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
Hauptverfasser: Harris, Holly R, Rice, Megan S, Shafrir, Amy L, Poole, Elizabeth M, Gupta, Mamta, Hecht, Jonathan L, Terry, Kathryn L, Tworoger, Shelley S
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container_end_page 102
container_issue 1
container_start_page 96
container_title Cancer epidemiology, biomarkers & prevention
container_volume 27
creator Harris, Holly R
Rice, Megan S
Shafrir, Amy L
Poole, Elizabeth M
Gupta, Mamta
Hecht, Jonathan L
Terry, Kathryn L
Tworoger, Shelley S
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
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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)( &lt; 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; &lt; 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. 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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; &lt; 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. 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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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