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Academic literature on the topic 'Evofosfamide'

Author: Grafiati
Published: 10 December 2022
Last updated: 29 January 2023

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Journal articles on the topic "Evofosfamide"

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Harms, Julia K., Tet-Woo Lee, Tao Wang, Amy Lai, Dennis Kee, John M. Chaplin, Nick P. McIvor, et al. "Impact of Tumour Hypoxia on Evofosfamide Sensitivity in Head and Neck Squamous Cell Carcinoma Patient-Derived Xenograft Models." Cells 8, no. 7 (July 13, 2019): 717. http://dx.doi.org/10.3390/cells8070717.

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Tumour hypoxia is a marker of poor prognosis and failure of chemoradiotherapy in head and neck squamous cell carcinoma (HNSCC), providing a strategy for therapeutic intervention in this setting. To evaluate the utility of the hypoxia-activated prodrug evofosfamide (TH-302) in HNSCC, we established ten early passage patient-derived xenograft (PDX) models of HNSCC that were characterised by their histopathology, hypoxia status, gene expression, and sensitivity to evofosfamide. All PDX models closely resembled the histology of the patient tumours they were derived from. Pimonidazole-positive tumour hypoxic fractions ranged from 1.7–7.9% in line with reported HNSCC clinical values, while mRNA expression of the Toustrup hypoxia gene signature showed close correlations between PDX and matched patient tumours, together suggesting the PDX models may accurately model clinical tumour hypoxia. Evofosfamide as a single agent (50 mg/kg IP, qd × 5 for three weeks) demonstrated antitumour efficacy that was variable across the PDX models, ranging from complete regressions in one p16-positive PDX model to lack of significant activity in the three most resistant models. Despite all PDX models showing evidence of tumour hypoxia, and hypoxia being essential for activation of evofosfamide, the antitumour activity of evofosfamide only weakly correlated with tumour hypoxia status determined by pimonidazole immunohistochemistry. Other candidate evofosfamide sensitivity genes—MKI67, POR, and SLFN11—did not strongly influence evofosfamide sensitivity in univariate analyses, although a weak significant relationship with MKI67 was observed, while SLFN11 expression was lost in PDX tumours. Overall, these data confirm that evofosfamide has antitumour activity in clinically-relevant PDX tumour models of HNSCC and support further clinical evaluation of this drug in HNSCC patients. Further research is required to identify those factors that, alongside hypoxia, can influence sensitivity to evofosfamide and could act as predictive biomarkers to support its use in precision medicine therapy of HNSCC.
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O'Connor, Liam J., Cindy Cazares-Körner, Jaideep Saha, Charles N. G. Evans, Michael R. L. Stratford, Ester M. Hammond, and Stuart J. Conway. "Efficient synthesis of 2-nitroimidazole derivatives and the bioreductive clinical candidate Evofosfamide (TH-302)." Organic Chemistry Frontiers 2, no. 9 (2015): 1026–29. http://dx.doi.org/10.1039/c5qo00211g.

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Jayaprakash, Priyamvada, Meghan Rice, Krithikaa Rajkumar Bhanu, Brittany Morrow, Joseph Marszalek, Jason Gay, Christopher Vellano, Benjamin Cowen, Dean Welsch, and Michael Curran. "622 Disrupted oxygen supply and tumor hyper- oxygen consumption contribute independently to prostate cancer immune privilege." Journal for ImmunoTherapy of Cancer 9, Suppl 2 (November 2021): A652. http://dx.doi.org/10.1136/jitc-2021-sitc2021.622.

