Publications
976 results found
Rosso L, Gray KR, Contractor KB, et al., 2009, New Method for Segmentation of Tumors from [18F] FLT PET Images using Predefined Kinetic Classes, EUROPEAN JOURNAL OF NUCLEAR MEDICINE AND MOLECULAR IMAGING, Vol: 36, Pages: S193-S193, ISSN: 1619-7070
WORTHAM NC, AHAMED E, NICHOL SM, et al., 2009, The DEAD-box protein p72 regulates ERα-/oestrogen-dependent transcription and cell growth, and is associated with improved survival in ERα-positive breast cancer, Oncogene, Vol: 28, Pages: 4053-4064, ISSN: 1476-5594
The DEAD-box RNA helicases p68 (DDX5) and p72 (DDX17) have been shown to act as transcriptional co-activators for a diverse range of transcription factors, including oestrogen receptor-α (ERα). Here, we show that, although both proteins interact with and co-activate ERα in reporter gene assays, small interfering RNA-mediated knockdown of p72, but not p68, results in a significant inhibition of oestrogen-dependent transcription of endogenous ERα-responsive genes and oestrogen-dependent growth of MCF-7 and ZR75-1 breast cancer cells. Furthermore, immunohistochemical staining of ERα-positive primary breast cancers for p68 and p72 indicate that p72 expression is associated with an increased period of relapse-free and overall survival (P=0.006 and 0.016, respectively), as well as being inversely associated with Her2 expression (P=0.008). Conversely, p68 shows no association with relapse-free period, or overall survival, but it is associated with an increased expression of Her2 (P=0.001), AIB-1 (P<0.001) and higher tumour grade (P=0.044). Our data thus highlight a crucial role for p72 in ERα co-activation and oestrogen-dependent cell growth and provide evidence in support of distinct but important roles for both p68 and p72 in regulating ERα activity in breast cancer.
Ali S, Heathcote DA, Kroll SHB, et al., 2009, The Development of a Selective Cyclin-Dependent Kinase Inhibitor That Shows Antitumor Activity, CANCER RESEARCH, Vol: 69, Pages: 6208-6215, ISSN: 0008-5472
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- Citations: 118
Tuthill M, Pell R, Guiliani R, et al., 2009, Peritoneal disease in breast cancer: A specific entity with an extremely poor prognosis, EUROPEAN JOURNAL OF CANCER, Vol: 45, Pages: 2146-2149, ISSN: 0959-8049
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- Citations: 28
Fu HL, Moss J, Shore I, et al., 2009, Ultrastructural localization of laminin and type IV collagen in normal human breast, ULTRASTRUCTURAL PATHOLOGY, Vol: 26, Pages: 77-80, ISSN: 0191-3123
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- Citations: 6
Francis RE, Myatt SS, Krol J, et al., 2009, FoxM1 is a downstream target and marker of HER2 overexpression in breast cancer, INTERNATIONAL JOURNAL OF ONCOLOGY, Vol: 35, Pages: 57-68, ISSN: 1019-6439
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- Citations: 97
Coombes RC, 2009, Editorial., Ther Adv Med Oncol, Vol: 1, ISSN: 1758-8340
Rasul S, Balasubramanian R, Filipovic A, et al., 2009, Inhibition of gamma-secretase induces G2/M arrest and triggers apoptosis in breast cancer cells, British Journal of Cancer, Vol: 100, Pages: 1879-1888, ISSN: 0007-0920
γ-Secretase activity is vital for the transmembrane cleavage of Notch receptors and the subsequent migration of their intracellular domains to the nucleus. Notch overexpression has been associated with breast, colon, cervical and prostate cancers. We tested the effect of three different γ-secretase inhibitors (GSIs) in breast cancer cells. One inhibitor (GSI1) was lethal to breast cancer cell lines at concentrations of 2 μM and above but had a minimal effect on the non-malignant breast lines. GSI1 was also cytotoxic for a wide variety of cancer cell lines in the NCI60 cell screen. GSI1 treatment resulted in a marked decrease in γ-secretase activity and downregulation of the Notch signalling pathway with no effects on expression of the γ-secretase components or ligands. Flow cytometric and western blot analyses indicated that GSI1 induces a G2/M arrest leading to apoptosis, through downregulation of Bcl-2, Bax and Bcl-XL. GSI1 also inhibited proteasome activity. Thus, the γ-secretase inhibitor GSI1 has a complex mode of action to inhibit breast cancer cell survival and may represent a novel therapy in breast cancer.
