Skip to main content
Top
Published in: Journal of Experimental & Clinical Cancer Research 1/2017

Open Access 01-12-2017 | Review

Drug repurposing for the treatment of glioblastoma multiforme

Authors: Claudia Abbruzzese, Silvia Matteoni, Michele Signore, Luca Cardone, Kavindra Nath, Jerry D. Glickson, Marco G. Paggi

Published in: Journal of Experimental & Clinical Cancer Research | Issue 1/2017

Login to get access

Abstract

Background

Glioblastoma Multiforme is the deadliest type of brain tumor and is characterized by very poor prognosis with a limited overall survival. Current optimal therapeutic approach has essentially remained unchanged for more than a decade, consisting in maximal surgical resection followed by radiotherapy plus temozolomide.

Main body

Such a dismal patient outcome represents a compelling need for innovative and effective therapeutic approaches. Given the development of new drugs is a process presently characterized by an immense increase in costs and development time, drug repositioning, finding new uses for existing approved drugs or drug repurposing, re-use of old drugs when novel molecular findings make them attractive again, are gaining significance in clinical pharmacology, since it allows faster and less expensive delivery of potentially useful drugs from the bench to the bedside. This is quite evident in glioblastoma, where a number of old drugs is now considered for clinical use, often in association with the first-line therapeutic intervention. Interestingly, most of these medications are, or have been, widely employed for decades in non-neoplastic pathologies without relevant side effects. Now, the refinement of their molecular mechanism(s) of action through up-to-date technologies is paving the way for their use in the therapeutic approach of glioblastoma as well as other cancer types.

