Literature DB >> 21252718

Phase II multicenter trial of voreloxin as second-line therapy in chemotherapy-sensitive or refractory small cell lung cancer.

Lee M Krug1, Jeffrey Crawford, David S Ettinger, Geoffrey I Shapiro, David Spigel, Tony Reiman, Jennifer S Temel, Glenn C Michelson, Donald Y Young, Ute Hoch, Daniel C Adelman.   

Abstract

INTRODUCTION: Voreloxin is an anticancer quinolone derivative that intercalates DNA and inhibits topoisomerase II, causing double-strand breaks in DNA, irreversible G2 arrest, and rapid onset of apoptosis. Based on preclinical activity of voreloxin in chemoresistant tumors, early phase I clinical activity, and a mechanism of action similar to other topoisomerase II inhibitors such as the anthracyclines and etoposide, this phase II trial was undertaken as second-line treatment of small cell lung cancer (SCLC).
METHODS: Patients with extensive stage SCLC previously treated with one prior chemotherapy regimen were eligible. Patients with chemotherapy-sensitive or chemotherapy-refractory disease were considered as separate cohorts. Voreloxin (48 mg/m) was administered on the first day of each 21-day cycle for up to six cycles. The primary end point was objective response rate.
RESULTS: Fifty-five patients were enrolled including 28 with refractory SCLC and 27 with sensitive SCLC; 47 were evaluable for response. Three patients with sensitive SCLC had an objective response, including one complete response and two partial responses (11% response rate based on intent to treat). No patients in the refractory cohort had a response. The primary grade 3 toxicity was neutropenia.
CONCLUSION: Voreloxin has minimal activity in relapsed SCLC when administered at 48 mg/m in a 3-week schedule.

Entities:  

Mesh:

Substances:

Year:  2011        PMID: 21252718     DOI: 10.1097/JTO.0b013e318200e509

Source DB:  PubMed          Journal:  J Thorac Oncol        ISSN: 1556-0864            Impact factor:   15.609


  5 in total

1.  Targeting the transposase domain of the DNA repair component Metnase to enhance chemotherapy.

Authors:  Elizabeth A Williamson; Leah Damiani; Andrei Leitao; Chelin Hu; Helen Hathaway; Tudor Oprea; Larry Sklar; Montaser Shaheen; Julie Bauman; Wei Wang; Jac A Nickoloff; Suk-Hee Lee; Robert Hromas
Journal:  Cancer Res       Date:  2012-10-22       Impact factor: 12.701

2.  Relevance of platinum-sensitivity status in relapsed/refractory extensive-stage small-cell lung cancer in the modern era: a patient-level analysis of southwest oncology group trials.

Authors:  Primo N Lara; James Moon; Mary W Redman; Thomas J Semrad; Karen Kelly; Jeffrey W Allen; Barbara J Gitlitz; Philip C Mack; David R Gandara
Journal:  J Thorac Oncol       Date:  2015-01       Impact factor: 15.609

Review 3.  Targeting acute myeloid leukemia with TP53-independent vosaroxin.

Authors:  Christopher B Benton; Farhad Ravandi
Journal:  Future Oncol       Date:  2016-09-12       Impact factor: 3.404

4.  The primary mechanism of cytotoxicity of the chemotherapeutic agent CX-5461 is topoisomerase II poisoning.

Authors:  Peter M Bruno; Mengrou Lu; Kady A Dennis; Haider Inam; Connor J Moore; John Sheehe; Stephen J Elledge; Michael T Hemann; Justin R Pritchard
Journal:  Proc Natl Acad Sci U S A       Date:  2020-02-10       Impact factor: 11.205

5.  Enhancement of radiosensitivity by the novel anticancer quinolone derivative vosaroxin in preclinical glioblastoma models.

Authors:  Giovanni Luca Gravina; Andrea Mancini; Claudia Mattei; Flora Vitale; Francesco Marampon; Alessandro Colapietro; Giulia Rossi; Luca Ventura; Antonella Vetuschi; Ernesto Di Cesare; Judith A Fox; Claudio Festuccia
Journal:  Oncotarget       Date:  2017-05-02
  5 in total

北京卡尤迪生物科技股份有限公司 © 2022-2023.