Sigmund Hsu
University of Texas Health Science Center at Houston
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Neuro-oncology | 2008
Vinay K. Puduvalli; Pierre Giglio; Morris D. Groves; Kenneth R. Hess; Mark R. Gilbert; Srikanth Mahankali; Edward F. Jackson; Victor A. Levin; Charles A. Conrad; Sigmund Hsu; Howard Colman; John F. de Groot; Melesa G. Ritterhouse; Sandra Ictech; W. K. Alfred Yung
This phase II study aimed at determining the efficacy and safety of irinotecan combined with thalidomide in adults with recurrent glioblastoma multiforme (GBM) not taking enzyme-inducing anticonvulsants (EIACs). Adult patients (> or =18 years) with recurrent GBM with up to three relapses following surgery and radiation therapy were eligible for this trial. The primary end point was rate of progression-free survival at 6 months (PFS-6); secondary end points were response rate, overall survival, and toxicity. Patients were treated in 6-week cycles with 125 mg/m(2) irinotecan weekly for 4 weeks followed by 2 weeks off treatment and 100 mg of thalidomide daily increased as tolerated to 400 mg/day. Of 32 evaluable patients, 8 (25%) were alive and progression free at 6 months. The median PFS was 13 weeks. One patient experienced a complete response, one a partial response, and 19 stable disease. Median overall survival time from entry into the study was 36 weeks, and the 1-year survival rate was 34%. Adverse events (grade 3 or 4) included diarrhea, abdominal cramps, lymphopenia, neutropenia, and fatigue. Two of the four deaths that occurred were possibly due to treatment-related toxicity. The combination of irinotecan, a cytotoxic agent, and thalidomide, an antiangiogenic agent, shows promising activity against recurrent GBM in patients not receiving EIACs and warrants further study. The results also provide support for similar strategies using combination therapies with newer targeted antiangiogenic agents to generate effective therapies against malignant gliomas.
Neuro-oncology | 2008
Morris D. Groves; Michael J. Glantz; Marc C. Chamberlain; Karen Baumgartner; Charles A. Conrad; Sigmund Hsu; Jeffrey S. Wefel; Mark R. Gilbert; Sandra Ictech; Kathy Hunter; Arthur D. Forman; Vinay K. Puduvalli; Howard Colman; Kenneth R. Hess; W. K. Alfred Yung
To determine the therapeutic efficacy (13-week and 26-week CNS progression-free survival [PFS], response rate, and overall survival) and safety of intraventricular (IVent) topotecan in patients with neoplastic meningitis (NM), we conducted a phase II, open-label, nonrandomized, single-arm trial of IVent topotecan in patients with NM using 400 mug of topotecan IVent twice weekly for 6 weeks, followed by evaluation with imaging, cerebrospinal fluid (CSF), and physical examinations. In the absence of disease progression, patients were then treated with IVent topotecan weekly for 6 weeks, twice monthly for 4 months, and monthly thereafter. Sixty-two patients (23 males and 39 females) were enrolled from April 2001 through March 2006. Median age and KPS at enrollment were 56 (range 5-83) and 80 (range 60-100), respectively. Primary cancers included breast (19), lung (13), CNS (14), and others (16). Forty patients (65%) completed the 6-week induction period, among whom 13 (21%) had CSF clearance of malignant cells. Kaplan-Meier estimates of PFS at 13 and 26 weeks were 30% (95% confidence interval [CI], 20%-45%) and 19% (95% CI, 11%-34%). Overall median survival (50 deaths) was 15 weeks (95% CI, 13-24 weeks). The most common side effect was chemical meningitis in 32% of patients (5% grade 3); 32% experienced no drug side effects. IVent topotecan is well tolerated, but provides no added benefit over other IVent therapies. Because of its modest side effect profile, combining IVent topotecan with other IVent or systemic interventions should be considered.
Neuro-oncology | 2015
Marta Penas-Prado; Kenneth R. Hess; Michael J. Fisch; Lore W. Lagrone; Morris D. Groves; Victor A. Levin; John F. de Groot; Vinay K. Puduvalli; Howard Colman; Gena Volas-Redd; Pierre Giglio; Charles A. Conrad; Michael Salacz; Justin D. Floyd; Monica Elena Loghin; Sigmund Hsu; Javier Gonzalez; Eric L. Chang; Shiao Y. Woo; Anita Mahajan; Kenneth D. Aldape; W. K. Alfred Yung; Mark R. Gilbert
BACKGROUND Chemoradiation, followed by adjuvant temozolomide, is the standard treatment for newly diagnosed glioblastoma. Adding other active agents may enhance treatment efficacy. METHODS The primary objective of this factorial phase II study was to determine if one of 3 potential chemotherapy agents added to dose-dense temozolomide (ddTMZ) improves progression-free survival (PFS) for patients with newly diagnosed glioblastoma. A prior phase I trial established the safety of combining ddTMZ with isotretinoin, celecoxib, and/or thalidomide. Adults with good performance status and no evidence of progression post chemoradiation were randomized into 8 arms: ddTMZ alone (7 days on/7 days off) or doublet, triplet, and quadruplet combinations with isotretinoin, celecoxib, and thalidomide. RESULTS The study enrolled 155 participants with a median age of 53 years (range, 18-84 y). None of the agents demonstrated improved PFS when compared with arms not containing that specific agent. There was no difference in PFS for triplet compared with doublet regimens, although a trend for improved overall survival (OS) was seen (20.1 vs 17.0 months, P = .15). Compared with ddTMZ, the ddTMZ + isotretinoin doublet had worse PFS (10.5 vs 6.5 months, P = .043) and OS (21.2 vs 11.7 months, P = .037). Trends were also seen for worse outcomes with isotretinoin-containing regimens, but there was no impact with celecoxib or thalidomide combinations. Treatment was well tolerated with expected high rates of lymphopenia. CONCLUSIONS The results do not establish a benefit for these combinations but indicate that adding isotretinoin to ddTMZ may be detrimental. This study demonstrated the feasibility and utility of the factorial design in efficiently testing drug combinations in newly diagnosed glioblastoma. CLINICALTRIALSGOV IDENTIFIER NCT00112502.
