Lifestyle and Reproductive Factors and Ovarian Cancer Risk by p53 and MAPK Expression
One model of ovarian cancer development model divides tumors into two types. Type I tumors are characterized by and mutations, which can activate mitogen-activated protein kinase (MAPK). Type II tumors are characterized by tubal precursor lesions with p53 mutations. We evaluated the association betw...
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Veröffentlicht in: | Cancer epidemiology, biomarkers & prevention biomarkers & prevention, 2018-01, Vol.27 (1), p.96-102 |
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description | One model of ovarian cancer development model divides tumors into two types. Type I tumors are characterized by
and
mutations, which can activate mitogen-activated protein kinase (MAPK). Type II tumors are characterized by tubal precursor lesions with p53 mutations. We evaluated the association between lifestyle and reproductive factors and risk of ovarian cancer defined by p53 and MAPK expression.
Epithelial ovarian cancer cases (
= 274) and controls (
= 1,907) were identified from the Nurses' Health Study and Nurses' Health Study II prospective cohorts, and the population-based New England Case-Control study. Reproductive and lifestyle exposures were assessed by questionnaire/interview. We performed immunohistochemical assays for p53 and MAPK expression. Odds ratios (ORs) and 95% confidence intervals (CIs) were estimated using polytomous logistic regression.
Parity was associated with a decreased risk of p53 wild-type tumors (OR = 0.31; 95% CI, 0.18-0.55), but not p53-mutant tumors (OR = 0.92; 95% CI, 0.54-1.59)(
< 0.01). Family history of breast or ovarian cancer was associated with risk of MAPK-negative (OR = 2.06; 95% CI, 1.39-3.06), but not MAPK-positive tumors (OR = 0.74; 95% CI, 0.43-1.27;
< 0.01). In cross-classified analyses, family history of breast or ovarian cancer was most strongly associated with p53-mutant/MAPK-negative tumors (OR = 2.33; 95% CI, 1.44-3.75). Differences by MAPK expression were also observed for estrogen plus progesterone hormone therapy use (
= 0.03).
These findings provide evidence that parity, family history, and estrogen plus progesterone hormone therapy use may be differentially associated with tumor subtypes defined by p53 and MAPK expression.
In future studies, other immunohistochemical markers or gene expression profiles that more clearly define these subtypes should be considered.
. |
doi_str_mv | 10.1158/1055-9965.EPI-17-0609 |
format | Article |
fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_5993043</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1964271827</sourcerecordid><originalsourceid>FETCH-LOGICAL-c439t-9c6f2b7d1b55d1c401b9f645a4446e1bd02f909c06c12efecdcf76db9d830a9a3</originalsourceid><addsrcrecordid>eNpdkV1P2zAUhq0JNFjZT9gUiRtuwo7jr_hmEqrKqCiiqsa15djOZpbGwU6q9d8vLVANrmzpfc4rHz8IfcFwiTErv2FgLJeSs8vZcp5jkQMH-QGdYkbKXAjGjsb7K3OCPqX0CABCMvYRnRQSE0I4P0UPC1-71G8bl-nWZivXxWAH0_uNy6616UNM--B-o6PXbTbVrXExW_n0J6u2WcfIPr67Wt5ms79ddCn50J6h41o3yX1-OSfo4Xr2c3qTL-5_zKdXi9xQIvtcGl4XlbC4YsxiQwFXsuaUaUopd7iyUNQSpAFucOFqZ6ypBbeVtCUBLTWZoO_Pvd1QrZ01ru2jblQX_VrHrQraq7dJ63-rX2GjmJQEKBkLLl4KYngaxo9Qa5-MaxrdujAkhSWnhcBlIUb0_B36GIbYjuupAoCXJRBKR4o9UyaGlKKrD4_BoHbi1E6K2klRoziFhdqJG-e-_r_JYerVFPkHDtOUaw</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2006880344</pqid></control><display><type>article</type><title>Lifestyle and Reproductive Factors and Ovarian Cancer Risk by p53 and MAPK Expression</title><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>American Association for Cancer Research</source><creator>Harris, Holly R ; Rice, Megan S ; Shafrir, Amy L ; Poole, Elizabeth M ; Gupta, Mamta ; Hecht, Jonathan L ; Terry, Kathryn L ; Tworoger, Shelley S</creator><creatorcontrib>Harris, Holly R ; Rice, Megan S ; Shafrir, Amy L ; Poole, Elizabeth M ; Gupta, Mamta ; Hecht, Jonathan L ; Terry, Kathryn L ; Tworoger, Shelley S</creatorcontrib><description>One model of ovarian cancer development model divides tumors into two types. Type I tumors are characterized by
and
mutations, which can activate mitogen-activated protein kinase (MAPK). Type II tumors are characterized by tubal precursor lesions with p53 mutations. We evaluated the association between lifestyle and reproductive factors and risk of ovarian cancer defined by p53 and MAPK expression.
