Inviting an author to review:
Find an author and click ‘Invite to review selected article’ near their name.
Search for authorsSearch for similar articles
14
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Impacts of smoking on endocrine treatment response in a prospective breast cancer cohort

      research-article

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Background:

          The association between smoking and breast cancer prognosis remains unclear. The purpose of this study was to investigate whether preoperative smoking was associated with prognosis in different treatment groups.

          Methods:

          This population-based cohort consisted of 1065 breast cancer patients without preoperative treatment included between 2002 and 2012 in Lund, Sweden. Smoking status was examined in relation to patient and tumour characteristics, and prognosis in different treatment groups.

          Results:

          At the preoperative visit, 21.0% smoked. Median follow-up time was 5.1 years. Overall, in the 1016 patients included in the survival analyses, there was no significant association between smoking and risk of breast cancer events (adjusted hazard ratio (adjHR): 1.45; 95% confidence interval (CI): 0.95–2.20). For the 309 aromatase inhibitor (AI)-treated patients ⩾50 years with oestrogen receptor-positive (ER+) tumours, smoking was associated with risk of breast cancer events (adjHR: 2.97; 95% CI: 1.44–6.13), distant metastasis (adjHR: 4.19; 95% CI: 1.81–9.72), and death (adjHR: 3.52; 95% CI: 1.59–7.81). Smoking was not associated with breast cancer events or distant metastasis in other treatment groups.

          Conclusions:

          Preoperative smoking was only associated with an increased risk for breast cancer events and distant metastasis in AI-treated patients. If confirmed, smoking status should be taken into consideration when selecting an endocrine therapy.

          Related collections

          Most cited references41

          • Record: found
          • Abstract: found
          • Article: not found

          Prostaglandin E2 synthesis and secretion: the role of PGE2 synthases.

          Prostaglandin E2 (PGE2) is a principal mediator of inflammation in diseases such as rheumatoid arthritis and osteoarthritis. Nonsteroidal anti-inflammatory medications (NSAIDs) and selective cyclooxygenase-2 (COX-2) inhibitors reduce PGE2 production to diminish the inflammation seen in these diseases, but have toxicities that may include both gastrointestinal bleeding and prothrombotic tendencies. In cells, arachidonic acid is transformed into PGE2 via cyclooxygenase (COX) enzymes and terminal prostaglandin E synthases (PGES). Accumulating data suggest that the interaction of various enzymes in the PGE2 synthetic pathway is complex and tightly regulated. In this review, we summarize the synthesis and secretion of PGE2. In particular, we focus on the three isoforms of the terminal PGES, and discuss the potential of targeting PGES as a more precise strategy for inhibiting PGE2 production.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Cytochrome P450-mediated metabolism of estrogens and its regulation in human.

            Estrogens are eliminated from the body by metabolic conversion to estrogenically inactive metabolites that are excreted in the urine and/or feces. The first step in the metabolism of estrogens is the hydroxylation catalyzed by cytochrome P450 (CYP) enzymes. Since most CYP isoforms are abundantly expressed in liver, the metabolism of estrogens mainly occurs in the liver. A major metabolite of estradiol, 2-hydroxyestradiol, is mainly catalyzed by CYP1A2 and CYP3A4 in liver, and by CYP1A1 in extrahepatic tissues. However, CYP1B1 which is highly expressed in estrogen target tissues including mammary, ovary, and uterus, specifically catalyzes the 4-hydroxylation of estradiol. Since 4-hydroxyestradiol generates free radicals from the reductive-oxidative cycling with the corresponding semiquinone and quinone forms, which cause cellular damage, the specific and local formation of 4-hydroxyestradiol is important for breast and endometrial carcinogenesis. Changes in the expression level of estrogen-metabolizing CYP isoforms not only alter the intensity of the action of estrogen but may also alter the profile of its physiological effect in liver and target tissues. Generally, many CYP isoforms are induced by the substrates themselves, resulting in enhanced metabolism and elimination from the body. Of particular interest is a novel finding that human CYP1B1 is regulated by estradiol via the estrogen receptor. This fact suggests that the regulation of CYP enzymes involved in estrogen metabolism by estrogen itself would be physiologically significant for the homeostasis of estrogens at local organs. In this mini-review, we discuss the CYP-mediated metabolism of estrogens and the regulation of the estrogen-metabolizing CYP enzymes in relation to the risk of cancer.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Increased levels of COX-2 and prostaglandin E2 contribute to elevated aromatase expression in inflamed breast tissue of obese women.

              Obesity is a risk factor for hormone receptor-positive breast cancer in postmenopausal women. Estrogen synthesis is catalyzed by aromatase, which is encoded by CYP19. We previously showed that aromatase expression and activity are increased in the breast tissue of overweight and obese women in the presence of characteristic inflammatory foci [crown-like structures of the breast (CLS-B)]. In preclinical studies, proinflammatory prostaglandin E(2) (PGE(2)) is a determinant of aromatase expression. We provide evidence that cyclooxygenase (COX)-2-derived PGE(2) stimulates the cyclic AMP (cAMP) → PKA signal transduction pathway that activates CYP19 transcription, resulting in increased aromatase expression and elevated progesterone receptor levels in breast tissues from overweight and obese women. We further demonstrate that a measure of in-breast inflammation (CLS-B index) is a better correlate of these biologic end points than body mass index. The obesity → inflammation → aromatase axis is likely to contribute to the increased risk of hormone receptor-positive breast cancer and the worse prognosis of obese patients with breast cancer. We show that obesity-associated inflammatory foci in the human breast are associated with elevated COX-2 levels and activation of the PGE2 → cAMP → PKA signal transduction pathway resulting in increased aromatase expression. These findings help to explain the link among obesity, low-grade chronic inflammation, and breast cancer with important clinical implications.
                Bookmark

                Author and article information

                Journal
                Br J Cancer
                Br. J. Cancer
                British Journal of Cancer
                Nature Publishing Group
                0007-0920
                1532-1827
                26 July 2016
                09 June 2016
                : 115
                : 3
                : 382-390
                Affiliations
                [1 ]Department of Clinical Sciences, Lund, Division of Oncology and Pathology, Lund University , Barngatan 2B, 22185 Lund, Sweden
                [2 ]CREATE Health and Department of Immunotechnology, Lund University , Medicon Village (Building 406), 223 81 Lund, Sweden
                [3 ]Department of Clinical Sciences, Lund, Division of Surgery, Lund University and Skåne University Hospital , 22185 Lund, Sweden
                Author notes
                Article
                bjc2016174
                10.1038/bjc.2016.174
                4973149
                27280635
                31c9e2fa-294b-4925-96d9-d6b0033dc4dd
                Copyright © 2016 Cancer Research UK

                From twelve months after its original publication, this work is licensed under the Creative Commons Attribution-NonCommercial-Share Alike 4.0 Unported License. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-sa/4.0/

                History
                : 16 November 2015
                : 11 May 2016
                : 16 May 2016
                Categories
                Epidemiology

                Oncology & Radiotherapy
                breast cancer,smoking,endocrine treatment,aromatase inhibitor,tamoxifen,prognosis

                Comments

                Comment on this article