Lee B, Franklin I, Lewis JS, et al., 2009, The efficacy of percutaneous vertebroplasty for vertebral metastases associated with solid malignancies, EUROPEAN JOURNAL OF CANCER, Vol: 45, Pages: 1597-1602, ISSN: 0959-8049
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- Citations: 39
Cleator SJ, Ahamed E, Coombes RC, et al., 2009, A 2009 Update on the Treatment of Patients with Hormone Receptor-Positive Breast Cancer, CLINICAL BREAST CANCER, Vol: 9, Pages: S6-S17, ISSN: 1526-8209
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- Citations: 61
Kenny LM, Coombes RC, Contractor K, et al., 2009, [11C]Choline-PET imaging of breast cancer, 45th Annual Meeting of the American-Society-of-Clinical-Oncology, Publisher: AMER SOC CLINICAL ONCOLOGY, ISSN: 0732-183X
Kenny LM, Coombes RC, Contractor K, et al., 2009, [11C]Choline-PET imaging of breast cancer., J Clin Oncol, Vol: 27
1110 Background: Molecular imaging techniques are increasingly being used in cancer diagnosis, staging, and assessment of response to treatment. This study sought to evaluate, for the first time, [(11)C]choline-PET in patients with breast cancer. The potential of [(11)C]choline-PET for differentiating tumours from normal tissue, correlation with molecular markers, determine its normal variability range, and finally the effect of trastuzumab on [(11)C]choline uptake in patients with breast cancer was investigated. METHODS: 21 patients with newly diagnosed and recurrent breast cancer AJCC stage II-IV were enrolled in the study, all of whom had a baseline dynamic [(11)C]choline-PET scan with arterial sampling. 14 patients had 2 [(11)C]choline-PET scans to examine reproducibility, and 7 had a scan after trastuzumab. Analysis of [(11)C]choline uptake was measured using SUV, Ki (irreversible retention), and IRF@60min (retention using spectral analysis). RESULTS: Breast tumour lesions were visualised by [(11)C]choline PET in all patients. The difference in tumour and non-tumour uptake were significant for SUV, Ki, and IRF@60 min (Wilcoxon p < 0.0001 for all parameters). [(11)C]choline uptake was reproducible in breast tumour lesions (r(2) = 0.945 for SUV, 0.894 for Ki, and 0.799 for IRF60). The metabolism analysis of arterial plasma samples in 19 patients showed that [(11)C]choline decreased rapidly post-injection such that at 60 mins the mean radioactivity in arterial plasma due to choline was 15.15 ± 2.16%.Early responses to trastuzumab were determined to be significant in 5 lesions which corresponded with 3 clinical responses. CONCLUSIONS: [(11)C]choline-PET is a promising imaging modality in breast cancer, and could play an important role for determining response to novel treatment strategies in vivo. No significant financial relationships to disclose.
Ngan S, Stronach EA, Photiou A, et al., 2009, Microarray coupled to quantitative RT-PCR analysis of androgen-regulated genes in human LNCaP prostate cancer cells, ONCOGENE, Vol: 28, Pages: 2051-2063, ISSN: 0950-9232
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- Citations: 54
Wang J, Jain S, Coombes CR, et al., 2009, Fulvestrant in Advanced Breast Cancer Following Tamoxifen and Aromatase Inhibition: A Single Center Experience, BREAST JOURNAL, Vol: 15, Pages: 247-253, ISSN: 1075-122X
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- Citations: 7
Giamas G, Castellano L, Feng Q, et al., 2009, CK1{delta} modulates the transcriptional activity of ER{alpha} via AIB1 in an estrogen-dependent manner and regulates ER{alpha}-AIB1 interactions., Nucleic Acids Res.