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BackgroundDespite the success of immunotherapy in immune-infiltrated ”hot” tumors like melanoma, ”cold” tumors like prostate cancer remain unresponsive [1,2,3]. We find that these tumors harbor regions of hypoxia that act as islands of immune privilege that exclude T cells, while retaining immunosuppressive myeloid cells. Targeting hypoxia using the hypoxia-activated prodrug, TH-302 (Evofosfamide) reduced hypoxic regions and co-operated with immune checkpoint blockade (anti-CTLA-4+anti PD-1) to drive tumor regression in transplantable and spontaneous murine prostate tumors [4]. In a Phase I clinical trial, the combination of Evofosfamide and anti CTLA-4 (Ipilimumab) elicited both objective responses and prolonged disease stabilization in late-stage ”cold” tumor patients. However, Evofosfamide reduces but does not eliminate hypoxia and patient tumors resistant to treatment with Evofosfamide and Ipilimumab were hyper-metabolic [5]. Heightened tumor oxidative metabolism has been shown to generate hypoxic zones that resist PD-1 blockade therapy [6] and treatment with Metformin, a mitochondrial complex I inhibitor may reduce hypoxia and improve responses [7]. We hypothesized that targeting tumor oxidative metabolism using mitochondrial complex I inhibitors might diminish tumor hypoxia and, in conjunction with Evofosfamide, sensitize unresponsive tumors to immunotherapy.MethodsWe investigated the capacity of two mitochondrial complex I inhibitors to reduce tumor oxidative metabolism, diminish myeloid suppressive capacity and improve anti-tumor T cell immunity, alone and in combination with Evofosfamide and checkpoint blockade. We assessed tumor burden and immune composition and characterized metabolic profiles using Seahorse XFe96 analyzer (Agilent).ResultsWhile Evofosfamide or inhibition of oxidative metabolism alone did not significantly impact tumor regression, dual combination and triple combination with checkpoint blockade led to a significant reduction in tumor burden. Assessment of the tumor immune microenvironment identified improvements in CD8 and CD4 effector T cell proliferation. In vitro metabolic and functional profiling of TRAMP-C2 prostate tumors, pre-activated T cells and myeloid derived suppressor cells revealed differential effects of complex I inhibition, with inhibition resulting in reduced tumor proliferation and myeloid suppressive function but increases in proliferation and cytotoxic function of pre-activated T cells.ConclusionsOur findings indicate that tumor hypoxia and associated immune suppressive programming can be reduced through both local tissue remodeling and limitation of tumor oxygen metabolism. Complex I inhibition selectively inhibits tumor and myeloid cell function, while sparing T cells. This provides opportunities to craft synergistic immuno-metabolic therapies with the potential to treat ”cold” tumor patients refractory to current FDA approved immunotherapeutics.ReferencesCurran MA, Montalvo W, Yagita H, and Allison JP. PD-1 and CTLA-4 combination blockade expands infiltrating T cells and reduces regulatory T and myeloid cells within B16 melanoma tumors. Proc Natl Acad Sci U S A. 2010; 107(9): 4275–80.Wolchok JD, Kluger H, Callahan MK, Postow MA, Rizvi NA, Lesokhin AM, et al. Nivolumab plus ipilimumab in advanced melanoma. N Engl J Med. 2013; 369(2): 122–33.Kwon ED, Drake CG, Scher HI, Fizazi K, Bossi A, van den Eertwegh AJ, et al. Ipilimumab versus placebo after radiotherapy in patients with metastatic castration-resistant prostate cancer that had progressed after docetaxel chemotherapy (CA184-043): a multicentre, randomised, doubleblind, phase 3 trial. Lancet Oncol. 2014;15(7):700–12.Jayaprakash P, Ai M, Liu A, Budhani P, Bartkowiak T, Sheng J, et al. Targeted hypoxia reduction restores T cell infiltration and sensitizes prostate cancer to immunotherapy. J Clin Invest. 2018; 128 (11): 5137–5149.Hegde A, Jayaprakash P, Couillault CA, Piha-Paul S, Karp D, Rodon J, et al. A Phase I Dose-Escalation Study to Evaluate the Safety and Tolerability of Evofosfamide in Combination with Ipilimumab in Advanced Solid Malignancies. Clin Cancer Res. 2021; 27(11): 3050–3060.Najjar YG, Menk AV, Sander C, Rao U, Karunamurthy A, Bhatia R, et al. Tumor cell oxidative metabolism as a barrier to PD-1 blockade immunotherapy in melanoma. JCI Insight. 2019 4(5): e124989. A.Scharping NE, Menk AV, Whetstone RD, Zeng X, Delgoffe GM. Efficacy of PD-1 Blockade Is Potentiated by Metformin-Induced Reduction of Tumor Hypoxia. Cancer Immunol Res. 2017; 5(1):9–16.
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Grande, Enrique, Daniel E. Castellano, Ana B. Custodio, Rocio Garcia-Carbonero, Encarnación González, Carlos López-López, Javier Munarriz, et al. "A phase II trial to assess the activity and safety of the hypoxia-activated prodrug evofosfamide (TH-302) in combination with sunitinib in patients with disseminated grade 1 and 2 pancreatic neuroendocrine tumors (pNET) as a first-line approach: The GETNE-1408 trial." Journal of Clinical Oncology 34, no. 4_suppl (February 1, 2016): TPS479. http://dx.doi.org/10.1200/jco.2016.34.4_suppl.tps479.

