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{"title"=>"Obesity-mediated regulation of HGF/c-met is associated with reduced basal-like breast cancer latency in Parous mice", "type"=>"journal", "authors"=>[{"first_name"=>"Sneha", "last_name"=>"Sundaram", "scopus_author_id"=>"7101967532"}, {"first_name"=>"Alex J.", "last_name"=>"Freemerman", "scopus_author_id"=>"6602463793"}, {"first_name"=>"Joseph A.", "last_name"=>"Galanko", "scopus_author_id"=>"6603715132"}, {"first_name"=>"Kirk K.", "last_name"=>"McNaughton", "scopus_author_id"=>"56872650700"}, {"first_name"=>"Katharine M.", "last_name"=>"Bendt", "scopus_author_id"=>"6507097749"}, {"first_name"=>"David B.", "last_name"=>"Darr", "scopus_author_id"=>"42061183700"}, {"first_name"=>"Melissa A.", "last_name"=>"Troester", "scopus_author_id"=>"6603045250"}, {"first_name"=>"Liza", "last_name"=>"Makowski", "scopus_author_id"=>"7004872137"}], "year"=>2014, "source"=>"PLoS ONE", "identifiers"=>{"issn"=>"19326203", "pui"=>"600310344", "doi"=>"10.1371/journal.pone.0111394", "sgr"=>"84908568810", "pmid"=>"25354395", "scopus"=>"2-s2.0-84908568810"}, "id"=>"9da62426-4e95-3958-a94c-6beef1e15dfa", "abstract"=>"It is widely thought that pregnancy reduces breast cancer risk, but this lacks consideration of breast cancer subtypes. While a full term pregnancy reduces risk for estrogen receptor positive (ER+) and luminal breast cancers, parity is associated with increased risk of basal-like breast cancer (BBC) subtype. Basal-like subtypes represent less than 10% of breast cancers and are highly aggressive, affecting primarily young, African American women. Our previous work demonstrated that high fat diet-induced obesity in nulliparous mice significantly blunted latency in C3(1)-TAg mice, a model of BBC, potentially through the hepatocyte growth factor (HGF)/c-Met oncogenic pathway. Experimental studies have examined parity and obesity individually, but to date, the joint effects of parity and obesity have not been studied. We investigated the role of obesity in parous mice on BBC. Parity alone dramatically blunted tumor latency compared to nulliparous controls with no effects on tumor number or growth, while obesity had only a minor role in further reducing latency. Obesity-associated metabolic mediators and hormones such as insulin, estrogen, and progesterone were not significantly regulated by obesity. Plasma IL-6 was also significantly elevated by obesity in parous mice. We have previously reported a potential role for stromal-derived hepatocyte growth factor (HGF) via its cognate receptor c-Met in the etiology of obesity-induced BBC tumor onset and in both human and murine primary coculture models of BBC-aggressiveness. Obesity-associated c-Met concentrations were 2.5-fold greater in normal mammary glands of parous mice. Taken together, our studies demonstrate that, parity in C3(1)-TAg mice dramatically reduced BBC latency compared to nulliparous mice. In parous mice, c-Met is regulated by obesity in unaffected mammary gland and is associated with tumor onset. C3(1)-TAg mice recapitulate epidemiologic findings such that parity drives increased BBC risk and potential microenvironmental alterations in c-Met signaling may play a role in etiology.", "link"=>"http://www.mendeley.com/research/obesitymediated-regulation-hgfcmet-associated-reduced-basallike-breast-cancer-latency-parous-mice", "reader_count"=>7, "reader_count_by_academic_status"=>{"Student > Doctoral Student"=>1, "Researcher"=>1, "Student > Ph. D. Student"=>3, "Student > Postgraduate"=>1, "Student > Master"=>1}, "reader_count_by_user_role"=>{"Student > Doctoral Student"=>1, "Researcher"=>1, "Student > Ph. D. Student"=>3, "Student > Postgraduate"=>1, "Student > Master"=>1}, "reader_count_by_subject_area"=>{"Environmental Science"=>1, "Biochemistry, Genetics and Molecular Biology"=>1, "Medicine and Dentistry"=>3, "Agricultural and Biological Sciences"=>1, "Immunology and Microbiology"=>1}, "reader_count_by_subdiscipline"=>{"Medicine and Dentistry"=>{"Medicine and Dentistry"=>3}, "Immunology and Microbiology"=>{"Immunology and Microbiology"=>1}, "Agricultural and Biological Sciences"=>{"Agricultural and Biological Sciences"=>1}, "Biochemistry, Genetics and Molecular Biology"=>{"Biochemistry, Genetics and Molecular Biology"=>1}, "Environmental Science"=>{"Environmental Science"=>1}}, "reader_count_by_country"=>{"Iraq"=>1}, "group_count"=>0}