Horlock C, Stott B, Dyson PJ, et al., 2009, The effects of trastuzumab on the CD4+CD25+FoxP3+and CD4+IL17A+T-cell axis in patients with breast cancer, BRITISH JOURNAL OF CANCER, Vol: 100, Pages: 1061-1067, ISSN: 0007-0920
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- Citations: 76
McGovern UB, Francis RE, Peck B, et al., 2009, Gefitinib (Iressa) represses FOXM1 expression via FOXO3a in breast cancer, MOLECULAR CANCER THERAPEUTICS, Vol: 8, Pages: 582-591, ISSN: 1535-7163
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- Citations: 111
Hurtado A, Holmes KA, Geistlinger TR, et al., 2009, Regulation of <i>ERBB2</i> by oestrogen receptor-PAX2 determines response to tamoxifen (vol 456, pg 663, 2008), NATURE, Vol: 457, ISSN: 0028-0836
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- Citations: 2
Filipovic A, Rashied S, Balasubramanian R, et al., 2009, Inhibiting nicastrin (NCT) stabilizes expression of e-cadherin and has potential in inducing mesenchymal to epithelial transition in breast cancer (BC)., 31st Annual San Antonio Breast Cancer Symposium, Publisher: AMER ASSOC CANCER RESEARCH, Pages: 224S-224S, ISSN: 0008-5472
Slade MJ, Payne R, Riethdorf S, et al., 2009, Comparison of bone marrow, disseminated tumour cells and blood-circulating tumour cells in breast cancer patients after primary treatment, BRITISH JOURNAL OF CANCER, Vol: 100, Pages: 160-166, ISSN: 0007-0920
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- Citations: 67
Ali S, 2009, Transcriptional coactivators and corepressors in endocrine response and resistance in breast cancer, Therapeutic Resistance to Anti-Hormonal Drugs in Breast Cancer: New Molecular Aspects and their Potential as Targets, Pages: 27-38, ISBN: 9781402085253
Regulation of gene expression by sequence-specific DNA binding proteins involves the co-ordinated action of a repertoire of transcriptional coregulator complexes, which together act to modify chromatin at gene promoters, thereby facilitating gene expression. The mechanisms by which such coregulators are recruited to the promoters of estrogen-responsive genes by estrogen receptor-\upalpha have been well studied in breast cancer cells. These studies have highlighted coactivator and corepressor proteins that appear to be critical for the agonist and antagonist actions of estrogen and anti-estrogens, and indicate that altered levels and/or activities of these proteins is an important feature of response and resistance to endocrine treatments in breast cancer. © Springer Science+Business Media B.V. 2009.
Payne RE, Yaguee E, Slade MJ, et al., 2009, Measurements of EGFR expression on circulating tumor cells are reproducible over time in metastatic breast cancer patients, PHARMACOGENOMICS, Vol: 10, Pages: 51-57, ISSN: 1462-2416
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- Citations: 53
Lee B, Lim A, Lalvani A, et al., 2008, The clinical significance of radiologically detected silent pulmonary nodules in early breast cancer, ANNALS OF ONCOLOGY, Vol: 19, Pages: 2001-2006, ISSN: 0923-7534
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- Citations: 23
Hurtado A, Holmes KA, Geistlinger TR, et al., 2008, Regulation of ERBB2 by oestrogen receptor-PAX2 determines response to tamoxifen, Nature, Vol: 456, Pages: 663-666
Crosstalk between the oestrogen receptor (ER) and ERBB2/HER-2 pathways has long been implicated in breast cancer aetiology and drug response, yet no direct connection at a transcriptional level has been shown. Here we show that oestrogen-ER and tamoxifen-ER complexes directly repress ERBB2 transcription by means of a cis-regulatory element within the ERBB2 gene in human cell lines. We implicate the paired box 2 gene product (PAX2), in a previously unrecognized role, as a crucial mediator of ER repression of ERBB2 by the anti-cancer drug tamoxifen. We show that PAX2 and the ER co-activator AIB-1/SRC-3 compete for binding and regulation of ERBB2 transcription, the outcome of which determines tamoxifen response in breast cancer cells. The repression of ERBB2 by ER-PAX2 links these two breast cancer subtypes and suggests that aggressive ERBB2-positive tumours can originate from ER-positive luminal tumours by circumventing this repressive mechanism. These data provide mechanistic insight into the molecular basis of endocrine resistance in breast cancer.