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TPS479 Background: Pancreatic-NETs are highly vascular tumors. The anti-angiogenetic sunitinib was approved in advanced pNETs based on prolongation of progression-free survival. Upregulation of several proangiogenic factors that reflects intratumor hypoxia conditions might drive resistance to sunitinib in pNETs. Evofosfamide is a prodrug that under hypoxic conditions preferentially releases a brominated version of isophosphoramide mustard and has shown activity in cell lines from neural crest derived tumors such as melanoma and glioblastoma/astrocytoma. We hypothesize that evofosfamide may have activity in the pathologic hypoxic conditions present in the tumor environment of neuroendocrine tumors inducing responses that may be consolidated and prolonged with sunitinib in patients with advanced pNETs that are naïve for systemic treatment. Methods: This is a prospective, non randomized, open-label, phase II study that is being conducted in 10 university sites belonging to the Spanish Task Force Group for NETs (GETNE) in Spain. Patients with histologically proven diagnosis of progressive unresectable or metastatic pNET with Ki67 < 20% and grade 1 or 2 will receive sunitinib orally at 37.5 mg PO daily on days 1 to 28 of a 28-day cycle (4 weeks) plus evofosfamide administered at 340 mg/m2 by IV infusion over 30-60 minutes on Days 8, 15 and 22 of a 28-day cycle (4 weeks). Hypoxia-related tumor markers, single nucleotide polymorphisms related to activity and metabolism of antiangiogenic agents (VEGFR2, VEGFR3, PDGFR-α, VEGF-A, IL8, CYP3A4, CYP3A5, ABCB1-2) will be correlated with clinical outcome. In this study it is planned to include 43 patientsbased on a two-stage Simon’s phase II design (α = 0.05, β = 80%). If the trial shows 8 responses or more among 43 patients, the treatment will be considered for further investigation. EudraCT number: 2014-004072-30 Clinical trial information: NCT02402062.
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Bailleul, Quentin, Pauline Navarin, Mélanie Arcicasa, Christine Bal-Mahieu, Angel Montero Carcaboso, Xuefen Le Bourhis, Alessandro Furlan, Samuel Meignan, and Pierre Leblond. "Evofosfamide Is Effective against Pediatric Aggressive Glioma Cell Lines in Hypoxic Conditions and Potentiates the Effect of Cytotoxic Chemotherapy and Ionizing Radiations." Cancers 13, no. 8 (April 9, 2021): 1804. http://dx.doi.org/10.3390/cancers13081804.

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Hypoxia is a hallmark of many solid tumors and is associated with resistance to anticancer treatments. Hypoxia-activated prodrugs (HAPs) were developed to target the hypoxic regions of these tumors. Among 2nd generation HAPs, Evofosfamide (Evo, also known as TH-302) exhibits preclinical and clinical activities against adult glioblastoma. In this study, we evaluated its potential in the field of pediatric neuro-oncology. We assessed the efficacy of Evo in vitro as a single drug, or in combination with SN38, doxorubicin, and etoposide, against three pediatric high-grade glioma (pHGG) and three diffuse intrinsic pontine glioma (DIPG) cell lines under hypoxic conditions. We also investigated radio-sensitizing effects using clonogenic assays. Evo inhibited the growth of all cell lines, mainly under hypoxia. We also highlighted a significant synergism between Evo and doxorubicin, SN38, or etoposide. Finally, Evo radio-sensitized the pHGG cell line tested, both with fractionated and single-dose irradiation schedules. Altogether, we report here the first preclinical proof of evidence about Evofosfamide efficiency against hypoxic pHGG and DIPG cells. Since such tumors are highly hypoxic, and Evo potentiates the effect of ionizing radiation and chemotherapy, it appears as a promising therapeutic strategy for children with brain tumors.
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Laubach, Jacob P., Noopur Raje, Andrew J. Yee, Philippe Armand, Robert L. Schlossman, Jacalyn Rosenblatt, Michael G. Martin, et al. "Final Results of a Phase 1/2 Open-Label Study to Assess the Safety, Tolerability and Preliminary Efficacy of Evofosfamide, a Hypoxia-Activated Prodrug, and Dexamethasone with or without Bortezomib in Subjects with Relapsed/Refractory Multiple Myeloma." Blood 128, no. 22 (December 2, 2016): 2122. http://dx.doi.org/10.1182/blood.v128.22.2122.2122.

