Alfredo Voloschin
Emory University
Network
Latest external collaboration on country level. Dive into details by clicking on the dots.
Publication
Featured researches published by Alfredo Voloschin.
Annals of Neurology | 2007
Josep Dalmau; Erdem Tüzün; Hai-Yan Wu; J. Masjuan; Jeffrey E. Rossi; Alfredo Voloschin; Joachim M. Baehring; Haruo Shimazaki; Reiji Koide; Dale King; Warren P. Mason; Lauren H. Sansing; Marc A. Dichter; Myrna R. Rosenfeld; David R. Lynch
To report the autoantigens of a new category of treatment‐responsive paraneoplastic encephalitis.
Blood | 2008
Elizabeth R. Gerstner; Lauren E. Abrey; David Schiff; Andrés J.M. Ferreri; Andrew Lister; Silvia Montoto; Richard Tsang; Eckhard Thiel; Francesc Graus; Dirk Behringer; Gerald Illerhaus; Susan A. Weaver; Patrick Y. Wen; Alfredo Voloschin; Nancy Lee Harris; Tracy T. Batchelor
Central nervous system (CNS) involvement by Hodgkin lymphoma (HL) is rare. As a result, there is limited guidance for clinicians on how to manage these patients. Detailed information was collected on 16 patients, the largest number to date, with meningeal or parenchymal CNS-HL confirmed by histopathology (15) or CSF (1). Eight patients presented with CNS-HL at diagnosis, 2 of whom had isolated CNS disease, while 8 patients developed CNS-HL at relapse. Patients received a range of treatments including surgery or radiation alone, radiation with chemotherapy, or chemotherapy alone. Median overall survival for all 16 patients was 60.9 months from first diagnosis of HL (systemic or CNS) and 43.8 months from diagnosis of CNS-HL. Although a majority of patients have died, long-term survival is possible in patients who achieve a complete response to treatment, particularly those who present with CNS involvement or involvement of the CNS is the sole site of relapsed disease.
Neuro-oncology | 2018
Antonio Omuro; Gordana Vlahovic; Michael Lim; Solmaz Sahebjam; Joachim M. Baehring; Timothy F. Cloughesy; Alfredo Voloschin; Shakti Ramkissoon; Keith L. Ligon; Robert Latek; Ricardo Zwirtes; Lewis C. Strauss; Prashni Paliwal; Christopher T. Harbison; David A. Reardon; John H. Sampson
Background Immunotherapies have demonstrated efficacy across a diverse set of tumors supporting further evaluation in glioblastoma. The objective of this study was to evaluate the safety/tolerability and describe immune-mediated effects of nivolumab ± ipilimumab in patients with recurrent glioblastoma. Exploratory efficacy outcomes are also reported. Methods Patients were randomized to receive nivolumab 3 mg/kg every 2 weeks (Q2W; NIVO3) or nivolumab 1 mg/kg + ipilimumab 3 mg/kg every 3 weeks (Q3W) for 4 doses, then nivolumab 3 mg/kg Q2W (NIVO1+IPI3). An alternative regimen of nivolumab 3 mg/kg + ipilimumab 1 mg/kg Q3W for 4 doses, then nivolumab 3 mg/kg Q2W (NIVO3+IPI1) was investigated in a nonrandomized arm. Results Forty patients were enrolled (NIVO3, n = 10; NIVO1+IPI3, n = 10; NIVO3+IPI1, n = 20). The most common treatment-related adverse events (AEs) were fatigue (NIVO3, 30%; NIVO1+IPI3, 80%; NIVO3+IPI1, 55%) and diarrhea (10%, 70%, 30%, respectively). AEs leading to discontinuation occurred in 10% (NIVO3), 30% (NIVO1+IPI3), and 20% (NIVO3+IPI1) of patients. Three patients achieved a partial response (NIVO3, n = 1; NIVO3+IPI1, n = 2) and 8 had stable disease for ≥12 weeks (NIVO3, n = 2; NIVO1+IPI3, n = 2; NIVO3+IPI1, n = 4 [Response Assessment in Neuro-Oncology criteria]). Most patients (68%) had tumor-cell programmed death ligand-1 expression ≥1%. Immune-mediated effects mimicking radiographic progression occurred in 2 patients. Conclusions Nivolumab monotherapy was better tolerated than nivolumab + ipilimumab; the tolerability of the combination was influenced by ipilimumab dose. These safety and exploratory findings merit further investigation of immunotherapies in glioblastoma.
Cancer | 2015
Jim Zhong; Arif N. Ali; Alfredo Voloschin; Yuan Liu; Walter J. Curran; Ian Crocker; Hui-Kuo Shu
Bevacizumab is a monoclonal antibody targeting vascular endothelial growth factor and is approved for the treatment of patients with recurrent glioblastoma (GBM). Previous authors have reported differential response to bevacizumab on an individual basis. Bevacizumab‐induced hypertension is a well‐documented side effect, and some reports have suggested this occurrence to be related to treatment outcome in other cancers. In the current study, the authors analyzed patients with recurrent GBM who were treated with bevacizumab based on whether the patients developed drug‐induced hypertension.
