Network


Latest external collaboration on country level. Dive into details by clicking on the dots.

Hotspot


Dive into the research topics where Michael Buckley is active.

Publication


Featured researches published by Michael Buckley.


PLOS ONE | 2010

A Phase II Trial of Sorafenib in Metastatic Melanoma with Tissue Correlates

Patrick A. Ott; Anne Hamilton; Christina Min; Sara Safarzadeh-Amiri; Lauren Goldberg; Joanne Yoon; Herman Yee; Michael Buckley; Paul J. Christos; John J. Wright; David Polsky; Iman Osman; Leonard Liebes; Anna C. Pavlick

Background Sorafenib monotherapy in patients with metastatic melanoma was explored in this multi-institutional phase II study. In correlative studies the impact of sorafenib on cyclin D1 and Ki67 was assessed. Methodology/Principal Findings Thirty-six patients treatment-naïve advanced melanoma patients received sorafenib 400 mg p.o. twice daily continuously. Tumor BRAFV600E mutational status was determined by routine DNA sequencing and mutation-specific PCR (MSPCR). Immunohistochemistry (IHC) staining for cyclin D1 and Ki67 was performed on available pre- and post treatment tumor samples. The main toxicities included diarrhea, alopecia, rash, mucositis, nausea, hand-foot syndrome, and intestinal perforation. One patient had a RECIST partial response (PR) lasting 175 days. Three patients experienced stable disease (SD) with a mean duration of 37 weeks. Routine BRAFV600E sequencing yielded 27 wild-type (wt) and 6 mutant tumors, whereas MSPCR identified 12 wt and 18 mutant tumors. No correlation was seen between BRAFV600E mutational status and clinical activity. No significant changes in expression of cyclin D1 or Ki67 with sorafenib treatment were demonstrable in the 15 patients with pre-and post-treatment tumor samples. Conclusions/Significance Sorafenib monotherapy has limited activity in advanced melanoma patients. BRAFV600E mutational status of the tumor was not associated with clinical activity and no significant effect of sorafenib on cyclin D1 or Ki67 was seen, suggesting that sorafenib is not an effective BRAF inhibitor or that additional signaling pathways are equally important in the patients who benefit from sorafenib. Trial registration Clinical Trials.gov NCT00119249


Journal of Translational Medicine | 2007

The histone deacetylase inhibitor belinostat (PXD101) suppresses bladder cancer cell growth in vitro and in vivo

Michael Buckley; Joanne Yoon; Herman Yee; Luis Chiriboga; Leonard Liebes; Gulshan Ara; Xiaozhong Qian; Dean F. Bajorin; Tung-Tien Sun; Xue-Ru Wu; Iman Osman

BackgroundTreatment options for patients with recurrent superficial bladder cancer are limited, necessitating aggressive exploration of new treatment strategies that effectively prevent recurrence and progression to invasive disease. We assessed the effects of belinostat (previously PXD101), a novel histone deacetylase inhibitor, on a panel of human bladder cancer cell lines representing superficial and invasive disease, and on a transgenic mouse model of superficial bladder cancer.MethodsGrowth inhibition and cell cycle distribution effect of belinostat on 5637, T24, J82, and RT4 urothelial lines were assessed. Ha-ras transgenic mice with established superficial bladder cancer were randomized to receive either belinostat or vehicle alone, and assessed for bladder weight, hematuria, gene expression profiling, and immunohistochemistry (IHC).ResultsBelinostat had a significant linear dose-dependent growth inhibition on all cell lines (IC50 range of 1.0–10.0 μM). The 5637 cell line, which was derived from a superficial papillary tumor, was the most sensitive to treatment. Belinostat (100 mg/kg, intraperitoneal, 5 days each week for 3 weeks) treated mice had less bladder weight (p < 0.05), and no hematuria compared with 6/10 control mice that developed at least one episode. IHC of bladder tumors showed less cell proliferation and a higher expression of p21WAF1 in the belinostat-treated mice. Gene expression profile analysis revealed 56 genes significantly different in the treated group; these included the upregulation of p21WAF1, induction of core histone deacetylase (HDAC), and cell communication genes.ConclusionOur data demonstrate that belinostat inhibits bladder cancer and supports the clinical evaluation of belinostat for the treatment of patients with superficial bladder cancer.


Journal of Translational Medicine | 2008

Assessing the clinical utility of measuring Insulin-like Growth Factor Binding Proteins in tissues and sera of melanoma patients

Jessie Z. Yu; Melanie Warycha; Paul J. Christos; Farbod Darvishian; Herman Yee; Hideko Kaminio; Russell S. Berman; Richard L. Shapiro; Michael Buckley; Leonard Liebes; Anna C. Pavlick; David Polsky; Peter C. Brooks; Iman Osman