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• http://doi.org/10.4049/jimmunol.1800002
• http://doi.org/10.1016/j.atherosclerosis.2017.10.009
• http://doi.org/10.1016/j.tem.2016.08.004
• http://doi.org/10.1186/s12935-016-0300-y
• http://doi.org/10.1111/imr.12856
• http://doi.org/10.1016/j.molmet.2016.04.005
• http://doi.org/10.1530/ERC-15-0400

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Figshare

• {"files"=>["https://ndownloader.figshare.com/files/1771027"], "description"=>"<p>Cytokine and chemokine concentrations of A) IL-6, B) TNF-α and C) MCP-1 were measured in plasma at sacrifice. n = 12. *P = 0.028. D) Plasma estrogen levels were determined using ELISA analysis. n = 14. E) Plasma progesterone levels were determined using ELISA analysis. n = 14.</p>", "links"=>[], "tags"=>["nulliparous mice", "African American women", "breast cancer risk", "obesity", "parity", "er", "tumor", "breast cancer subtypes", "bbc", "luminal breast cancers", "parous mice", "Hepatocyte Growth Factor", "role", "il", "hgf"], "article_id"=>1222285, "categories"=>["Uncategorised"], "users"=>["Sneha Sundaram", "Alex J. Freemerman", "Joseph A. Galanko", "Kirk K. McNaughton", "Katharine M. Bendt", "David B. Darr", "Melissa A. Troester", "Liza Makowski"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0111394.g003", "stats"=>{"downloads"=>0, "page_views"=>14, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_IL_6_concentration_was_elevated_but_plasma_levels_of_other_inflammatory_mediators_and_reproductive_hormones_were_not_increased_by_obesity_in_parous_mice_/1222285", "title"=>"IL-6 concentration was elevated but plasma levels of other inflammatory mediators and reproductive hormones were not increased by obesity in parous mice.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2014-10-29 03:10:52"}
• {"files"=>["https://ndownloader.figshare.com/files/1771035", "https://ndownloader.figshare.com/files/1771036"], "description"=>"<div><p>It is widely thought that pregnancy reduces breast cancer risk, but this lacks consideration of breast cancer subtypes. While a full term pregnancy reduces risk for estrogen receptor positive (ER+) and luminal breast cancers, parity is associated with increased risk of basal-like breast cancer (BBC) subtype. Basal-like subtypes represent less than 10% of breast cancers and are highly aggressive, affecting primarily young, African American women. Our previous work demonstrated that high fat diet-induced obesity in nulliparous mice significantly blunted latency in C3(1)-T_Ag mice, a model of BBC, potentially through the hepatocyte growth factor (HGF)/c-Met oncogenic pathway. Experimental studies have examined parity and obesity individually, but to date, the joint effects of parity and obesity have not been studied. We investigated the role of obesity in parous mice on BBC. Parity alone dramatically blunted tumor latency compared to nulliparous controls with no effects on tumor number or growth, while obesity had only a minor role in further reducing latency. Obesity-associated metabolic mediators and hormones such as insulin, estrogen, and progesterone were not significantly regulated by obesity. Plasma IL-6 was also significantly elevated by obesity in parous mice. We have previously reported a potential role for stromal-derived hepatocyte growth factor (HGF) via its cognate receptor c-Met