Epithelial ovarian cancer cases (
= 274) and controls (
= 1,907) were identified from the Nurses' Health Study and Nurses' Health Study II prospective cohorts, and the population-based New England Case-Control study. Reproductive and lifestyle exposures were assessed by questionnaire/interview. We performed immunohistochemical assays for p53 and MAPK expression. Odds ratios (ORs) and 95% confidence intervals (CIs) were estimated using polytomous logistic regression.
Parity was associated with a decreased risk of p53 wild-type tumors (OR = 0.31; 95% CI, 0.18-0.55), but not p53-mutant tumors (OR = 0.92; 95% CI, 0.54-1.59)(
< 0.01). Family history of breast or ovarian cancer was associated with risk of MAPK-negative (OR = 2.06; 95% CI, 1.39-3.06), but not MAPK-positive tumors (OR = 0.74; 95% CI, 0.43-1.27;
< 0.01). In cross-classified analyses, family history of breast or ovarian cancer was most strongly associated with p53-mutant/MAPK-negative tumors (OR = 2.33; 95% CI, 1.44-3.75). Differences by MAPK expression were also observed for estrogen plus progesterone hormone therapy use (
= 0.03).
These findings provide evidence that parity, family history, and estrogen plus progesterone hormone therapy use may be differentially associated with tumor subtypes defined by p53 and MAPK expression.
In future studies, other immunohistochemical markers or gene expression profiles that more clearly define these subtypes should be considered.
.</description><identifier>ISSN: 1055-9965</identifier><identifier>EISSN: 1538-7755</identifier><identifier>DOI: 10.1158/1055-9965.EPI-17-0609</identifier><identifier>PMID: 29133366</identifier><language>eng</language><publisher>United States: American Association for Cancer Research, Inc</publisher><subject>Bioindicators ; Breast cancer ; Endocrine therapy ; Estrogens ; Family medical history ; Gene expression ; Genetics ; Health risk assessment ; Health risks ; Kinases ; Lesions ; Lifestyles ; MAP kinase ; Medical personnel ; Mutation ; Ovarian cancer ; Ovarian carcinoma ; p53 Protein ; Parity ; Progesterone ; Protein kinase ; Risk factors ; Tumors</subject><ispartof>Cancer epidemiology, biomarkers & prevention, 2018-01, Vol.27 (1), p.96-102</ispartof><rights>2017 American Association for Cancer Research.</rights><rights>Copyright American Association for Cancer Research, Inc. Jan 2018</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c439t-9c6f2b7d1b55d1c401b9f645a4446e1bd02f909c06c12efecdcf76db9d830a9a3</citedby><cites>FETCH-LOGICAL-c439t-9c6f2b7d1b55d1c401b9f645a4446e1bd02f909c06c12efecdcf76db9d830a9a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,315,781,785,886,3357,27928,27929</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29133366$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Harris, Holly R</creatorcontrib><creatorcontrib>Rice, Megan S</creatorcontrib><creatorcontrib>Shafrir, Amy L</creatorcontrib><creatorcontrib>Poole, Elizabeth M</creatorcontrib><creatorcontrib>Gupta, Mamta</creatorcontrib><creatorcontrib>Hecht, Jonathan L</creatorcontrib><creatorcontrib>Terry, Kathryn L</creatorcontrib><creatorcontrib>Tworoger, Shelley S</creatorcontrib><title>Lifestyle and Reproductive Factors and Ovarian Cancer Risk by p53 and MAPK Expression</title><title>Cancer epidemiology, biomarkers & prevention</title><addtitle>Cancer Epidemiol Biomarkers Prev</addtitle><description>One model of ovarian cancer development model divides tumors into two types. Type I tumors are characterized by
and
mutations, which can activate mitogen-activated protein kinase (MAPK). Type II tumors are characterized by tubal precursor lesions with p53 mutations. We evaluated the association between lifestyle and reproductive factors and risk of ovarian cancer defined by p53 and MAPK expression.