BackgroundDifferent Insulin-like Growth Factor Binding Proteins (IGFBPs) have been investigated as potential biomarkers in several types of tumors. In this study, we examined both IGFBP-3 and -4 levels in tissues and sera of melanoma patients representing different stages of melanoma progression.MethodsThe study cohort consisted of 132 melanoma patients (primary, n = 72; metastatic, n = 60; 64 Male, 68 Female; Median Age = 56) prospectively enrolled in the New York University School of Medicine Interdisciplinary Melanoma Cooperative Group (NYU IMCG) between August 2002 and December 2006. We assessed tumor-expression and circulating sera levels of IGFBP-3 and -4 using immunohistochemistry and ELISA assays. Correlations with clinicopathologic parameters were examined using Wilcoxon rank-sum tests and Spearman-rank correlation coefficients.ResultsMedian IGFBP-4 tumor expression was significantly greater in primary versus metastatic patients (70% versus 10%, p = 0.01) A trend for greater median IGFBP-3 sera concentration was observed in metastatic versus primary patients (4.9 μg/ml vs. 3.4 μg/ml, respectively, p = 0.09). However, sera levels fell within a normal range for IGFBP-3. Neither IGFBP-3 nor -4 correlated with survival in this subset of patients.ConclusionDecreased IGFBP-4 tumor expression might be a step in the progression from primary to metastatic melanoma. Our data lend support to a recently-described novel tumor suppressor role of secreting IGFBPs in melanoma. However, data do not support the clinical utility of measuring levels of IGFBP-3 and -4 in sera of melanoma patients.


Bioorganic & Medicinal Chemistry Letters | 2014

Targeted amplification of delivery to cell surface receptors by dendrimer self-assembly

Steven Isaacman; Michael Buckley; Xiaojian Wang; Edwin Wang; Leonard Liebes; James W. Canary

Nanometer-scale architectures assembled on cell surface receptors from smaller macromolecular constituents generated a large amplification of fluorescence. A targeted dendrimer was synthesized from a cystamine-core G4 PAMAM dendrimer, and contained an anti-BrE3 monoclonal antibody as the targeting group, several fluorophores and an average of 12 aldehyde moieties as complementary bio-orthogonal reactive sites for the covalent assembly. A cargo dendrimer, derived from a PAMAM G4 dendrimer, contained several fluorophores as the cargo for delivery and five hydrazine moieties as complimentary bio-orthogonal reactive sites. The system is designed to be flexible and allow for facile incorporation of a variety of targeting ligands.


Molecular Cancer Therapeutics | 2002

PS-341, a novel proteasome inhibitor, induces Bcl-2 phosphorylation and cleavage in association with G2-M phase arrest and apoptosis

Yi He Ling; Leonard Liebes; Bruce Ng; Michael Buckley; Peter J. Elliott; Julian Adams; Jian Dong Jiang; Franco M. Muggia; Roman Perez-Soler


Cancer Research | 2008

Androgen Receptor Overexpression in Prostate Cancer Linked to Purα Loss from a Novel Repressor Complex

Longgui G. Wang; Edward M. Johnson; Yayoi Kinoshita; James S. Babb; Michael Buckley; Leonard Liebes; Jonathan Melamed; Xiaomei Liu; Ralf Kurek; Liliana Ossowski; Anna C. Ferrari


Atherosclerosis | 2004

Oxalic acid alters intracellular calcium in endothelial cells

Phoebe A. Recht; Gerard J Tepedino; Neil W Siecke; Michael Buckley; John T. H. Mandeville; Frederick R. Maxfield; Richard I. Levin


International Journal of Radiation Oncology Biology Physics | 2006

The vitamin-like dietary supplement para-aminobenzoic acid enhances the antitumor activity of ionizing radiation

Sandhya Xavier; Shannon M. MacDonald; Jennifer M. Roth; Maresa Caunt; Abebe Akalu; Danielle Morais; Michael Buckley; Leonard Liebes; Silvia C. Formenti; Peter C. Brooks


Journal of Clinical Oncology | 2008

Phase II trial of sorafenib (S [BAY 43–9006]) in metastatic melanoma (MM) including detection of BRAF with mutant specific-PCR (MS-PCR) and altered proliferation pathways-final outcome analysis

C. J. Min; Leonard Liebes; J. Escalon; Anne Hamilton; Herman Yee; Michael Buckley; John J. Wright; Iman Osman; David Polsky; Anna C. Pavlick


Journal of Clinical Oncology | 2008

Androgen receptor (AR) overexpression and sensitivity to hormones reversed by epigenetic therapy that restores Purα to a transcriptional repressor complex (RC) of AR deregulated in hormone refractory prostate cancer (HRPC)

Anna C. Ferrari; L. Wang; E. M. Johnson; Yayoi Kinoshita; James S. Babb; Michael Buckley; Leonard Liebes; Jonathan Melamed; Xiaomei Liu; L. Ossowski

Collaboration


Dive into the Michael Buckley's collaboration.

Top Co-Authors

Avatar
Top Co-Authors

Avatar
Top Co-Authors

Avatar
Top Co-Authors

Avatar
Top Co-Authors

Avatar
Top Co-Authors

Avatar
Top Co-Authors

Avatar
Top Co-Authors

Avatar
Top Co-Authors

Avatar
Top Co-Authors

Avatar
Researchain Logo
Decentralizing Knowledge