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Abrahamsson, Annelie
Publications (10 of 15) Show all publications
Vazquez Rodriguez, G., Abrahamsson, A., Jensen, L. D. & Dabrosin, C. (2018). Adipocytes Promote Early Steps of Breast Cancer Cell Dissemination via Interleukin-8. Frontiers in Immunology, 9, 1-17, Article ID 1767.
Open this publication in new window or tab >>Adipocytes Promote Early Steps of Breast Cancer Cell Dissemination via Interleukin-8
2018 (English)In: Frontiers in Immunology, ISSN 1664-3224, E-ISSN 1664-3224, Vol. 9, p. 1-17, article id 1767Article in journal (Refereed) Published
Abstract [en]

Fat is a major tissue component in human breast cancer (BC). Whether breast adipocytes (BAd) affect early stages of BC metastasis is yet unknown. BC progression is dependent on angiogenesis and inflammation, and interleukin-8 (IL-8) and vascular endothelial growth factor (VEGF) are key regulators of these events. Here, we show that BAd increased the dissemination of estrogen receptor positive BC cells (BCC) in vivo in the zebrafish model of metastasis, while dissemination of the more aggressive and metastatic BCC such as estrogen receptor negative was unaffected. While anti-VEGF and anti-IL-8 exhibited equal inhibition of angiogenesis at the primary tumor site, anti-IL-8 reduced BCC dissemination whereas anti-VEGF had minor effects on this early metastatic event. Mechanistically, overexpression of cell-adhesion molecules in BCC and neutrophils via IL-8 increased the dissemination of BCC. Importantly, the extracellular in vivo levels of IL-8 were 40-fold higher than those of VEGF in human BC. Our results suggest that IL-8 is a clinical relevant and promising therapeutic target for human BC.

Place, publisher, year, edition, pages
Frontiers Media S.A., 2018
Keywords
breast cancer, microdialysis, zebrafish, angiogenesis, inflammation
National Category
Cancer and Oncology
Identifiers
urn:nbn:se:liu:diva-150059 (URN)10.3389/fimmu.2018.01767 (DOI)000440193400002 ()
Funder
Swedish Cancer Society, 2015/309Swedish Research Council, 2013-2457
Available from: 2018-08-08 Created: 2018-08-08 Last updated: 2018-08-30
Vazquez Rodriguez, G., Abrahamsson, A., Jensen, L. & Dabrosin, C. (2017). Estradiol promotes breast cancer cell migration via recruitment and activation of neutrophils. Cancer Immunology research, 5(3), 234-247, Article ID 28159748.
Open this publication in new window or tab >>Estradiol promotes breast cancer cell migration via recruitment and activation of neutrophils
2017 (English)In: Cancer Immunology research, ISSN 2326-6066, Vol. 5, no 3, p. 234-247, article id 28159748Article in journal (Refereed) Published
Abstract [en]

Estradiol (E2) plays a key role in breast cancer progression. Most breast cancer recurrences express the estrogen receptor (ER), but nearly 50% of patients are resistant to antiestrogen therapy. Novel therapeutic targets of ER-positive breast cancers are needed. Protumoral neutrophils expressing the lymphocyte function-associated antigen 1 (LFA-1) integrin may mediate cancer metastasis, and TGFβ1 is the major chemoattractant for neutrophils. The role of E2 in neutrophil–ER+ breast cancer cell interactions is unknown. We studied this in vivo using murine breast cancers in immunocompetent mice and human breast cancers in nude mice. Cell dissemination was evaluated in a zebrafish model, and microdialysis of breast cancer patients was performed. In vitro studies were done with mammosphere cultures of breast cancer cells and human neutrophils. We found that E2 increased the number of LFA-1+ neutrophils recruited to the invasive edge of mouse tumors, increased TGFβ1 secretion and promoted neutrophil infiltration in mammospheres, and induced overexpression of LFA-1 in neutrophils. In zebrafish, in the presence of E2, neutrophils increased dissemination of ER+ breast cancer cells via LFA-1 and TGFβ1, thus causing noninvasive cancer cells to be highly metastatic. Time-lapse imaging in zebrafish revealed close interactions of neutrophils with cancer cells, which drove breast cancer metastasis. We also found that extracellular TGFβ1 was overproduced in human breast cancer tissue compared with adjacent normal breast tissue. Thus, E2 can regulate immune/cancer cell interactions in tumor microenvironments. Our results indicate that extracellular TGFβ1 is a relevant target in human breast cancer.

