High Expression of Obesity-Linked Phosphatase SHIP2 in Invasive Breast Cancer Correlates with Reduced Disease-Free Survival
SH2-containing 5′-inositol phosphatase (SHIP2) is a known regulator of insulin function. Genetic knockout of SHIP2 in mice causes mild insulin hypersensitivity and prevents high-fat-diet-induced obesity. SHIP2 also regulates actin remodeling and epidermal growth factor receptor (EGFR) turnover and s...
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| Veröffentlicht in: | Tumor biology 2008-01, Vol.29 (5), p.330-341 |
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| creator | Prasad, Nagendra K. Tandon, Manish Handa, Anant Moore, George E. Babbs, Charles F. Snyder, Paul W. Bose, Shikha |
| description | SH2-containing 5′-inositol phosphatase (SHIP2) is a known regulator of insulin function. Genetic knockout of SHIP2 in mice causes mild insulin hypersensitivity and prevents high-fat-diet-induced obesity. SHIP2 also regulates actin remodeling and epidermal growth factor receptor (EGFR) turnover and supports breast cancer; and metastatic growth. To determine the clinical significance of SHIP2 expression in breast cancer and its relationship to relevant oncogenic molecules, SHIP2 expression was determined immunohistochemically in 285 primary breast cancers; 140 ductal carcinomas in situ (DCIS) and 145 invasive carcinomas. Forty-five percent of the specimens showed high SHIP2 levels in cancer cells while only 15% of adjacent normal cells expressed high SHIP2 levels (p < 0.0001). In cancer cells, the risk of SHIP2 overexpression is elevated (a) in women aged ≤50 years (relative risk, RR = 4.13; 95% confidence interval, CI, 2.5–6.9) compared to women aged >50 years (RR = 2.37; 95% CI 1.6–3.5; p = 0.0003), and (b) in invasive carcinomas (RR = 3.52; 95% CI 2.3–5.5) compared with DCIS (RR = 2.22; 95% CI 1.5–3.5; p = 0.0009). Patients with higher SHIP2 levels in invasive carcinomas had significantly reduced disease-free (p = 0.0025) and overall survival periods (p = 0.0228). In invasive carcinomas, SHIP2 correlated with estrogen receptor absence (p = 0.003) and EGFR presence (p = 0.0147). In conclusion, SHIP2 is an important biomarker for breast cancer. |
| doi_str_mv | 10.1159/000172970 |
| format | Article |
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Genetic knockout of SHIP2 in mice causes mild insulin hypersensitivity and prevents high-fat-diet-induced obesity. SHIP2 also regulates actin remodeling and epidermal growth factor receptor (EGFR) turnover and supports breast cancer; and metastatic growth. To determine the clinical significance of SHIP2 expression in breast cancer and its relationship to relevant oncogenic molecules, SHIP2 expression was determined immunohistochemically in 285 primary breast cancers; 140 ductal carcinomas in situ (DCIS) and 145 invasive carcinomas. Forty-five percent of the specimens showed high SHIP2 levels in cancer cells while only 15% of adjacent normal cells expressed high SHIP2 levels (p < 0.0001). In cancer cells, the risk of SHIP2 overexpression is elevated (a) in women aged ≤50 years (relative risk, RR = 4.13; 95% confidence interval, CI, 2.5–6.9) compared to women aged >50 years (RR = 2.37; 95% CI 1.6–3.5; p = 0.0003), and (b) in invasive carcinomas (RR = 3.52; 95% CI 2.3–5.5) compared with DCIS (RR = 2.22; 95% CI 1.5–3.5; p = 0.0009). Patients with higher SHIP2 levels in invasive carcinomas had significantly reduced disease-free (p = 0.0025) and overall survival periods (p = 0.0228). In invasive carcinomas, SHIP2 correlated with estrogen receptor absence (p = 0.003) and EGFR presence (p = 0.0147). In conclusion, SHIP2 is an important biomarker for breast cancer.