Breast Neoplasms: Murray N

Murray N, Winstanley J, Bennett A, Francis K, Anonymous00077. · Cancer Research UK Clinical Centre, University of Southampton, Somers Cancer Research Building, Southampton General Hospital, Southampton SO16 6YD. · BMJ. · Pubmed #19244303 No free full text.

This publication has no abstract.

Murray N, Brunt M, Macbeth F, Winstanley J, Anonymous00048. · No affiliation provided · Clin Oncol (R Coll Radiol). · Pubmed #19419851 No free full text.

This publication has no abstract.

Barrett-Lee PJ, Dixon JM, Farrell C, Jones A, Leonard R, Murray N, Palmieri C, Plummer CJ, Stanley A, Verrill MW. · Breast Unit, Velindre Cancer Centre, Cardiff, UK. · Ann Oncol. · Pubmed #19153118 No free full text.

Abstract: Anthracyclines are considered to be among the most active agents for the treatment of breast cancer. However, their use is limited by cumulative, dose-related cardiotoxicity. Such cardiotoxicity results in a permanent loss of cardiac myocytes and a progressive reduction in cardiac function following each subsequent dose of anthracycline. Initially, damage to the heart is subclinical; however, increasingly impaired cardiac function can result in cardiovascular symptoms, with serious cardiac injury resulting in chronic heart failure. Since the early detection and treatment of cardiotoxicity can reduce its clinical effects, it is important that oncologists are aware of these adverse effects and manage them appropriately. This review examines the risk factors for anthracycline-associated cardiotoxicity and offers recommendations on strategies to reduce the cardiotoxicity of anthracyclines in the management of patients with advanced breast cancer.

Chu QS, Cianfrocca ME, Goldstein LJ, Gale M, Murray N, Loftiss J, Arya N, Koch KM, Pandite L, Fleming RA, Paul E, Rowinsky EK. · Institute for Drug Development, Cancer Therapy and Research Center, San Antonio, Texas, USA. · Clin Cancer Res. · Pubmed #18628463 links to  free full text

Abstract: PURPOSE: The main objectives of this phase I and pharmacokinetic, open-label study were to determine the optimally tolerated regimen (OTR), safety, pharmacokinetics, and clinical activity of lapatinib in combination with letrozole in patients with advanced solid malignancies. EXPERIMENTAL DESIGN: Patients with advanced breast cancer with immunohistochemically detectable estrogen or progesterone receptors or other cancers were eligible. Doses of lapatinib were escalated in cohorts of three subjects from 1,250 to a maximum of 1,500 mg/d based on dose-limiting toxicities in the first treatment cycle. The letrozole dose was fixed at 2.5 mg/d. Additional patients were enrolled at the OTR dose level to further evaluate safety and for pharmacokinetic analyses. RESULTS: Thirty-nine patients were enrolled in the study: 12 in the dose-escalation group, 7 in the OTR safety group, and 20 in the pharmacokinetic group. The OTR dose level was identified as 1,500 mg/d lapatinib and 2.5 mg/d letrozole. The most common (>25% of patients) drug-related adverse events were diarrhea (77%), rash (62%), nausea (46%), and fatigue (26%). No significant differences were observed in the pharmacokinetic variables (C(max) and AUC) of lapatinib and letrozole when coadministered compared with single-agent administration. One patient with endometrial cancer had a confirmed partial response. CONCLUSIONS: Clinically relevant doses of lapatinib in combination with letrozole were well tolerated and did not result in a pharmacokinetic interaction, and clinical antitumor activity was observed.

Zeidan BA, Cutress RI, Murray N, Coulton GR, Hastie C, Packham G, Townsend PA. · Human Genetics Division, Southampton General Hospital, University of Southampton, Southampton, SO16 6YD, UK. · Cancer Genomics Proteomics. · Pubmed #19487543 No free full text.

Abstract: Large cohorts of archival samples are stored in tissue banks worldwide yet their contribution to biomarker discovery is limited. Proteomic profiling technologies have potential for early screening and diagnosis of cancer, and data from such samples can be the answer for many clinical questions. Here we introduce the notion of archival samples proteomics. Using SELDI-TOF MS analysis, we compared 30-year-old archival serum samples of healthy volunteers and patients diagnosed with non metastatic breast cancer. To validate the reproducibility of our results, analysis of the same samples was repeated in a different centre under standardised settings. Plausible differentially expressed protein peaks between the breast cancer and control groups were repeatedly detected. Our pilot study showed highly reproducible and concordant results between two independent analyses conducted in different centres. The feasibility and reliability of profiling serum archives of women with breast cancer was tested in this pilot study. Our results imply that proteomic profiling of serum may have an important role in biomarkers discovery regardless of the storage period. Clearly, multicentre validation of larger archival cohorts is vital.

Taylor M, Bolton LM, Johnson P, Elliott T, Murray N. · Cancer Research - UK Clinical Centre, University of Southampton, MP824, Southampton General Hospital, Tremona Road, Southampton SO16 6YD, UK. · Breast Cancer Res. · Pubmed #17650306 links to  free full text

Abstract: INTRODUCTION: Cancer-testis antigens (CTAGs) are expressed solely in germ cells and in malignant tissues. They are targets of immune responses mediated by cytotoxic T cells in some cancers, and there is much interest in developing vaccines that induce these responses. The purpose of the present study was to ascertain the frequency of expression of CTAGs in breast cancer. METHODS: Breast tumours were collected sequentially in the Southampton Tumour Bank from donors who had given written informed consent. Stored samples where there was sufficient material were sampled in sequence. An initial series of 42 tumours was screened for expression of 17 different CTAGs. A second panel of 40 tumours was screened for the expression of those antigens present in the first panel. RESULTS: Ninety-three per cent of tumours in the first series expressed at least one CTAG, and 62% expressed the single antigen CTAG1. Eighty per cent of tumours in the second series expressed at least one CTAG, 50% expressing CTAG1. Tumours exhibiting higher risk features tended to express more CTAGs. CONCLUSION: More than two-thirds of breast cancers would be covered by a vaccine directed against just three CTAGs - CTAG1, BAGE1, and MAGEA10 - all of which are known to be targets of cytotoxic-T-lymphocyte responses.

Cathomas R, Pelosi E, Smart J, Murray N, Simmonds P. · No affiliation provided · Clin Oncol (R Coll Radiol). · Pubmed #15997927 No free full text.

This publication has no abstract.