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Abstract Purpose: This phase 1/2 study was conducted to determine the maximum tolerated dose (MTD), safety, tolerability, and clinical activity of the hypoxia-activated prodrug evofosfamide (TH-302) and dexamethasone with or without bortezomib in relapsed/refractory multiple myeloma. Patients & Methods: Patients were enrolled to stage A (evofosfamide + dexamethasone) followed by stage B (evofosfamide + bortezomib + dexamethasone). Stage A enrollment began in March 2012 and ended in May 2014. In total 34 patients were enrolled to stage A, with 31 patients being treated. Stage B enrollment began in June 2014 and ended in July 2015. In total 28 patients were enrolled and treated on stage B. Patients enrolled on study were diagnosed with relapsed/ refractory multiple myeloma (RRMM), had adequate hepatic, renal, and hematologic function, as well as an ECOG performance status of ≤2, and had all received at least 2 prior lines of therapy including an immunomodulatory agent and a proteasome inhibitor. In stage B, patients previously receiving bortezomib must not have discontinued due to toxicity. Patients must have had measureable disease as determined by the International Working Group (IMWG) criteria. In stage A, evofosfamide was administered IV in conjunction with a fixed oral dose of 40 mg dexamethasone on Days 1, 4, 8 and 11 of a 21-day cycle. In stage B, evofosfamide was administered in conjunction with a fixed oral dose of 40 mg dexamethasone and a fixed IV or SC dose of 1.3 mg/m2 bortezomib. Stage A dose escalation began at a dose of 240 mg/m2 evofosfamide and increased stepwise in a 3+3 design until reaching the MTD of 480 mg/m2. The recommended phase 2 dose (RP2D) was set at 340 mg/m2 and a dose expansion cohort of 15 treated patients were treated at the RP2D. Stage B dose escalation began at a dose of 240 mg/m2 and concluded at the 340 mg/m2 RP2D of stage A. There were no DLTs observed in this cohort. A total of 24 patients were treated at the RP2D. Results: Of the 31 patients treated on stage A, the median age was 65, with a range of 53-86. The median number of prior treatments was 6 (range: 2-13). Of the 28 patients treated on stage B, the median age was 62, with a range of 45-83. The median number of prior treatments was 8 (range: 3 - 16). All patients had prior bortezomib exposure with a median number of bortezomib containing regimens in stage B of 3 (range: 1-6). The most common stage A grade 3/4 events were anemia (36%), neutropenia (32%), thrombocytopenia (39%), leukopenia (23%), cellulitis (10%) and pneumonia (10%). Four pts (13%) discontinued due to an adverse event. The most common Arm B grade 3/4 events were thrombocytopenia (61%), neutropenia (32%), anemia (25%), leukopenia (18%) and pneumonia (14%). Two patients (7%) discontinued due to an adverse event. Of the 31 patients evaluable for response in stage A, 4 Partial Responses and 2 Minimal Responses were reported for a clinical benefit rate of 19%. Twenty patients (65%) in stage A had stable Disease. Of the 28 patients evaluable for response in stage B, 1 Complete Response, 2 Partial Responses and 2 Minimal Responses were reported for a clinical benefit rate of 18%. Eighteen patients (64%) in stage B had Stable Disease. Conclusion: A 340 mg/m2 twice a week dose of the hypoxia- activated agent evofosfamide was established as the recommended Phase 2 dose when combined with dexamethasone with or without bortezomib. Clinical activity was noted along with a majority of patients having stable disease or better even in this heavily pre-treated refractory population of MM. The use of hypoxia-activated agents holds promise as a novel therapeutic target in MM. Disclosures Raje: Amgen: Consultancy, Membership on an entity's Board of Directors or advisory committees; Celgene: Consultancy, Membership on an entity's Board of Directors or advisory committees; Takeda: Consultancy, Membership on an entity's Board of Directors or advisory committees; Merck: Membership on an entity's Board of Directors or advisory committees; Novartis: Consultancy, Membership on an entity's Board of Directors or advisory committees; Roche: Consultancy, Membership on an entity's Board of Directors or advisory committees; BMS: Consultancy, Membership on an entity's Board of Directors or advisory committees; AstraZeneca: Research Funding; Eli Lilly: Research Funding. Armand:Pfizer: Research Funding; Roche: Research Funding; Bristol-Myers Squibb: Consultancy, Research Funding; Infinity Pharmaceuticals: Consultancy; Sequenta Inc: Research Funding; Merck: Consultancy, Research Funding. Rosenblatt:BMS: Research Funding; Astex: Research Funding; DCPrime: Research Funding. Shain:Amgen/Onyx: Membership on an entity's Board of Directors or advisory committees, Speakers Bureau; Novartis: Speakers Bureau; Takeda/Millennium: Membership on an entity's Board of Directors or advisory committees, Speakers Bureau; Signal Genetics: Research Funding; Celgene: Membership on an entity's Board of Directors or advisory committees, Research Funding, Speakers Bureau. Anderson:Oncopep: Other: Scientific Founder; Onyx: Membership on an entity's Board of Directors or advisory committees; Acetylon: Other: Scientific Founder; Sonofi Aventis: Membership on an entity's Board of Directors or advisory committees; Gilead: Membership on an entity's Board of Directors or advisory committees; Celgene: Membership on an entity's Board of Directors or advisory committees. Richardson:Jazz Pharmaceuticals: Consultancy, Membership on an entity's Board of Directors or advisory committees. Ghobrial:Amgen: Honoraria; BMS: Honoraria, Research Funding; Novartis: Honoraria; Noxxon: Honoraria; Takeda: Honoraria; Celgene: Honoraria, Research Funding.
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Higgins, Jack P., Nenad Sarapa, Jason Kim, and Eric Poma. "Unexpected pharmacokinetics of evofosfamide observed in phase III MAESTRO study." Journal of Clinical Oncology 36, no. 15_suppl (May 20, 2018): 2568. http://dx.doi.org/10.1200/jco.2018.36.15_suppl.2568.