</description><identifier>ISSN: 1010-4283</identifier><identifier>EISSN: 1423-0380</identifier><identifier>DOI: 10.1159/000172970</identifier><identifier>PMID: 19065064</identifier><language>eng</language><publisher>Basel, Switzerland: Springer Nature B.V</publisher><subject>Adult ; Aged ; Aged, 80 and over ; Biomarkers, Tumor - metabolism ; Blotting, Western ; Breast Neoplasms - metabolism ; Breast Neoplasms - mortality ; Breast Neoplasms - pathology ; Carcinoma, Ductal, Breast - metabolism ; Carcinoma, Ductal, Breast - mortality ; Carcinoma, Ductal, Breast - pathology ; Carcinoma, Intraductal, Noninfiltrating - metabolism ; Carcinoma, Intraductal, Noninfiltrating - mortality ; Carcinoma, Intraductal, Noninfiltrating - pathology ; Case-Control Studies ; Female ; Humans ; Immunoenzyme Techniques ; Middle Aged ; Neoplasm Invasiveness ; Phosphatidylinositol-3,4,5-Trisphosphate 5-Phosphatases ; Phosphoric Monoester Hydrolases - metabolism ; Prognosis ; PTEN Phosphohydrolase - metabolism ; Research Article ; src Homology Domains ; Survival Rate</subject><ispartof>Tumor biology, 2008-01, Vol.29 (5), p.330-341</ispartof><rights>2008 S. Karger AG, Basel</rights><rights>Copyright 2008 S. Karger AG, Basel.</rights><rights>Copyright (c) 2008 S. Karger AG, Basel</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c362t-923af3469ee792c64c81fbcbc6b105ff4a422b639aa36801b37e381657cc94913</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,2422,27903,27904</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19065064$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Prasad, Nagendra K.</creatorcontrib><creatorcontrib>Tandon, Manish</creatorcontrib><creatorcontrib>Handa, Anant</creatorcontrib><creatorcontrib>Moore, George E.</creatorcontrib><creatorcontrib>Babbs, Charles F.</creatorcontrib><creatorcontrib>Snyder, Paul W.</creatorcontrib><creatorcontrib>Bose, Shikha</creatorcontrib><title>High Expression of Obesity-Linked Phosphatase SHIP2 in Invasive Breast Cancer Correlates with Reduced Disease-Free Survival</title><title>Tumor biology</title><addtitle>Tumor Biol</addtitle><description>SH2-containing 5′-inositol phosphatase (SHIP2) is a known regulator of insulin function. Genetic knockout of SHIP2 in mice causes mild insulin hypersensitivity and prevents high-fat-diet-induced obesity. SHIP2 also regulates actin remodeling and epidermal growth factor receptor (EGFR) turnover and supports breast cancer; and metastatic growth. To determine the clinical significance of SHIP2 expression in breast cancer and its relationship to relevant oncogenic molecules, SHIP2 expression was determined immunohistochemically in 285 primary breast cancers; 140 ductal carcinomas in situ (DCIS) and 145 invasive carcinomas. Forty-five percent of the specimens showed high SHIP2 levels in cancer cells while only 15% of adjacent normal cells expressed high SHIP2 levels (p < 0.0001). In cancer cells, the risk of SHIP2 overexpression is elevated (a) in women aged ≤50 years (relative risk, RR = 4.13; 95% confidence interval, CI, 2.5–6.9) compared to women aged >50 years (RR = 2.37; 95% CI 1.6–3.5; p = 0.0003), and (b) in invasive carcinomas (RR = 3.52; 95% CI 2.3–5.5) compared with DCIS (RR = 2.22; 95% CI 1.5–3.5; p = 0.0009). Patients with higher SHIP2 levels in invasive carcinomas had significantly reduced disease-free (p = 0.0025) and overall survival periods (p = 0.0228). In invasive carcinomas, SHIP2 correlated with estrogen receptor absence (p = 0.003) and EGFR presence (p = 0.0147). In conclusion, SHIP2 is an important biomarker for breast cancer.