in the etiology of obesity-induced BBC tumor onset and in both human and murine primary coculture models of BBC-aggressiveness. Obesity-associated c-Met concentrations were 2.5-fold greater in normal mammary glands of parous mice. Taken together, our studies demonstrate that, parity in C3(1)-T_Ag mice dramatically reduced BBC latency compared to nulliparous mice. In parous mice, c-Met is regulated by obesity in unaffected mammary gland and is associated with tumor onset. C3(1)-T_Ag mice recapitulate epidemiologic findings such that parity drives increased BBC risk and potential microenvironmental alterations in c-Met signaling may play a role in etiology.</p></div>", "links"=>[], "tags"=>["nulliparous mice", "African American women", "breast cancer risk", "obesity", "parity", "er", "tumor", "breast cancer subtypes", "bbc", "luminal breast cancers", "parous mice", "Hepatocyte Growth Factor", "role", "il", "hgf"], "article_id"=>1222293, "categories"=>["Uncategorised"], "users"=>["Sneha Sundaram", "Alex J. Freemerman", "Joseph A. Galanko", "Kirk K. McNaughton", "Katharine M. Bendt", "David B. Darr", "Melissa A. Troester", "Liza Makowski"], "doi"=>["https://dx.doi.org/10.1371/journal.pone.0111394.s001", "https://dx.doi.org/10.1371/journal.pone.0111394.s002"], "stats"=>{"downloads"=>9, "page_views"=>15, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Obesity_Mediated_Regulation_of_HGF_c_Met_Is_Associated_with_Reduced_Basal_Like_Breast_Cancer_Latency_in_Parous_Mice_/1222293", "title"=>"Obesity-Mediated Regulation of HGF/c-Met Is Associated with Reduced Basal-Like Breast Cancer Latency in Parous Mice", "pos_in_sequence"=>0, "defined_type"=>4, "published_date"=>"2014-10-29 03:10:52"}
• {"files"=>["https://ndownloader.figshare.com/files/1771025"], "description"=>"<p>A) C3(1)-T_Ag body weight was measured weekly over the course of the study until mice were sacrificed. Diet was initiated at 10 weeks of age (week 0 on diet) in n = 15 mice. *P<0.05 over weeks 1–6. B) Body fat content by MRI was measured monthly until sacrifice. Percent fat content over total body mass is shown. n = 15. *P<0.0001 at 4 weeks on diet, and P = 0.0049 at 8 weeks on diets. C) Blood glucose levels were measured from tail vein blood in mice fasted 6 hours. n = 15 mice. D) Insulin was measured at sacrifice in 6 hour fasted mice. n = 12. E) Homeostasis model assessment of insulin resistance (HOMA_IR) was calculated from measures at sacrifice. n = 12.</p>", "links"=>[], "tags"=>["nulliparous mice", "African American women", "breast cancer risk", "obesity", "parity", "er", "tumor", "breast cancer subtypes", "bbc", "luminal breast cancers", "parous mice", "Hepatocyte Growth Factor", "role", "il", "hgf"], "article_id"=>1222283, "categories"=>["Uncategorised"], "users"=>["Sneha Sundaram", "Alex J. Freemerman", "Joseph A. Galanko", "Kirk K. McNaughton", "Katharine M. Bendt", "David B. Darr", "Melissa A. Troester", "Liza Makowski"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0111394.g002", "stats"=>{"downloads"=>1, "page_views"=>39, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Diet_induced_obesity_affects_body_weight_adiposity_and_leptin_but_not_metabolic_parameters_in_parous_mice_/1222283", "title"=>"Diet-induced obesity affects body weight, adiposity, and leptin but not metabolic parameters in parous mice.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2014-10-29 03:10:52"}