Place, publisher, year, edition, pages
American Association for Cancer Research, 2017
National Category
Clinical Medicine
Identifiers
urn:nbn:se:liu:diva-135330 (URN)10.1158/2326-6066.CIR-16-0150 (DOI)000396023000006 ()28159748 (PubMedID)
Funder
Swedish Cancer Society, 2015/309Swedish Research Council, 2013-2457Linköpings universitet
Note

Funding agencies: Swedish Cancer Society [2015/309]; Swedish Research Council [2013-2457]; LiU-Cancer; Research Funds of Linkoping University Hospital

Available from: 2017-03-13 Created: 2017-03-13 Last updated: 2018-05-02
Abrahamsson, A., Rzepecka, A. & Dabrosin, C. (2017). Increased nutrient availability in dense breast tissue of postmenopausal women in vivo. Scientific Reports, 7, Article ID 42733.
Open this publication in new window or tab >>Increased nutrient availability in dense breast tissue of postmenopausal women in vivo
2017 (English)In: Scientific Reports, ISSN 2045-2322, E-ISSN 2045-2322, Vol. 7, article id 42733Article in journal (Refereed) Published
Abstract [en]

Metabolic reprogramming is a hallmark of cancer. Nutrient availability in the tissue microenvironment determines cellular events and may play a role in breast carcinogenesis. High mammographic density is an independent risk factor for breast cancer. Whether nutrient availability differs in normal breast tissues with various densities is unknown. Therefore we investigated whether breast tissues with various densities exhibited differences in nutrient availability. Healthy postmenopausal women from the regular mammographic screening program who had either predominantly fatty breast tissue (nondense), n = 18, or extremely dense breast tissue (dense), n = 20, were included. Microdialysis was performed for the in vivo sampling of amino acids (AAs), analyzed by ultra-high performance liquid chromatography with tandem mass spectroscopy, glucose, lactate and vascular endothelial growth factor (VEGF) in breast tissues and, as a control, in abdominal subcutaneous (s.c.) fat. We found that dense breast tissue exhibited significantly increased levels of 20 proteinogenic AAs and that 18 of these AAs correlated significantly with VEGF. No differences were found in the s.c. fat, except for one AA, suggesting tissue-specific alterations in the breast. Glucose and lactate were unaltered. Our findings provide novel insights into the biology of dense breast tissue that may be explored for breast cancer prevention strategies.

Place, publisher, year, edition, pages
NATURE PUBLISHING GROUP, 2017
National Category
Cancer and Oncology
Identifiers
urn:nbn:se:liu:diva-135389 (URN)10.1038/srep42733 (DOI)000394294800001 ()28198437 (PubMedID)
Note

Funding Agencies|Swedish Cancer Society [2015/309]; Swedish Research Council [2013-2457]; LiU-Cancer; Linkoping University Hospital

Available from: 2017-03-14 Created: 2017-03-14 Last updated: 2018-05-02
Morad, V., Abrahamsson, A., Kjölhede, P. & Dabrosin, C. (2016). Adipokines and Vascular Endothelial Growth Factor in Normal Human Breast Tissue in Vivo - Correlations and Attenuation by Dietary Flaxseed. Journal of mammary gland biology and neoplasia, 21(1-2), 69-76
Open this publication in new window or tab >>Adipokines and Vascular Endothelial Growth Factor in Normal Human Breast Tissue in Vivo - Correlations and Attenuation by Dietary Flaxseed
2016 (English)In: Journal of mammary gland biology and neoplasia, ISSN 1083-3021, E-ISSN 1573-7039, Vol. 21, no 1-2, p. 69-76Article in journal (Refereed) Published
Abstract [en]

