assessment of patients with HCC after resection is an important clinical issue. We recently reported that aberrant expression of Aurora B is observed in primary HCC, and that it can be a predictive factor for HCC recurrence exceeding Milan criteria after curative hepatectomy. In this study we investigated the expression of the newly observed Aurora B splicing variant forms in HCC, and their roles in hepatocarcinogenisis. The expression of Aurora B and splicing variant forms were screened in 125 HCC patients (94 chronic hepatitis with cirrhosis background liver specimens), 18 metastatic liver cancer patients and 16 normal liver specimens by cDNA microarray, reverse transcription – polymerase chain reaction (RT–PCR) and Real time quentitative Reverse Transcription PCR (qRT‐PCR). The results showed that expression of Aurora B splicing variant 2 (AURKB‐Sv2) variant form was absent in normal liver and was higher in metastatic liver cancer than HCC. This aberrant expression was associated with the advanced stages of HCC (P < 0.01), correlated with a poor outcome (P = 0.008) and short disease‐free period (P = 0.018). Furthermore, AURKB‐Sv2 variant form is associated with a higher level of serum α‐fetoprotein, protein induced by vitamin K absence or antagonist‐II (PIVKAII), tumor capsular invasion, multiple tumor formation and at an age younger than those with other variant forms (P < 0.05). The results thus suggest that AURKB‐Sv2 variant form is more significantly associated with the advanced stages of HCC than others and is a marker of poor prognosis. Founded in the tumor capsular invasion and multiple tumor regions, suggests that this might play a role in enhancing multiple malignant tumor formation and recurrence of HCC in hepatocarcinogenesis. This is the first study to report clinicopathological significance of aberrant expression of AURKB‐Sv2 variant form in hepatocellular carcinoma. (Cancer Sci 2009; 100: 472–480)</description><subject>Aged</subject><subject>Aurora Kinase B</subject><subject>Aurora Kinases</subject><subject>Biological and medical sciences</subject><subject>Biomarkers, Tumor - analysis</subject><subject>Blotting, Western</subject><subject>Carcinoma, Hepatocellular - enzymology</subject><subject>Carcinoma, Hepatocellular - genetics</subject><subject>Carcinoma, Hepatocellular - pathology</subject><subject>Female</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Humans</subject><subject>Isoenzymes - biosynthesis</subject><subject>Kaplan-Meier Estimate</subject><subject>Liver Neoplasms - enzymology</subject><subject>Liver Neoplasms - genetics</subject><subject>Liver Neoplasms - pathology</subject><subject>Liver. Biliary tract. Portal circulation. Exocrine pancreas</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Neoplasm Recurrence, Local - enzymology</subject><subject>Neoplasm Recurrence, Local - genetics</subject><subject>Neoplasm Recurrence, Local - pathology</subject><subject>Oligonucleotide Array Sequence Analysis</subject><subject>Original</subject><subject>Prognosis</subject><subject>Protein Serine-Threonine Kinases - biosynthesis</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>Tumors</subject><issn>1347-9032</issn><issn>1349-7006</issn><issn>1349-7006</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkU2P0zAQhi0EYpfCX0C-wC1hnDhOfECoWy0f0kocgLM169isq8QudlK6_x5nWxU4gS8eaZ53vl5CKIOS5fdmW7Kay6IFEGUF0JXAQHTl4RG5PCceP8RtIaGuLsizlLYAteCSPyUXTOZU1l2S_vqwiyYlFzwNlq7nGCLSK4q-pzhMJnqc3N7QPUaHfqI2xDFR5-md2eEUtBmGecBINUbtfBjxqOy3qE3GJ5fSbJ6TJxaHZF6c_hX59v766-ZjcfP5w6fN-qbQoqm7ArkFroHXfcObrm24ZaKVBm9rLSVay6oerBYdt3knoUVr216AQGgNVpWQ9Yq8O9bdzbej6ZcJIg5qF92I8V4FdOrvjHd36nvYq3zT3DBXXZHXpwox_JhNmtTo0rIkehPmpISQooFG_BOsgEObT5zB7gjqGFKKxp7HYbD0ZWqrFs_U4plazFQPZqpDlr78c53fwpN7GXh1AjBpHGxEr106cxVjHYh82hV5e-R-usHc__cAarP-skT1L5TkvAw</recordid><startdate>200903</startdate><enddate>200903</enddate><creator>Yasen, Mahmut</creator><creator>Mizushima, Hiroshi</creator><creator>Mogushi, Kaoru</creator><creator>Obulhasim, Gulanbar</creator><creator>Miyaguchi, Ken</creator><creator>Inoue, Kazuhiko</creator><creator>Nakahara, Izumi</creator><creator>Ohta, Tsutomu</creator><creator>Aihara, Arihiro</creator><creator>Tanaka, Shinji</creator><creator>Arii, Shigeki</creator><creator>Tanaka, Hiroshi</creator><general>Blackwell Publishing Asia</general><general>Blackwell</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>7U9</scope><scope>H94</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>200903</creationdate><title>Expression of Aurora B and alternative variant forms in hepatocellular carcinoma and adjacent tissue</title><author>Yasen, Mahmut ; Mizushima, Hiroshi ; Mogushi, Kaoru ; Obulhasim, Gulanbar ; Miyaguchi, Ken ; Inoue, Kazuhiko ; Nakahara, Izumi ; Ohta, Tsutomu ; Aihara, Arihiro ; Tanaka, Shinji ; Arii, Shigeki ; Tanaka, Hiroshi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c6538-a4f04c043d5458754f1679eab3c99aff12d0fc684f9036c67f7d606a07ea22693</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Aged</topic><topic>Aurora Kinase B</topic><topic>Aurora Kinases</topic><topic>Biological and medical sciences</topic><topic>Biomarkers, Tumor - analysis</topic><topic>Blotting, Western</topic><topic>Carcinoma, Hepatocellular - enzymology</topic><topic>Carcinoma, Hepatocellular - genetics</topic><topic>Carcinoma, Hepatocellular - pathology</topic><topic>Female</topic><topic>Gastroenterology. Liver. Pancreas. Abdomen</topic><topic>Humans</topic><topic>Isoenzymes - biosynthesis</topic><topic>Kaplan-Meier Estimate</topic><topic>Liver Neoplasms - enzymology</topic><topic>Liver Neoplasms - genetics</topic><topic>Liver Neoplasms - pathology</topic><topic>Liver. Biliary tract. Portal circulation. Exocrine pancreas</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Neoplasm Recurrence, Local - enzymology</topic><topic>Neoplasm Recurrence, Local - genetics</topic><topic>Neoplasm Recurrence, Local - pathology</topic><topic>Oligonucleotide Array Sequence Analysis</topic><topic>Original</topic><topic>Prognosis</topic><topic>Protein Serine-Threonine Kinases - biosynthesis</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yasen, Mahmut</creatorcontrib><creatorcontrib>Mizushima, Hiroshi</creatorcontrib><creatorcontrib>Mogushi, Kaoru</creatorcontrib><creatorcontrib>Obulhasim, Gulanbar</creatorcontrib><creatorcontrib>Miyaguchi, Ken</creatorcontrib><creatorcontrib>Inoue, Kazuhiko</creatorcontrib><creatorcontrib>Nakahara, Izumi</creatorcontrib><creatorcontrib>Ohta, Tsutomu</creatorcontrib><creatorcontrib>Aihara, Arihiro</creatorcontrib><creatorcontrib>Tanaka, Shinji</creatorcontrib><creatorcontrib>Arii, Shigeki</creatorcontrib><creatorcontrib>Tanaka, Hiroshi</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>Virology and AIDS 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>Yasen, Mahmut</au><au>Mizushima, Hiroshi</au><au>Mogushi, Kaoru</au><au>Obulhasim, Gulanbar</au><au>Miyaguchi, Ken</au><au>Inoue, Kazuhiko</au><au>Nakahara, Izumi</au><au>Ohta, Tsutomu</au><au>Aihara, Arihiro</au><au>Tanaka, Shinji</au><au>Arii, Shigeki</au><au>Tanaka, Hiroshi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Expression of Aurora B and alternative variant forms in hepatocellular carcinoma