</description><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Biomarkers, Tumor - metabolism</subject><subject>Blotting, Western</subject><subject>Breast Neoplasms - metabolism</subject><subject>Breast Neoplasms - mortality</subject><subject>Breast Neoplasms - pathology</subject><subject>Carcinoma, Ductal, Breast - metabolism</subject><subject>Carcinoma, Ductal, Breast - mortality</subject><subject>Carcinoma, Ductal, Breast - pathology</subject><subject>Carcinoma, Intraductal, Noninfiltrating - metabolism</subject><subject>Carcinoma, Intraductal, Noninfiltrating - mortality</subject><subject>Carcinoma, Intraductal, Noninfiltrating - pathology</subject><subject>Case-Control Studies</subject><subject>Female</subject><subject>Humans</subject><subject>Immunoenzyme Techniques</subject><subject>Middle Aged</subject><subject>Neoplasm Invasiveness</subject><subject>Phosphatidylinositol-3,4,5-Trisphosphate 5-Phosphatases</subject><subject>Phosphoric Monoester Hydrolases - metabolism</subject><subject>Prognosis</subject><subject>PTEN Phosphohydrolase - metabolism</subject><subject>Research Article</subject><subject>src Homology Domains</subject><subject>Survival Rate</subject><issn>1010-4283</issn><issn>1423-0380</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqF0c9rFDEUB_AgFlurB-8iwYPgYerLj0kmR11bd2GhxR_nIZN90007O7PmzawW_3kju7Tgpac8yOd94fFl7JWAMyFK9wEAhJXOwhN2IrRUBagKnuYZBBRaVuqYPSe6yap0zjxjx8KBKcHoE_ZnHq_X_Pz3NiFRHHo-tPyyQYrjXbGM_S2u-NV6oO3aj56Qf5svriSPPV_0O09xh_xTQk8jn_k-YOKzISXs_IjEf8Vxzb_iago543OkzLC4SJhDprSLO9-9YEet7whfHt5T9uPi_PtsXiwvvyxmH5dFUEaOhZPKt0obh2idDEaHSrRNaIJpBJRtq72WsjHKea9MBaJRFlUlTGlDcNoJdcre7XO3afg5IY31JlLArvM9DhPVxlUVGKsfhRKctFLaDN_-B2-GKfX5iFrmf3DWyoze71FIA1HCtt6muPHprhZQ_-utvu8t2zeHwKnZ4OpBHorK4PUe3Pp0jekB7Pf_Aj4vmkw</recordid><startdate>20080101</startdate><enddate>20080101</enddate><creator>Prasad, Nagendra K.</creator><creator>Tandon, Manish</creator><creator>Handa, Anant</creator><creator>Moore, George E.</creator><creator>Babbs, Charles F.</creator><creator>Snyder, Paul W.</creator><creator>Bose, Shikha</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>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7T5</scope><scope>7TO</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</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>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M7P</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>7TS</scope><scope>7X8</scope></search><sort><creationdate>20080101</creationdate><title>High Expression of Obesity-Linked Phosphatase SHIP2 in Invasive Breast Cancer Correlates with Reduced Disease-Free Survival</title><author>Prasad, Nagendra K. ; Tandon, Manish ; Handa, Anant ; Moore, George E. ; Babbs, Charles F. ; Snyder, Paul W. ; Bose, Shikha</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c362t-923af3469ee792c64c81fbcbc6b105ff4a422b639aa36801b37e381657cc94913</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Biomarkers, Tumor - metabolism</topic><topic>Blotting, Western</topic><topic>Breast Neoplasms - metabolism</topic><topic>Breast Neoplasms - mortality</topic><topic>Breast Neoplasms - pathology</topic><topic>Carcinoma, Ductal, Breast - metabolism</topic><topic>Carcinoma, Ductal, Breast - mortality</topic><topic>Carcinoma, Ductal, Breast - pathology</topic><topic>Carcinoma, Intraductal, Noninfiltrating - metabolism</topic><topic>Carcinoma, Intraductal, Noninfiltrating - mortality</topic><topic>Carcinoma, Intraductal, Noninfiltrating - pathology</topic><topic>Case-Control Studies</topic><topic>Female</topic><topic>Humans</topic><topic>Immunoenzyme Techniques</topic><topic>Middle Aged</topic><topic>Neoplasm Invasiveness</topic><topic>Phosphatidylinositol-3,4,5-Trisphosphate 5-Phosphatases</topic><topic>Phosphoric Monoester Hydrolases - metabolism</topic><topic>Prognosis</topic><topic>PTEN Phosphohydrolase - metabolism</topic><topic>Research Article</topic><topic>src Homology Domains</topic><topic>Survival Rate</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Prasad, Nagendra K.</creatorcontrib><creatorcontrib>Tandon, Manish</creatorcontrib><creatorcontrib>Handa, Anant</creatorcontrib><creatorcontrib>Moore, George E.</creatorcontrib><creatorcontrib>Babbs, Charles F.</creatorcontrib><creatorcontrib>Snyder, Paul W.