Exposure to sex steroids increases the risk of breast cancer but the exact mechanisms are yet to be elucidated. Events in the microenvironment are important for carcinogenesis. Diet containing phytoestrogens can affect the breast microenvironment and alter the risk of breast cancer. It has previously been shown that estrogen regulates extracellular levels of leptin, adiponectin, and VEGF in normal breast tissue in vivo. Whether these proteins correlate in breast tissue in vivo or if diet addition of flaxseed, a major source of phytoestrogens in Western diets, alters adipokine levels in breast tissue are unknown. We used microdialysis to sample proteins of normal human breast tissue and abdominal subcutaneous fat in situ in 34 pre-and postmenopausal women. In vitro, co-culture of breast cancer cells and primary human adipocytes was used. In vivo, in normal breast tissue, a significant positive correlation between VEGF and leptin was detected. No correlations were found in fat tissue. Co-culture of adipocytes and breast cancer cells per se increased the secretion of VEGF and leptin and enhanced the effects of estradiol compared to culture of either cell type alone. In vitro, inhibition of VEGF diminished the release of leptin while inhibition of leptin had no influence on VEGF secretion. The levels of leptin decreased and adiponectin increased after a dietary addition of 25 g of flaxseed/day for one menstrual cycle. We conclude that VEGF and leptin correlate significantly in normal human breast tissue in vivo and that dietary addition of flaxseed affect adipokine levels in the breast.

Place, publisher, year, edition, pages
SPRINGER/PLENUM PUBLISHERS, 2016
Keywords
Flaxseed; Diet; Microdialysis; Estrogen; Leptin; Adiponectin
National Category
Cancer and Oncology
Identifiers
urn:nbn:se:liu:diva-130433 (URN)10.1007/s10911-016-9352-9 (DOI)000379327000009 ()27059487 (PubMedID)
Available from: 2016-08-07 Created: 2016-08-05 Last updated: 2019-06-28
Svensson, S., Abrahamsson, A., Vazquez Rodriguez, G., Olsson, A.-K., Jensen, L., Cao, Y. & Dabrosin, C. (2015). CCL2 and CCL5 Are Novel Therapeutic Targets for Estrogen-Dependent Breast Cancer. Clinical Cancer Research, 21(16), 3794-3805
Open this publication in new window or tab >>CCL2 and CCL5 Are Novel Therapeutic Targets for Estrogen-Dependent Breast Cancer
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2015 (English)In: Clinical Cancer Research, ISSN 1078-0432, E-ISSN 1557-3265, Vol. 21, no 16, p. 3794-3805Article in journal (Refereed) Published
Abstract [en]

Purpose: Novel therapeutic targets of estrogen receptor (ER)-positive breast cancers are urgently needed because current antiestrogen therapy causes severe adverse effects, nearly 50% of patients are intrinsically resistant, and the majority of recurrences have maintained ER expression. We investigated the role of estrogen-dependent chemokine expression and subsequent cancer growth in human tissues and experimental breast cancer models. Experimental Design: For in vivo sampling of human chemokines, microdialysis was used in breast cancers of women or normal human breast tissue before and after tamoxifen therapy. Estrogen exposure and targeted therapies were assessed in immune competent PyMT murine breast cancer, orthotopic human breast cancers in nude mice, cell culture of cancer cells, and freshly isolated human macrophages. Cancer cell dissemination was investigated using zebrafish. Results: ER+ cancers in women produced high levels of extracellular CCL2 and CCL5 in vivo, which was associated with infiltration of tumor-associated macrophages. In experimental breast cancer, estradiol enhanced macrophage influx and angiogenesis through increased release of CCL2, CCL5, and vascular endothelial growth factor. These effects were inhibited by anti-CCL2 or anti-CCL5 therapy, which resulted in potent inhibition of cancer growth. In addition, estradiol induced a protumorigenic activation of the macrophages. In a zebrafish model, macrophages increased cancer cell dissemination via CCL2 and CCL5 in the presence of estradiol, which was inhibited with anti-CCL2 and anti-CCL5 treatment. Conclusions: Our findings shed new light on the mechanisms underlying the progression of ER+ breast cancer and indicate the potential of novel therapies targeting CCL2 and CCL5 pathways. (C)2015 AACR.

Place, publisher, year, edition, pages
AMER ASSOC CANCER RESEARCH, 2015
National Category
Cancer and Oncology
Identifiers
urn:nbn:se:liu:diva-122122 (URN)10.1158/1078-0432.CCR-15-0204 (DOI)000361909100027 ()25901081 (PubMedID)
Note

Funding Agencies|Swedish Cancer Society [2009/799]; Swedish Research Council [2010-3458]; LiU-Cancer; Linkoping University Hospital

Available from: 2015-10-19 Created: 2015-10-19 Last updated: 2018-08-08
Morad, V., Abrahamsson, A., Kjölhede, P. & Dabrosin, C. (2015). Correlation between vascular endothelial growth factor and leptin in normal human breast tissue in vivo.
Open this publication in new window or tab >>Correlation between vascular endothelial growth factor and leptin in normal human breast tissue in vivo
2015 (English)Manuscript (preprint) (Other academic)
Abstract [en]

Introduction: Events in the microenvironment are important for carcinogenesis of the breast. Adipocytes, which produce adipokines with paracrine effects, are the most abundant cell type in breast tissue. Exposure to sex steroids affects the risk of breast cancer. It has previously been shown that estrogen regulates the extracellular levels of leptin, adiponectin, IL-1β, and VEGF in normal human breast tissue in vivo.