and adjacent tissue</atitle><jtitle>Cancer science</jtitle><addtitle>Cancer Sci</addtitle><date>2009-03</date><risdate>2009</risdate><volume>100</volume><issue>3</issue><spage>472</spage><epage>480</epage><pages>472-480</pages><issn>1347-9032</issn><issn>1349-7006</issn><eissn>1349-7006</eissn><abstract>Surgical resection is the effective treatment modality for hepatocellular carcinoma (HCC); however, rapid recurrence of the tumors are frequently observed even after apparently curative resection. The recurrence and prognostic assessment of patients with HCC after resection is an important clinical issue. We recently reported that aberrant expression of Aurora B is observed in primary HCC, and that it can be a predictive factor for HCC recurrence exceeding Milan criteria after curative hepatectomy. In this study we investigated the expression of the newly observed Aurora B splicing variant forms in HCC, and their roles in hepatocarcinogenisis. The expression of Aurora B and splicing variant forms were screened in 125 HCC patients (94 chronic hepatitis with cirrhosis background liver specimens), 18 metastatic liver cancer patients and 16 normal liver specimens by cDNA microarray, reverse transcription – polymerase chain reaction (RT–PCR) and Real time quentitative Reverse Transcription PCR (qRT‐PCR). The results showed that expression of Aurora B splicing variant 2 (AURKB‐Sv2) variant form was absent in normal liver and was higher in metastatic liver cancer than HCC. This aberrant expression was associated with the advanced stages of HCC (P < 0.01), correlated with a poor outcome (P = 0.008) and short disease‐free period (P = 0.018). Furthermore, AURKB‐Sv2 variant form is associated with a higher level of serum α‐fetoprotein, protein induced by vitamin K absence or antagonist‐II (PIVKAII), tumor capsular invasion, multiple tumor formation and at an age younger than those with other variant forms (P < 0.05). The results thus suggest that AURKB‐Sv2 variant form is more significantly associated with the advanced stages of HCC than others and is a marker of poor prognosis. Founded in the tumor capsular invasion and multiple tumor regions, suggests that this might play a role in enhancing multiple malignant tumor formation and recurrence of HCC in hepatocarcinogenesis. This is the first study to report clinicopathological significance of aberrant expression of AURKB‐Sv2 variant form in hepatocellular carcinoma. (Cancer Sci 2009; 100: 472–480)</abstract><cop>Melbourne, Australia</cop><pub>Blackwell Publishing Asia</pub><pmid>19134008</pmid><doi>10.1111/j.1349-7006.2008.01068.x</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Aged Aurora Kinase B Aurora Kinases Biological and medical sciences Biomarkers, Tumor - analysis Blotting, Western Carcinoma, Hepatocellular - enzymology Carcinoma, Hepatocellular - genetics Carcinoma, Hepatocellular - pathology Female Gastroenterology. Liver. Pancreas. Abdomen Humans Isoenzymes - biosynthesis Kaplan-Meier Estimate Liver Neoplasms - enzymology Liver Neoplasms - genetics Liver Neoplasms - pathology Liver. Biliary tract. Portal circulation. Exocrine pancreas Male Medical sciences Neoplasm Recurrence, Local - enzymology Neoplasm Recurrence, Local - genetics Neoplasm Recurrence, Local - pathology Oligonucleotide Array Sequence Analysis Original Prognosis Protein Serine-Threonine Kinases - biosynthesis Reverse Transcriptase Polymerase Chain Reaction Tumors |
| title | Expression of Aurora B and alternative variant forms in hepatocellular carcinoma and adjacent tissue |
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