Neuro-oncology | 2005
Alfredo Voloschin; David N. Louis; Garth R. Cosgrove; Tracy T. Batchelor
A 38-year-old woman presented with an infiltrative tumor of the right frontal lobe and genu of the corpus callosum that was deemed only partially resectable. A stereotactic biopsy was performed, which revealed a right frontal oligoastrocytoma that had some anaplastic features as well as allelic loss of chromosome arms 1p and 19q. The patient was treated with temozolomide for 24 months. The partial response of the tumor to chemotherapy rendered the lesion amenable to gross total resection, which was performed subsequently. The patient remains alive and well without evidence of recurrence 7 months after resection and 48 months after initial diagnosis. Thus, preoperative chemotherapy decreased tumor mass to a degree that subsequently enabled a gross total resection. This treatment strategy, although common in the treatment of other solid tumors, is rarely utilized in adult neuro-oncology and raises another potential role for chromosome testing in oligodendroglial tumor management.
Cancer | 2018
Jaymin Jhaveri; Yuan Liu; Mudit Chowdhary; Z.S. Buchwald; Theresa W. Gillespie; Jeffrey J. Olson; Alfredo Voloschin; Bree R. Eaton; Hui-Kuo Shu; Ian Crocker; Walter J. Curran; Kirtesh R. Patel
The addition of chemotherapy to adjuvant radiotherapy (chemotherapy and radiation therapy [CRT]) improves overall survival (OS) for patients with high‐risk grade 2 gliomas; however, the impact of chemotherapy alone (CA) is unknown. This study compares the OS of patients with high‐risk grade 2 gliomas treated with CA versus CRT.
Cancer Research | 2012
Hyunsuk Shim; Li Wei; Scott N. Hwang; Andrew H. Miller; Ying Guo; Chad A. Holder; William L. Read; Katarzyna Kopcewicz; Alfredo Voloschin; Daniel J. Brat; Xiaoping Hu; Hui-Kuo Shu; Peter B. Barker; Jeffrey J. Olson
Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL A major impediment to the development of new therapies for glioblastoma is a lack of biomarkers indicating response. The current standard for assessing tumor progression relies on changes in size of the enhancing components of the tumor on standard MRI. While this was adequate when patients were treated with radiation alone, the addition of temozolomide has significantly increased the incidence of “pseudoprogression” while use of anti-angiogenic agents (e.g. cediranib) has increased the incidence of “pseudoresponse” complicating the interpretation of standard imaging. Tissue biopsy following treatment can assess tumor viability but this is invasive and impractical. Also, many newer agents do not produce a traditional tumor “response”. Epigenetic modifications are now recognized as a frequent development in the early phases of tumorigenesis, playing a central role in tumor development. Epigenetic alterations differ significantly from genetic modifications in that they may be readily revertible by ‘‘epigenetic drugs’’ such as inhibitors of histone deacetylases (HDAC). HDACs As a promising new modality for cancer therapy the first generation of HDAC inhibitors (HDACi) are currently being tested in phase I/II clinical trials. Glioblastomas benefit from therapy with HDACi, such as vorinostat, or SAHA, demonstrating tumor redifferentiation/cytostasis rather than tumor size reduction. This limits the utility of traditional imaging methods such as MRI. Magnetic resonance spectroscopic imaging (MRSI) quantitates amino acids and other metabolic substances in tumor and normal brain, allowing characterization of metabolic processes in live tissue. Our preclinical MRSI results show that after only three days of treatment with SAHA, elevated alanine and lactate levels and reduced myo-inositol (MI), N-acetyl aspartate (NAA), and creatine levels in gliomas return toward normal brain levels. In our patient study of SAHA and temozolomide in recurrent GBMs, MRSI showed normalization (or restoration) of glioblastoma metabolism toward normal brain tissue-like metabolism following only 7 days of SAHA treatment in 50% of enrolled patients (metabolic responders). In contrast, MRSI showed no changes at day 7 in the other 50% of enrolled GBM patients (non-metabolic responders, p < 0.001). These results provide an exciting insight of the mechanisms by which HDACi exert their effect on glioblastomas. The increased biosynthetic needs of tumor cells demand a reprogramming of cellular metabolism. This creates increased energy demands and makes tumor cells more vulnerable to interventions targeting their metabolism. The mechanism by which HDACi induces redifferentiation/cytostasis in tumors may be by targeting tumor metabolism. The changes, as measured by MRSI, may serve as novel early predictors of response to HDACi-containing combination therapy in glioblastomas. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr LB-159. doi:1538-7445.AM2012-LB-159
Brain | 2005
Beau M. Ances; Roberta Vitaliani; Robert A. Taylor; David S. Liebeskind; Alfredo Voloschin; David J. Houghton; Steven L. Galetta; Marc A. Dichter; Abass Alavi; Myrna R. Rosenfeld; Josep Dalmau
Journal of Neuro-oncology | 2008
Alfredo Voloschin; Rebecca A. Betensky; Patrick Y. Wen; Fred H. Hochberg; Tracy T. Batchelor
Journal of Neuroimmunology | 2008
Erica L. Carpenter; Barbara A. Vance; Rachel S. Klein; Alfredo Voloschin; Josep Dalmau; Robert H. Vonderheide