Objective: We aimed to determine if there were any relationships between leptin, adiponectin, IL-1β, and/or VEGF in normal human breast tissue in vivo and to elucidate the role of adipocytes in the regulation of these factors.

Design and methods: Microdialysis was used to sample proteins of normal human breast tissue and abdominal subcutaneous (s.c.) fat in situ in pre-and postmenopausal women. An in vitro co-culture model of breast cancer cells and primary mature human adipocytes was used.

Results: In vivo, in normal breast tissue, significant positive correlations between VEGF and leptin, and VEGF and leptin/adiponectin ratio were detected. No correlations were found in s.c. abdominal fat tissue. Co-culture of adipocytes and breast cancer cells per se increased the secretion of VEGF and leptin and enhanced the effects of estradiol compared to culture of either cell type alone. In vitro, inhibition of VEGF diminished the release of leptin while inhibition of leptin had no influence on VEGF secretion. In breast tissue, significant correlations between IL-1β and leptin and VEGF were revealed.

Conclusions: Our results suggest that VEGF regulates leptin in normal human breast tissue. Moreover, physical contact between adipocytes and breast cancer cells, induces phenotypic changes and enhances the effects of estradiol. These mechanisms may be involved in breast cancer progression.

National Category
Clinical Medicine
Identifiers
urn:nbn:se:liu:diva-117982 (URN)
Available from: 2015-05-19 Created: 2015-05-19 Last updated: 2019-06-28Bibliographically approved
Abrahamsson, A. & Dabrosin, C. (2015). Tissue specific expression of extracellular microRNA in human breast cancers and normal human breast tissue in vivo. OncoTarget, 6(26), 22959-22969
Open this publication in new window or tab >>Tissue specific expression of extracellular microRNA in human breast cancers and normal human breast tissue in vivo
2015 (English)In: OncoTarget, ISSN 1949-2553, E-ISSN 1949-2553, Vol. 6, no 26, p. 22959-22969Article in journal (Refereed) Published
Abstract [en]

Extracellular circulating microRNAs (miRNAs) have been suggested to be biomarkers for disease monitoring but data are inconsistent, one reason being that blood miRNA is of heterogeneous origin. Here, we sampled extracellular microRNAs locally in situ using microdialysis. Three different cohorts of women were included; postmenopausal women with ongoing breast cancer investigated within the cancer and in normal adjacent breast tissue, postmenopausal women investigated in their normal healthy breast and subcutaneous fat before and after six weeks of tamoxifen therapy, premenopausal women during the menstrual cycle. Samples were initially screened using TaqMan array cards with subsequently absolute quantification. 124 miRNA were expressed in microdialysates. After absolute quantifications extracellular miRNA-21 was found to be significantly increased in breast cancer. In addition, the levels were significantly higher in pre-menopausal breast tissue compared with postmenopausal. In breast tissue of pre-menopausal women miRNA-21 exhibited a cyclic variation during the menstrual cycle and in postmenopausal women six weeks of tamoxifen treatment decreased miRNA-21 suggesting that this miRNA may be important for breast carcinogenesis. None of these changes were found in plasma or microdialysates from subcutaneous fat. Our data revealed tissue specific changes of extracellular circulating miRNAs that would be otherwise unraveled using blood samples.