McParland BJ, Miller MP, Spinks TJ, et al., 2008, The biodistribution and radiation dosimetry of the Arg-Gly-Asp peptide 18F-AH111585 in healthy volunteers, Journal of Nuclear Medicine, Vol: 49, Pages: 1664-1667
We report the safety, biodistribution, and internal radiation dosimetry of a new PET tracer, (18)F-AH111585, a peptide with a high affinity for the alpha(v)beta(3) integrin receptor involved in angiogenesis. METHODS: PET scans of 8 healthy volunteers were acquired at time points up to 4 h after a bolus injection of (18)F-AH111585. (18)F activity in whole blood and plasma and excreted urine were measured up to 4 h after injection. In vivo (18)F activities in up to 12 source regions were determined from quantitative analysis of the images. The cumulated activities subsequently calculated were then used to determine the internal radiation dosimetry, including the effective dose. RESULTS: Injection of (18)F-AH111585 was well tolerated in all subjects, with no serious or drug-related adverse events reported. The main route of (18)F excretion was renal (37%), and the 3 highest initial uptakes were by liver (15%); combined walls of the small, upper large, and lower large intestines (11%); and kidneys (9%). The 3 highest absorbed doses were received by the urinary bladder wall (124 microGy/MBq), kidneys (102 microGy/MBq), and cardiac wall (59 microGy/MBq). The effective dose was 26 microGy/MBq. CONCLUSION: (18)F-AH111585 is a safe PET tracer with a dosimetry profile comparable to other common (18)F PET tracers.
McParland BJ, Miller MP, Spinks TJ, et al., 2008, The Biodistribution and Radiation Dosimetry of the Arg-Gly-Asp Peptide <SUP>18</SUP>F-AH111585 in Healthy Volunteers, JOURNAL OF NUCLEAR MEDICINE, Vol: 49, Pages: 1664-1667, ISSN: 0161-5505
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- Citations: 67
Mintz PJ, Habib NA, Jones JL, et al., 2008, The phosphorylated membrane estrogen receptor and cytoplasmic signaling and apoptosis proteins in human breast cancer, CANCER, Vol: 113, Pages: 1489-1495, ISSN: 0008-543X
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- Citations: 15
Fuller-Pace FV, Ali S, 2008, The DEAD box RNA helicases p68 (Ddx5) and p72 (Ddx17): novel transcriptional co-regulators, BIOCHEMICAL SOCIETY TRANSACTIONS, Vol: 36, Pages: 609-612, ISSN: 0300-5127
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- Citations: 83
Palmieri C, Coombes RC, Kim S-B, et al., 2008, Ethnicity and breast cancer research, LANCET, Vol: 372, Pages: 188-189, ISSN: 0140-6736
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- Citations: 4
Kwok JM-M, Myatt SS, Marson CM, et al., 2008, Thiostrepton selectively targets breast cancer cells through inhibition of forkhead box M1 expression, MOLECULAR CANCER THERAPEUTICS, Vol: 7, Pages: 2022-2032, ISSN: 1535-7163
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- Citations: 193
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