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Pourmorteza, Mohsen, Zia U. Rahman, and Mark Young. "Evofosfamide, a new horizon in the treatment of pancreatic cancer." Anti-Cancer Drugs 27, no. 8 (September 2016): 723–25. http://dx.doi.org/10.1097/cad.0000000000000386.

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Spiegelberg, Linda, Stefan J. van Hoof, Rianne Biemans, Natasja G. Lieuwes, Damiënne Marcus, Raymon Niemans, Jan Theys, et al. "Evofosfamide sensitizes esophageal carcinomas to radiation without increasing normal tissue toxicity." Radiotherapy and Oncology 141 (December 2019): 247–55. http://dx.doi.org/10.1016/j.radonc.2019.06.034.

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Anderson, Robert F., Dan Li, and Francis W. Hunter. "Antagonism in effectiveness of evofosfamide and doxorubicin through intermolecular electron transfer." Free Radical Biology and Medicine 113 (December 2017): 564–70. http://dx.doi.org/10.1016/j.freeradbiomed.2017.10.385.

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Dissertations / Theses on the topic "Evofosfamide"

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Liapis, Vasilios. "Targeting Cancer in the Bone with the Hypoxia Activated Pro-Drug Evofosfamide." Thesis, 2017. http://hdl.handle.net/2440/119332.