Place, publisher, year, edition, pages
Albany, NY, United States: Impact Journals LLC, 2015
Keywords
mammary gland; microdialysis; sex steroids; estrogen; tamoxifen
National Category
Clinical Medicine
Identifiers
urn:nbn:se:liu:diva-122668 (URN)10.18632/oncotarget.4038 (DOI)000362954800106 ()
Note

Funding Agencies|Swedish Cancer Society [2012/454]; Swedish Research Council [2013-2457]; Linkoping University

Available from: 2015-11-16 Created: 2015-11-13 Last updated: 2017-12-01
Morad, V., Abrahamsson, A. & Dabrosin, C. (2014). Estradiol Affects Extracellular Leptin: Adiponectin Ratio in Human Breast Tissue in Vivo. Journal of Clinical Endocrinology and Metabolism, 99(9), 3460-3467
Open this publication in new window or tab >>Estradiol Affects Extracellular Leptin: Adiponectin Ratio in Human Breast Tissue in Vivo
2014 (English)In: Journal of Clinical Endocrinology and Metabolism, ISSN 0021-972X, E-ISSN 1945-7197, Vol. 99, no 9, p. 3460-3467Article in journal (Refereed) Published
Abstract [en]

Context: Exposure to sex steroids is associated with increased breast cancer risk, and adipokines, leptin and adiponectin have been implicated in cancer progression. However, it is not known whether sex steroids affect adipokine secretion in breast tissue. Objective: To elucidate the role of estrogen and tamoxifen on adipokine release in normal human breast tissue and breast cancer. Setting and Design: Microdialysis sampling was used to collect extracellular in vivo leptin and adiponectin from normal human breast tissue in premenopausal healthy volunteers during the menstrual cycle and in postmenopausal women before tamoxifen treatment and after 6 weeks of treatment. In women with breast cancer, microdialysis was performed intratumorally before surgery. In addition, whole normal breast tissue biopsies were cultured ex vivo, and murine breast cancer models were evaluated. Results: In normal breast tissue, plasma estradiol negatively correlated with local extracellular adiponectin levels (r = -0.34; P less than .05) and positively correlated with leptin (r = 0.37; P less than .05) and leptin: adiponectin ratio (r = 0.38; P less than .05). In postmenopausal women, tamoxifen treatment increased adiponectin (P less than 0.05) and decreased leptin (P less than .01) and the leptin: adiponectin ratio (P less than .01). These in vivo results were confirmed in breast tissue biopsies cultured ex vivo. In patients with breast cancer, extracellular leptin was higher (P less than .01) and adiponectin lower (P less than .05) in tumors than in normal adjacent breast tissue. In a murine model of breast cancer, estrogen exposure increased leptin secretion (P less than .05). Conclusions: Estrogen exposure may have a critical role in the regulation of adipokines in human breast tissue and may serve as therapeutic targets for treatment and prevention.

Place, publisher, year, edition, pages
Endocrine Society, 2014
National Category
Clinical Medicine
Identifiers
urn:nbn:se:liu:diva-111611 (URN)10.1210/jc.2014-1129 (DOI)000342341400088 ()24796929 (PubMedID)
Note

Funding Agencies|Swedish Cancer Society [2012/454]; Swedish Research Council [2010-3458]; Research Funds of Linkoping University Hospital

Available from: 2014-10-27 Created: 2014-10-27 Last updated: 2017-12-05
Söderlund, K., Svensson, S., Abrahamsson, A., Bendrik, C., Robertson, J., Gauldie, J., . . . Dabrosin, C. (2013). Inflammation Induced by MMP-9 Enhances Tumor Regression of Experimental Breast Cancer. Journal of Immunology, 190(8), 4420-4430
Open this publication in new window or tab >>Inflammation Induced by MMP-9 Enhances Tumor Regression of Experimental Breast Cancer
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2013 (English)In: Journal of Immunology, ISSN 0022-1767, E-ISSN 1550-6606, Vol. 190, no 8, p. 4420-4430Article in journal (Refereed) Published
Abstract [en]