• {"files"=>["https://ndownloader.figshare.com/files/1771024"], "description"=>"<p>A) Upon initiation of diet at 10 weeks of age, parous mice were palpated three times a week for tumor onset (first tumor detected) (N = 15). Using the Kaplan-Meier analysis the hazard ratio comparing 60% to 10% was 1.151 (95% CI of ratio: 0.67 to 1.98). Median latencies in 10% and 60%-fed mice were 18.00 and 17.43 weeks, respectively. Using a chi-square test with a degree of freedom of 1, 10% vs. 60% equaled 0.61. B) Mean latencies of total tumors palpated from initial until sacrifice are shown. N = 30 tumors in 15 mice per group. *P = 0.002. C) Representative 40X photomicrographs of the IHC analysis of membrane localized c-Met staining (arrows). D) Total c-Met protein levels in normal mammary glands were quantified. *P = 0.003.</p>", "links"=>[], "tags"=>["nulliparous mice", "African American women", "breast cancer risk", "obesity", "parity", "er", "tumor", "breast cancer subtypes", "bbc", "luminal breast cancers", "parous mice", "Hepatocyte Growth Factor", "role", "il", "hgf"], "article_id"=>1222282, "categories"=>["Uncategorised"], "users"=>["Sneha Sundaram", "Alex J. Freemerman", "Joseph A. Galanko", "Kirk K. McNaughton", "Katharine M. Bendt", "David B. Darr", "Melissa A. Troester", "Liza Makowski"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0111394.g001", "stats"=>{"downloads"=>0, "page_views"=>9, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Obesity_and_parity_regulated_a_decrease_in_BBC_latency_and_elevated_c_Met_in_normal_mammary_glands_/1222282", "title"=>"Obesity and parity regulated a decrease in BBC latency and elevated c-Met in normal mammary glands.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2014-10-29 03:10:52"}
• {"files"=>["https://ndownloader.figshare.com/files/1771033"], "description"=>"<p>Initial tumor latency was defined as the age at which first tumor palpated. Mean ± standard error of mean of tumor latency of the first tumor palpated. N = 15 per group.</p><p>Tumor latency in C3(1)-T_Ag nulliparous and parous mice.</p>", "links"=>[], "tags"=>["nulliparous mice", "African American women", "breast cancer risk", "obesity", "parity", "er", "tumor", "breast cancer subtypes", "bbc", "luminal breast cancers", "parous mice", "Hepatocyte Growth Factor", "role", "il", "hgf"], "article_id"=>1222291, "categories"=>["Uncategorised"], "users"=>["Sneha Sundaram", "Alex J. Freemerman", "Joseph A. Galanko", "Kirk K. McNaughton", "Katharine M. Bendt", "David B. Darr", "Melissa A. Troester", "Liza Makowski"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0111394.t001", "stats"=>{"downloads"=>5, "page_views"=>8, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Tumor_latency_in_C3_1_T_Ag_nulliparous_and_parous_mice_/1222291", "title"=>"Tumor latency in C3(1)-T_Ag nulliparous and parous mice.", "pos_in_sequence"=>0, "defined_type"=>3, "published_date"=>"2014-10-29 03:10:52"}
• {"files"=>["https://ndownloader.figshare.com/files/1771032"], "description"=>"<p>A) Representative 20X photomicrographs of SV40 T-antigen (T_Ag) staining in normal mammary gland (A). Arrows indicate positive SV40 T_Ag staining. B) SV40 T_Ag levels in normal mammary glands (B) were quantified. n = 2 sections from 5 mice per diet group were digitally quantified. *P = 0.044.</p>", "links"=>[], "tags"=>["nulliparous mice", "African American women", "breast cancer risk", "obesity", "parity", "er", "tumor", "breast cancer subtypes", "bbc", "luminal breast cancers", "parous mice", "Hepatocyte Growth Factor", "role", "il", "hgf"], "article_id"=>1222290, "categories"=>["Uncategorised"], "users"=>["Sneha Sundaram", "Alex J. Freemerman", "Joseph A. Galanko", "Kirk K. McNaughton", "Katharine M. Bendt", "David B. Darr", "Melissa A. Troester", "Liza Makowski"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0111394.g004", "stats"=>{"downloads"=>0, "page_views"=>21, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Normal_mammary_gland_and_tumor_levels_of_SV40_T_Ag_are_not_increased_by_obesity_in_parous_mice_/1222290", "title"=>"Normal mammary gland and tumor levels of SV40-T_Ag are not increased by obesity in parous mice.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2014-10-29 03:10:52"}

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Relative Metric

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F1000Prime