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Tumour hypoxia is widely recognised as a major cause of treatment failure and poor outcome for a variety of malignancies. Tumour hypoxia also results in resistance to conventional anticancer therapies leading to an increase in malignancy and metastases to other sites, in particular, the bone. Bone metastases occur in more than 75% of patients with breast, prostate and lung cancer. Tumours in the bone are often resistant to anticancer therapy due to the hypoxic nature of the bone micro-environment, resulting in their recurrence and metastasis. Hypoxia also offers treatment opportunities, exemplified by the development of highly active compounds that target hypoxic zones known as Hypoxia Activated Pro-drugs. Evofosfamide is a hypoxia activated pro-drug created by the conjugation of 2-nitroimidazole to bromo-isophosphoramide (Br-IPM). When Evofosfamide is delivered to regions of hypoxia, Br-IPM, the DNA cross linking toxin is released resulting in cancer cell death. The cytotoxic activity of evofosfamide against osteosarcoma cells was assessed in vitro and its anticancer efficacy as a single agent and in combination with doxorubicin was evaluated in an orthotopic mouse model of human osteosarcoma (OS). In vitro, evofosfamide was cytotoxic to osteosarcoma cells selectively under hypoxic conditions, whereas primary normal human osteoblasts were protected. Animals transplanted with OS cells directly into their tibiae and left untreated developed mixed osteolytic/osteosclerotic bone lesions and subsequently developed lung metastases. Evofosfamide reduced tumor burden in bone and cooperated with doxorubicin to protect the bone from osteosarcoma induced bone destruction, while also reducing lung metastases. In addition, under hypoxic conditions in vitro, evofosfamide cooperated with Pro Apoptotic Receptor Agonists (PARAs) dulanermin and drozitumab, resulting in a dose-dependent increase in cytotoxicity to osteosarcoma cells selectively under hypoxic conditions. In contrast primary normal human osteoblasts under the same hypoxic conditions were resistant. In vivo, evofosfamide cooperated with drozitumab, reducing tumor burden in the orthotopic mouse model of human osteosarcoma and protected the bone from osteosarcoma-induced bone destruction while also reducing the growth of pulmonary metastases. In order to assess the anticancer efficacy of evofosfamide against breast cancer, a panel of human breast cancer cell lines were treated with evofosfamide and shown to be highly cytotoxic under hypoxia. Osteolytic MDA-MB-231-TXSA cells were transplanted into the mammary fat pad or into the tibiae of mice, allowed to establish and treated with evofosfamide, paclitaxel, or both. In vivo evofosfamide demonstrated tumor suppressive activity as a single agent and cooperated with paclitaxel to reduce mammary tumor growth. Breast cancer cells transplanted into the tibiae of mice developed osteolytic lesions. Treatment with evofosfamide or paclitaxel resulted in a significant delay in tumor growth and with an overall reduction in tumor burden in bone, whereas combined treatment resulted in a significantly greater reduction in tumor burden in the tibia of mice. In conclusion the preclinical data presented in this thesis demonstrate that evofosfamide may be an attractive therapeutic agent when used alone and in combination with chemotherapy or PARAs for the treatment of osteosarcoma and breast cancer.
Thesis (Ph.D.) -- University of Adelaide, Adelaide Medical School, 2017
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Conference papers on the topic "Evofosfamide"

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Meng, Fanying, Deepthi Bhupathi, Geraldine Chan, and Charles P. Hart. "Abstract 2803: Distinct roles of intracellular ROS in cisplatin and evofosfamide cytotoxicity." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-2803.

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Nytko-Karouzakis, Katarzyna J., Ivo Grgic, Janosch Ott, and Martin Pruschy. "Abstract A163: The combined treatment modality of a hypoxia-activated prodrug (Evofosfamide) with ionizing radiation." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics; November 5-9, 2015; Boston, MA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1535-7163.targ-15-a163.

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Perassi, Bruna Victorasso Jardim, Wei Mu, Dominique F. Abrahams, Michal R. Tomaszewski, Jan Poleszczuk, Jack Higgins, Gary V. Martinez, and Robert J. Gillies. "Abstract 2772: Targeting hypoxic habitats with hypoxia pro-drug evofosfamide in preclinical models of sarcoma." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-2772.

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Hunter, Francis W., Avik Shome, Dan Li, Way W. Wong, Peter Tsai, Nooriyah Poonawala, Purvi M. Kakadiya, et al. "Abstract 169: Preclinical efficacy and sensitivity determinants of evofosfamide in molecularly defined models of head and neck squamous cell carcinoma." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-169.

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Lavranos, Tina C., Daniel Inglis, Donna Beaumont, Annabell F. Leske, Chloe Hawkins, Michaela Scherer, Charles Hart, Jessica Sun, Brian Elenbaas, and Gabriel Kremmidiotis. "Abstract B174: Complementary activity of the vascular disruption agent BNC105 and the hypoxia-activated prodrug evofosfamide (TH-302) in suppressing the growth of preclinical renal and breast solid tumors." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics; November 5-9, 2015; Boston, MA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1535-7163.targ-15-b174.

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