219 research outputs found
sj-docx-1-mpp-10.1177_23814683231171363 – Supplemental material for Estimating the Cost of 3 Risk Prediction Strategies for Potential Use in the United Kingdom National Breast Screening Program
No full textSupplemental material, sj-docx-1-mpp-10.1177_23814683231171363 for Estimating the Cost of 3 Risk Prediction Strategies for Potential Use in the United Kingdom National Breast Screening Program by Stuart J. Wright, Martin Eden, Helen Ruane, Helen Byers, D. Gareth Evans, Michelle Harvie, Sacha J. Howell, Anthony Howell, David French and Katherine Payne in MDM Policy & Practice</p
sj-zip-1-whe-10.1177_17455057231160348 – Supplemental material for Optimising the delivery of breast cancer risk assessment for women aged 30–39 years: A qualitative study of women’s views
No full textSupplemental material, sj-zip-1-whe-10.1177_17455057231160348 for Optimising the delivery of breast cancer risk assessment for women aged 30–39 years: A qualitative study of women’s views by Sarah Hindmarch, Louise Gorman, Rhiannon E Hawkes, Sacha J Howell and David P French in Women’s Health</p
Increased risk of breast cancer in neurofibromatosis type 1: current insights
No full textSacha J Howell,1 Kimberley Hockenhull,1 Zena Salih,1 D Gareth Evans2,3 1Department of Medical Oncology, The Christie NHS Foundation Trust, 2Division of Evolution and Genomic Sciences, School of Biological Sciences, Faculty of Biology, Medicine and Health, University of Manchester, Manchester Academic Health Science Centre, 3Manchester Centre for Genomic Medicine, Central Manchester University Hospitals NHS Foundation Trust, Manchester, UK Abstract: Neurofibromatosis type 1 (NF1) is an autosomal dominant condition caused by mutation/deletion of the NF1 gene. The gene product, neurofibromin, is a tumor suppressor which represses the activity of the Ras oncogene. Central nervous system (CNS) tumors have long been associated with NF1, but their association with several other malignancies has been demonstrated. In this review, we summarize the epidemiological data that irrefutably support a link between NF1 and an increased risk of early-onset breast cancer, to levels at which annual mammography is currently recommended in national high-risk screening programs. We discuss the reasons for the observed adverse breast cancer prognosis in NF1 cases, including late presentation and more aggressive tumor subtypes, and recommend that a collaborative breast screening study be initiated to better serve this currently underserved population of women. Keywords: breast cancer, neurofibromatosis type 1, NF
Endocrine therapy
No full textThe link between ovarian hormones and breast cancer began to be formed as early as 1882 when TW Nunn observed the spontaneous regression of breast cancer in a woman 6 months after her menstruation ceased [1]. Oophorectomy was first proposed by the German clinician, Schinzinger, on the basis of his observation that younger women had more aggressive breast cancer [2]. However, it was not until 1896 that Beatson reported the first results of therapeutic oophorectomy in women with recurrent and locally advanced breast cancer, demonstrating regressions in three cases [3]. This paved the way for several other surgeons to replicate his work and demonstrate response rates in the order of 20-30% in terms of pain control and objective regression [4-6]. Oestrogen itself wasn't isolated and identified until 1923, and the first man-made oestrogen was synthesised in 1933 [7, 8]. In the mid 1940s, such synthetic oestrogens became some of the first addivive systemic therapies for breast cancer and it wasn't until the early 1970s that the first systemic anti-oestrogen, tamoxifen, came into clinical practice (Table 18.1). Tamoxifen, largely overtook additive oestrogen therapy, not due to increased efficacy, but rather its better tolerability. The majority of subsequent developments in breast cancer endocrine pharmacotherapy have centred around the generation of alternative strategies to abrogate the effects of oestrogen on breast cancer cells, including inhibition of the aromatase enzyme, oestrogen receptor (ER) downregulation and pharmacological suppression of ovarian oestrogen production (Table 18.1). In the following chapter, we review the available data on such endocrine agents. As with the drug development paradigm in all fields of oncology, we start with advanced breast cancer and then describe how such therapies have been translated to the adjuvant and neoadjuvant settings. Table 18.1 Timeline of the introduction of endocrine therapies in use today a Therapy Authorb (reference) Date Ovarian ablation (OA) Beatson [3] 1896 Ovarian irradiation DeCourmelles [9] 1922 Androgens Ulrich [97] 1938 Oestrogens Haddow [84] 1944 Progestins Escher [106] 1951 Hypophysectomy Perrault [61] 1952 Adrenalectomy Huggins [69] 1953 Tamoxifen Cole [32] 1971 Aminoglutethamide Griffiths [71] 1973 LHRHHanalogues Klijn [19] 1982 Raloxifine Buzdar [42] 1988 Letrozole Iveson [162] 1993 Exemestane Zilembo [163] 1995 Pureanti-oestrogens Howell [55] 1995 Anastrazole Jonat [164] 1996 aIncludes the important conceptual advances of hypophysectomy and adrenalectomy bfirst author of first paper</p