Oncologist | 2017
Adrienne Johnson; Eric Allan Severson; Jo-Anne Vergilio; Julia A. Elvin; James Suh; Sugganth Daniel; Mandy Covert; Garrett Michael Frampton; Sigmund Hsu; Glenn J. Lesser; Kimberly Stogner‐Underwood; Ryan T. Mott; Sarah Rush; Jennifer Stanke; Sonika Dahiya; James Sun; Prasanth Reddy; Zachary R. Chalmers; Rachel L. Erlich; Yakov Chudnovsky; David Fabrizio; Alexa B. Schrock; Siraj M. Ali; Vincent A. Miller; Philip J. Stephens; Jeffrey S. Ross; John R. Crawford; Shakti Ramkissoon
This study highlights the value of comprehensive genomic profiling in the largest known cohort of pediatric glioma patients and explores the most common alterations across diagnosis and anatomic location. Tumor mutational burden and associated genetic factors that may predispose patients to developing a hypermutator phenotype are also discussed.
Oncoscience | 2016
Adan Rios; Sigmund Hsu; Angel I. Blanco; Jamie Buryanek; Arthur L. Day; Mary F. McGuire; Robert E. Brown
Glioblastoma multiforme (GBM) is a CNS (central nervous system) malignancy with a low cure rate. Median time to progression after standard treatment is 7 months and median overall survival is 15 months [1]. Post-treatment vasculogenesis promoted by recruitment of bone marrow derived cells (BMDCs, CD11b+ myelomonocytes) is one of main mechanisms of GBM resistance to initial chemoradiotherapy treatment [2]. Local secretion of SDF-1, cognate ligand of BMDCs CXCR4 receptors attracts BMDCs to the post-radiation tumor site.[3]. This SDF-1 hypoxia-dependent effect can be blocked by AMD3100 (plerixafor) [4]. We report a GBM case treated after chemo- radiotherapy with plerixafor and a combination of an mTOR, a Sirt1 and an EGFRvIII inhibitor. After one year temozolomide and the EGFRvIII inhibitor were stopped. Plerixafor, and the MTOR and Sirt-1 inhibitors were continued. He is in clinical and radiologic remission 30 months from the initiation of his adjuvant treatment. To our knowledge, this is the first report of a patient treated for over two years with a CXCR4 inhibitor (plerixafor), as part of his adjuvant treatment. We believe there is sufficient experimental evidence to consider AMD3100 (plerixafor) part of the adjuvant treatment of GBM. Significance The adjuvant inhibition of GBM vasculogenesis(a process different from local angiogenesis) by specifically blocking the migration of BMDCs to the primary tumor site with inhibitors of the CXCR4/SDF-1 axis represents a potential novel therapeutic approach to GBM. There is significant pre-clinical evidence and validation for its use as demonstrated in a patient derived tumor xenograft model of GBM. Together with other specific anti-tumoral therapies, the active inhibition of vasculogenesis in the adjuvant treatment of GBM is deserving of further exploration.
Journal of Biological Chemistry | 1994
Julie A. Rosenthal; Sigmund Hsu; Dinesh Schneider; Lisa N. Gentile; Norma J. Messier; Charles A. Vaslet; Edward Hawrot
Journal of Clinical Oncology | 2006
Mark R. Gilbert; P. Gaupp; Vivien Liu; Charles A. Conrad; Howard Colman; Morris D. Groves; Vinay K. Puduvalli; Victor A. Levin; Sigmund Hsu; J. Horowitz; W. K. Yung
Journal of Neuro-oncology | 2011
Tobias Walbert; Mark R. Gilbert; Morris D. Groves; Vinay K. Puduvalli; W. K. Alfred Yung; Charles A. Conrad; George C. Bobustuc; Howard Colman; Sigmund Hsu; B. Nebiyou Bekele; Wei Qiao; Victor A. Levin
Neurosurgery | 2017
Yoshua Esquenazi; Elliott Friedman; Zheyu Liu; Jay Jiguang Zhu; Sigmund Hsu; Nitin Tandon
Journal of Clinical Oncology | 2005
Morris D. Groves; Vinay K. Puduvalli; Mark R. Gilbert; Charles A. Conrad; Sigmund Hsu; Howard Colman; Kenneth R. Hess; Victor A. Levin; W. K. A. Yung