</creatorcontrib><creatorcontrib>Bose, Shikha</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Immunology Abstracts</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>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science 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>Research Library Prep</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Biological Science Database</collection><collection>Research Library (Corporate)</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 Basic</collection><collection>Physical Education Index</collection><collection>MEDLINE - Academic</collection><jtitle>Tumor biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Prasad, Nagendra K.</au><au>Tandon, Manish</au><au>Handa, Anant</au><au>Moore, George E.</au><au>Babbs, Charles F.</au><au>Snyder, Paul W.</au><au>Bose, Shikha</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>High Expression of Obesity-Linked Phosphatase SHIP2 in Invasive Breast Cancer Correlates with Reduced Disease-Free Survival</atitle><jtitle>Tumor biology</jtitle><addtitle>Tumor Biol</addtitle><date>2008-01-01</date><risdate>2008</risdate><volume>29</volume><issue>5</issue><spage>330</spage><epage>341</epage><pages>330-341</pages><issn>1010-4283</issn><eissn>1423-0380</eissn><abstract>SH2-containing 5′-inositol phosphatase (SHIP2) is a known regulator of insulin function. Genetic knockout of SHIP2 in mice causes mild insulin hypersensitivity and prevents high-fat-diet-induced obesity. SHIP2 also regulates actin remodeling and epidermal growth factor receptor (EGFR) turnover and supports breast cancer; and metastatic growth. To determine the clinical significance of SHIP2 expression in breast cancer and its relationship to relevant oncogenic molecules, SHIP2 expression was determined immunohistochemically in 285 primary breast cancers; 140 ductal carcinomas in situ (DCIS) and 145 invasive carcinomas. Forty-five percent of the specimens showed high SHIP2 levels in cancer cells while only 15% of adjacent normal cells expressed high SHIP2 levels (p < 0.0001). In cancer cells, the risk of SHIP2 overexpression is elevated (a) in women aged ≤50 years (relative risk, RR = 4.13; 95% confidence interval, CI, 2.5–6.9) compared to women aged >50 years (RR = 2.37; 95% CI 1.6–3.5; p = 0.0003), and (b) in invasive carcinomas (RR = 3.52; 95% CI 2.3–5.5) compared with DCIS (RR = 2.22; 95% CI 1.5–3.5; p = 0.0009). Patients with higher SHIP2 levels in invasive carcinomas had significantly reduced disease-free (p = 0.0025) and overall survival periods (p = 0.0228). In invasive carcinomas, SHIP2 correlated with estrogen receptor absence (p = 0.003) and EGFR presence (p = 0.0147). In conclusion, SHIP2 is an important biomarker for breast cancer.</abstract><cop>Basel, Switzerland</cop><pub>Springer Nature B.V</pub><pmid>19065064</pmid><doi>10.1159/000172970</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adult Aged Aged, 80 and over Biomarkers, Tumor - metabolism Blotting, Western Breast Neoplasms - metabolism Breast Neoplasms - mortality Breast Neoplasms - pathology Carcinoma, Ductal, Breast - metabolism Carcinoma, Ductal, Breast - mortality Carcinoma, Ductal, Breast - pathology Carcinoma, Intraductal, Noninfiltrating - metabolism Carcinoma, Intraductal, Noninfiltrating - mortality Carcinoma, Intraductal, Noninfiltrating - pathology Case-Control Studies Female Humans Immunoenzyme Techniques Middle Aged Neoplasm Invasiveness Phosphatidylinositol-3,4,5-Trisphosphate 5-Phosphatases Phosphoric Monoester Hydrolases - metabolism Prognosis PTEN Phosphohydrolase - metabolism Research Article src Homology Domains Survival Rate |
| title | High Expression of Obesity-Linked Phosphatase SHIP2 in Invasive Breast Cancer Correlates with Reduced Disease-Free Survival |
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