Resistance to Endocrine Therapy in Breast Cancer: Are Breast Cancer Stem Cells Implicated?:Ciara S. O’Brien, Sacha J. Howell, Gillian Farnie and Robert B. Clarke
No full textResistance to Endocrine Therapy in Breast Cancer: Are Breast Cancer Stem Cells Implicated?:Ciara S. O’Brien, Sacha J. Howell, Gillian Farnie and Robert B. Clarke
No full textPharmacogenetics in the management of breast cancer
No full textThe estrogen receptor (ER) and human epidermal growth factor receptor 2 (HER2) represent key pharmacogenomic targets for effective therapies in breast oncology. Furthermore, recent advances in genomic approaches to clarify prognosis have refined the use of cytotoxic chemotherapy, although a great many women still receive unnecessary and often ineffective treatment. Pharmacogenetic factors involved in the metabolism of some of these drugs, and in particular the influence of CYP2D6 polymorphisms in the metabolism of tamoxifen, have begun to change clinical practice. The routine genotyping of drug metabolic pathways may well become another standard measure in breast oncology in the near future. © 2010 Springer Science+Business Media B.V
Influence of the substrate and tip shape on the characterization of thin films by electrostatic force microscopy
Full text linkPersonal use of this material is permitted. Permission from IEEE must be obtained for all other uses, in any current or future media, including reprinting/republishing this material for advertising or promotional purposes, creating new collective works, for resale or redistribution to servers or lists, or reuse of any copyrighted component of this work in other works. G. M. Sacha, "Influence of the Substrate and Tip Shape on the Characterization of Thin Films by Electrostatic Force Microscopy", IEEE Transactions on Nanotechnology, vol.12, no.2, pp.152-156, Marzo 2013.Electrostatic force microscopy has been shown to be a useful tool to determine the dielectric constant of nanoscaled thin films that play a key role in many electrical, optical and biological phenomena. Previous approaches have made use of simple analytical models to analyze the experimental data for these materials. Here we show that the electrostatic force shows a completely different behavior when the shape of the tip and sample are taken into account. We present a complete study of the interaction between the whole tip and the layers below the thin film. We demonstrate that physical magnitudes such as the surface charge density distribution and the size of the materials have a strong influence on the EFM signal. The EFM sensitivity to the substrate below the thin film decreases with the substrate thickness and saturates for thicknesses above two times the length of the tip, when it is close to that of an infinite medium.Author acknowledges interesting discussion from J. J. Sáenz, C. Gómez-Navarro, J. Gómez-Herrero and E. Castellano-Hernández. This work was supported by TIN2010-
19607. Author acknowledges support from the Spanish Ramón y Cajal Program
Advances in the treatment of luminal breast cancer
No full textPurpose of Review: Recent advances in the genomic analysis of breast cancers show promise in better defining endocrine sensitive subtypes. In addition, several key trials have recently reported results that better define the optimal sequence of endocrine agents and approaches to overcome endocrine resistance. Recent Findings: In clinical practice 'luminal' breast cancer is commonly used interchangeably with estrogen receptor positivity by immunohistochemistry. Genomic analysis better defines this subgroup of tumours but also highlights the complexity of the genetic landscape. These advances are discussed, along with pivotal data from contemporary clinical trials of endocrine therapy, the treatment modality most relevant to the 'luminal' subgroup. The review focuses on data from trials in advanced breast cancer. Four studies (FIRST, FACT, SWOG S0226 and SoFEA) have recently reported and improved our understanding of the optimal sequence of endocrine agents, in particular the estrogen receptor downregulator fulvestrant. The TAMRAD and BOLERO2 trials reported significant improvements in outcome with tamoxifen and exemestane, respectively, when these standard agents were combined with the mammalian target of rapamycin inhibitor everolimus. Summary: Overall these data represent significant advances for women with metastatic breast cancer that will be translated into the early breast cancer setting in the near future. © 2013 Wolters Kluwer Health | Lippincott Williams & Wilkins
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