Epithelial ovarian cancer cases (
= 274) and controls (
= 1,907) were identified from the Nurses' Health Study and Nurses' Health Study II prospective cohorts, and the population-based New England Case-Control study. Reproductive and lifestyle exposures were assessed by questionnaire/interview. We performed immunohistochemical assays for p53 and MAPK expression. Odds ratios (ORs) and 95% confidence intervals (CIs) were estimated using polytomous logistic regression.
Parity was associated with a decreased risk of p53 wild-type tumors (OR = 0.31; 95% CI, 0.18-0.55), but not p53-mutant tumors (OR = 0.92; 95% CI, 0.54-1.59)(
< 0.01). Family history of breast or ovarian cancer was associated with risk of MAPK-negative (OR = 2.06; 95% CI, 1.39-3.06), but not MAPK-positive tumors (OR = 0.74; 95% CI, 0.43-1.27;
< 0.01). In cross-classified analyses, family history of breast or ovarian cancer was most strongly associated with p53-mutant/MAPK-negative tumors (OR = 2.33; 95% CI, 1.44-3.75). Differences by MAPK expression were also observed for estrogen plus progesterone hormone therapy use (
= 0.03).
These findings provide evidence that parity, family history, and estrogen plus progesterone hormone therapy use may be differentially associated with tumor subtypes defined by p53 and MAPK expression.
In future studies, other immunohistochemical markers or gene expression profiles that more clearly define these subtypes should be considered.
.</description><subject>Bioindicators</subject><subject>Breast cancer</subject><subject>Endocrine therapy</subject><subject>Estrogens</subject><subject>Family medical history</subject><subject>Gene expression</subject><subject>Genetics</subject><subject>Health risk assessment</subject><subject>Health risks</subject><subject>Kinases</subject><subject>Lesions</subject><subject>Lifestyles</subject><subject>MAP kinase</subject><subject>Medical personnel</subject><subject>Mutation</subject><subject>Ovarian cancer</subject><subject>Ovarian carcinoma</subject><subject>p53 Protein</subject><subject>Parity</subject><subject>Progesterone</subject><subject>Protein kinase</subject><subject>Risk factors</subject><subject>Tumors</subject><issn>1055-9965</issn><issn>1538-7755</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><recordid>eNpdkV1P2zAUhq0JNFjZT9gUiRtuwo7jr_hmEqrKqCiiqsa15djOZpbGwU6q9d8vLVANrmzpfc4rHz8IfcFwiTErv2FgLJeSs8vZcp5jkQMH-QGdYkbKXAjGjsb7K3OCPqX0CABCMvYRnRQSE0I4P0UPC1-71G8bl-nWZivXxWAH0_uNy6616UNM--B-o6PXbTbVrXExW_n0J6u2WcfIPr67Wt5ms79ddCn50J6h41o3yX1-OSfo4Xr2c3qTL-5_zKdXi9xQIvtcGl4XlbC4YsxiQwFXsuaUaUopd7iyUNQSpAFucOFqZ6ypBbeVtCUBLTWZoO_Pvd1QrZ01ru2jblQX_VrHrQraq7dJ63-rX2GjmJQEKBkLLl4KYngaxo9Qa5-MaxrdujAkhSWnhcBlIUb0_B36GIbYjuupAoCXJRBKR4o9UyaGlKKrD4_BoHbi1E6K2klRoziFhdqJG-e-_r_JYerVFPkHDtOUaw</recordid><startdate>20180101</startdate><enddate>20180101</enddate><creator>Harris, Holly R</creator><creator>Rice, Megan S</creator><creator>Shafrir, Amy L</creator><creator>Poole, Elizabeth M</creator><creator>Gupta, Mamta</creator><creator>Hecht, Jonathan L</creator><creator>Terry, Kathryn L</creator><creator>Tworoger, Shelley S</creator><general>American Association for Cancer Research, Inc</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7TM</scope><scope>7TO</scope><scope>H94</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20180101</creationdate><title>Lifestyle and Reproductive Factors and Ovarian Cancer Risk by p53 and MAPK Expression</title><author>Harris, Holly R ; Rice, Megan S ; Shafrir, Amy L ; Poole, Elizabeth M ; Gupta, Mamta ; Hecht, Jonathan L ; Terry, Kathryn L ; Tworoger, Shelley S</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c439t-9c6f2b7d1b55d1c401b9f645a4446e1bd02f909c06c12efecdcf76db9d830a9a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Bioindicators</topic><topic>Breast cancer</topic><topic>Endocrine therapy</topic><topic>Estrogens</topic><topic>Family medical history</topic><topic>Gene expression</topic><topic>Genetics</topic><topic>Health risk assessment</topic><topic>Health risks</topic><topic>Kinases</topic><topic>Lesions</topic><topic>Lifestyles</topic><topic>MAP kinase</topic><topic>Medical