Matrix metalloproteinases (MMPs) have been suggested as therapeutic targets in cancer treatment, but broad-spectrum MMP inhibitors have failed in clinical trials. Recent data suggest that several MMPs including MMP-9 exert both pro-and antitumorigenic properties. This is also the case of the natural inhibitors of MMPs, tissue inhibitor of metalloproteinases (TIMPs). The inhibitor of MMP-9 is TIMP-1, and high levels of this enzyme have been associated with decreased survival in breast cancer. Inflammation is one hallmark of cancer progression, and MMPs/TIMPs may be involved in the local immune regulation. We investigated the role of MMP-9/TIMP-1 in regulating innate antitumor immunity in breast cancer. Breast cancers were established in nude mice and treated with intratumoral injections of adenoviruses carrying the human TIMP-1 or MMP-9 gene (AdMMP-9). In vivo microdialysis for sampling of cancer cell-derived (human) and stroma-derived (murine) proteins, immunostainings, as well as cell cultures were performed. We report a dose-dependent decrease of tumor growth and angiogenesis after AdMMP-9 treatment. In addition to increased generation of endostatin, AdMMP-9 promoted an antitumor immune response by inducing massive neutrophil infiltration. Neutrophil depletion prior to gene transfer abolished the therapeutic effects of AdMMP-9. Additionally, AdMMP-9 activated tumor-infiltrating macrophages into a tumor-inhibiting phenotype both in vivo and in vitro. AdMMP-9 also inhibited tumor growth in immune-competent mice bearing breast cancers. Adenoviruses carrying the human TIMP-1 gene had no effect on tumor growth or the immune response. Our novel data identify MMP-9 as a potent player in modulating the innate immune response into antitumor activities. The Journal of Immunology, 2013, 190: 4420-4430.

Place, publisher, year, edition, pages
American Association of Immunologists, 2013
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-92700 (URN)10.4049/jimmunol.1202610 (DOI)000317274500059 ()
Note

Funding Agencies|Swedish Cancer Society|2009/799|Swedish Research Council|2010-3458|Research Funds of Linkoping University Hospital||

Available from: 2013-05-16 Created: 2013-05-16 Last updated: 2017-12-06Bibliographically approved
Abrahamsson, A., Morad, V., Saarinen, N. M. & Dabrosin, C. (2012). Estradiol, Tamoxifen, and Flaxseed Alter IL-1 beta and IL-1Ra Levels in Normal Human Breast Tissue in Vivo. Journal of Clinical Endocrinology and Metabolism, 97(11), E2044-E2054
Open this publication in new window or tab >>Estradiol, Tamoxifen, and Flaxseed Alter IL-1 beta and IL-1Ra Levels in Normal Human Breast Tissue in Vivo
2012 (English)In: Journal of Clinical Endocrinology and Metabolism, ISSN 0021-972X, E-ISSN 1945-7197, Vol. 97, no 11, p. E2044-E2054Article in journal (Refereed) Published
Abstract [en]

Introduction: Sex steroid exposure increases the risk of breast cancer by unclear mechanisms. Diet modifications may be one breast cancer prevention strategy. The proinflammatory cytokine family of IL-1 is implicated in cancer progression. IL-1Ra is an endogenous inhibitor of the proinflammatory IL-1 alpha and IL-1 beta. less thanbrgreater than less thanbrgreater thanObjective: The objective of this study was to elucidate whether estrogen, tamoxifen, and/or diet modification altered IL-1 levels in normal human breast tissue. less thanbrgreater than less thanbrgreater thanDesign and Methods: Microdialysis was performed in healthy women under various hormone exposures, tamoxifen therapy, and diet modifications and in breast cancers of women before surgery. Breast tissue biopsies from reduction mammoplasties were cultured. less thanbrgreater than less thanbrgreater thanResults: We show a significant positive correlation between estradiol and in vivo levels of IL-1 beta in breast tissue and abdominal sc fat, whereas IL-1Ra exhibited a significant negative correlation with estradiol in breast tissue. Tamoxifen or a dietary addition of 25 g flaxseed per day resulted in significantly increased levels of IL-1Ra in the breast. These results were confirmed in ex vivo culture of breast biopsies. Immunohistochemistry of the biopsies did not reveal any changes in cellular content of the IL-1s, suggesting that mainly the secreted levels were affected. In breast cancer patients, intratumoral levels of IL-1 beta were significantly higher compared with normal adjacent breast tissue. less thanbrgreater than less thanbrgreater thanConclusion: IL-1 may be under the control of estrogen in vivo and may be attenuated by antiestrogen therapy and diet modifications. The increased IL-1 beta in breast cancers of women strongly suggests IL-1 as a potential therapeutic target in breast cancer treatment and prevention.

Place, publisher, year, edition, pages
Endocrine Society, 2012
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-86651 (URN)10.1210/jc.2012-2288 (DOI)000310710500002 ()
Note

Funding Agencies|Swedish Cancer Society|2009/799|Swedish Research Council|2010-3458|Research Funds of Linkoping University Hospital||

Available from: 2012-12-20 Created: 2012-12-20 Last updated: 2017-12-06
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