personnel</topic><topic>Mutation</topic><topic>Ovarian cancer</topic><topic>Ovarian carcinoma</topic><topic>p53 Protein</topic><topic>Parity</topic><topic>Progesterone</topic><topic>Protein kinase</topic><topic>Risk factors</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Harris, Holly R</creatorcontrib><creatorcontrib>Rice, Megan S</creatorcontrib><creatorcontrib>Shafrir, Amy L</creatorcontrib><creatorcontrib>Poole, Elizabeth M</creatorcontrib><creatorcontrib>Gupta, Mamta</creatorcontrib><creatorcontrib>Hecht, Jonathan L</creatorcontrib><creatorcontrib>Terry, Kathryn L</creatorcontrib><creatorcontrib>Tworoger, Shelley S</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>Nucleic Acids Abstracts</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 epidemiology, biomarkers & prevention</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Harris, Holly R</au><au>Rice, Megan S</au><au>Shafrir, Amy L</au><au>Poole, Elizabeth M</au><au>Gupta, Mamta</au><au>Hecht, Jonathan L</au><au>Terry, Kathryn L</au><au>Tworoger, Shelley S</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Lifestyle and Reproductive Factors and Ovarian Cancer Risk by p53 and MAPK Expression</atitle><jtitle>Cancer epidemiology, biomarkers & prevention</jtitle><addtitle>Cancer Epidemiol Biomarkers Prev</addtitle><date>2018-01-01</date><risdate>2018</risdate><volume>27</volume><issue>1</issue><spage>96</spage><epage>102</epage><pages>96-102</pages><issn>1055-9965</issn><eissn>1538-7755</eissn><abstract>One model of ovarian cancer development model divides tumors into two types. Type I tumors are characterized by
and
mutations, which can activate mitogen-activated protein kinase (MAPK). Type II tumors are characterized by tubal precursor lesions with p53 mutations. We evaluated the association between lifestyle and reproductive factors and risk of ovarian cancer defined by p53 and MAPK expression.
Epithelial ovarian cancer cases (
= 274) and controls (
= 1,907) were identified from the Nurses' Health Study and Nurses' Health Study II prospective cohorts, and the population-based New England Case-Control study. Reproductive and lifestyle exposures were assessed by questionnaire/interview. We performed immunohistochemical assays for p53 and MAPK expression. Odds ratios (ORs) and 95% confidence intervals (CIs) were estimated using polytomous logistic regression.
Parity was associated with a decreased risk of p53 wild-type tumors (OR = 0.31; 95% CI, 0.18-0.55), but not p53-mutant tumors (OR = 0.92; 95% CI, 0.54-1.59)(
< 0.01). Family history of breast or ovarian cancer was associated with risk of MAPK-negative (OR = 2.06; 95% CI, 1.39-3.06), but not MAPK-positive tumors (OR = 0.74; 95% CI, 0.43-1.27;
< 0.01). In cross-classified analyses, family history of breast or ovarian cancer was most strongly associated with p53-mutant/MAPK-negative tumors (OR = 2.33; 95% CI, 1.44-3.75). Differences by MAPK expression were also observed for estrogen plus progesterone hormone therapy use (
= 0.03).
These findings provide evidence that parity, family history, and estrogen plus progesterone hormone therapy use may be differentially associated with tumor subtypes defined by p53 and MAPK expression.
In future studies, other immunohistochemical markers or gene expression profiles that more clearly define these subtypes should be considered.
.</abstract><cop>United States</cop><pub>American Association for Cancer Research, Inc</pub><pmid>29133366</pmid><doi>10.1158/1055-9965.EPI-17-0609</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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source | Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; American Association for Cancer Research |
subjects | Bioindicators Breast cancer Endocrine therapy Estrogens Family medical history Gene expression Genetics Health risk assessment Health risks Kinases Lesions Lifestyles MAP kinase Medical personnel Mutation Ovarian cancer Ovarian carcinoma p53 Protein Parity Progesterone Protein kinase Risk factors Tumors |
title | Lifestyle and Reproductive Factors and Ovarian Cancer Risk by p53 and MAPK Expression |
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