Short conclusion

The spiraling costs of new antineoplastic drugs and the long time required for them to reach the market demands a profoundly different approach to keep lifesaving therapies affordable for cancer patients. In this context, repurposing can represent a relatively inexpensive, safe and fast approach to glioblastoma treatment. To this end, pros and cons must be accurately considered.
Literature
1.
go back to reference Stupp R, Mason WP, van den Bent MJ, Weller M, Fisher B, Taphoorn MJ, et al. Radiotherapy plus concomitant and adjuvant temozolomide for glioblastoma. N Engl J Med. 2005;352(10):987–96. doi: 10.1056/NEJMoa043330.PubMedCrossRef Stupp R, Mason WP, van den Bent MJ, Weller M, Fisher B, Taphoorn MJ, et al. Radiotherapy plus concomitant and adjuvant temozolomide for glioblastoma. N Engl J Med. 2005;352(10):987–96. doi: 10.​1056/​NEJMoa043330.PubMedCrossRef
6.
go back to reference Zappacosta AR. Reversal of baldness in patient receiving minoxidil for hypertension. N Engl J Med. 1980;303(25):1480–1.PubMed Zappacosta AR. Reversal of baldness in patient receiving minoxidil for hypertension. N Engl J Med. 1980;303(25):1480–1.PubMed
10.
go back to reference Furman PA, Fyfe JA, St Clair MH, Weinhold K, Rideout JL, Freeman GA, et al. Phosphorylation of 3′-azido-3′-deoxythymidine and selective interaction of the 5′-triphosphate with human immunodeficiency virus reverse transcriptase. Proc Natl Acad Sci U S A. 1986;83(21):8333–7.PubMedPubMedCentralCrossRef Furman PA, Fyfe JA, St Clair MH, Weinhold K, Rideout JL, Freeman GA, et al. Phosphorylation of 3′-azido-3′-deoxythymidine and selective interaction of the 5′-triphosphate with human immunodeficiency virus reverse transcriptase. Proc Natl Acad Sci U S A. 1986;83(21):8333–7.PubMedPubMedCentralCrossRef
28.
go back to reference Parkinson H, Sarkans U, Kolesnikov N, Abeygunawardena N, Burdett T, Dylag M, et al. ArrayExpress update--an archive of microarray and high-throughput sequencing-based functional genomics experiments. Nucleic Acids Res. 2011;39(Database):D1002–4. doi: 10.1093/nar/gkq1040.PubMedCrossRef Parkinson H, Sarkans U, Kolesnikov N, Abeygunawardena N, Burdett T, Dylag M, et al. ArrayExpress update--an archive of microarray and high-throughput sequencing-based functional genomics experiments. Nucleic Acids Res. 2011;39(Database):D1002–4. doi: 10.​1093/​nar/​gkq1040.PubMedCrossRef
29.
go back to reference Barrett T, Suzek TO, Troup DB, Wilhite SE, Ngau WC, Ledoux P, et al. NCBI GEO: mining millions of expression profiles--database and tools. Nucleic Acids Res. 2005;33(Database issue):D562–6. doi: 10.1093/nar/gki022.PubMedCrossRef Barrett T, Suzek TO, Troup DB, Wilhite SE, Ngau WC, Ledoux P, et al. NCBI GEO: mining millions of expression profiles--database and tools. Nucleic Acids Res. 2005;33(Database issue):D562–6. doi: 10.​1093/​nar/​gki022.PubMedCrossRef
30.
go back to reference Lamb J, Crawford ED, Peck D, Modell JW, Blat IC, Wrobel MJ, et al. The connectivity map: using gene-expression signatures to connect small molecules, genes, and disease. Science. 2006;313(5795):1929–35. doi: 10.1126/science.1132939.PubMedCrossRef Lamb J, Crawford ED, Peck D, Modell JW, Blat IC, Wrobel MJ, et al. The connectivity map: using gene-expression signatures to connect small molecules, genes, and disease. Science. 2006;313(5795):1929–35. doi: 10.​1126/​science.​1132939.PubMedCrossRef
33.
36.
go back to reference Ghosh JC, Siegelin MD, Vaira V, Faversani A, Tavecchio M, Chae YC, et al. Adaptive mitochondrial reprogramming and resistance to PI3K therapy. J Natl Cancer Inst. 2015;107(3) doi: 10.1093/jnci/dju502. Ghosh JC, Siegelin MD, Vaira V, Faversani A, Tavecchio M, Chae YC, et al. Adaptive mitochondrial reprogramming and resistance to PI3K therapy. J Natl Cancer Inst. 2015;107(3) doi: 10.​1093/​jnci/​dju502.
38.
42.
go back to reference Cheng F, Hong H, Yang S, Wei Y. Individualized network-based drug repositioning infrastructure for precision oncology in the panomics era. Brief Bioinform. 2017;18(4):682–97. doi: 10.1093/bib/bbw051. PubMed Cheng F, Hong H, Yang S, Wei Y. Individualized network-based drug repositioning infrastructure for precision oncology in the panomics era. Brief Bioinform. 2017;18(4):682–97. doi: 10.​1093/​bib/​bbw051.​ PubMed
45.
go back to reference Chen X, Wong YK, Wang J, Zhang J, Lee YM, Shen HM, et al. Target identification with quantitative activity based protein profiling (ABPP). Proteomics. 2017;17(3–4) doi: 10.1002/pmic.201600212. Chen X, Wong YK, Wang J, Zhang J, Lee YM, Shen HM, et al. Target identification with quantitative activity based protein profiling (ABPP). Proteomics. 2017;17(3–4) doi: 10.​1002/​pmic.​201600212.
53.
54.
go back to reference Lun X, Wells JC, Grinshtein N, King JC, Hao X, Dang NH, et al. Disulfiram when combined with copper enhances the therapeutic effects of temozolomide for the treatment of glioblastoma. Clin Cancer Res. 2016; doi: 10.1158/1078-0432.CCR-15-1798. Lun X, Wells JC, Grinshtein N, King JC, Hao X, Dang NH, et al. Disulfiram when combined with copper enhances the therapeutic effects of temozolomide for the treatment of glioblastoma. Clin Cancer Res. 2016; doi: 10.​1158/​1078-0432.​CCR-15-1798.
57.
go back to reference Paranjpe A, Zhang R, Ali-Osman F, Bobustuc GC, Srivenugopal KS. Disulfiram is a direct and potent inhibitor of human O6-methylguanine-DNA methyltransferase (MGMT) in brain tumor cells and mouse brain and markedly increases the alkylating DNA damage. Carcinogenesis. 2014;35(3):692–702. doi: 10.1093/carcin/bgt366.PubMedCrossRef Paranjpe A, Zhang R, Ali-Osman F, Bobustuc GC, Srivenugopal KS. Disulfiram is a direct and potent inhibitor of human O6-methylguanine-DNA methyltransferase (MGMT) in brain tumor cells and mouse brain and markedly increases the alkylating DNA damage. Carcinogenesis. 2014;35(3):692–702. doi: 10.​1093/​carcin/​bgt366.PubMedCrossRef
59.
go back to reference Hegazy AM, Yamada D, Kobayashi M, Kohno S, Ueno M, Ali MA, et al. Therapeutic strategy for targeting aggressive malignant gliomas by disrupting their energy balance. J Biol Chem. 2016; doi: 10.1074/jbc.M116.734756. Hegazy AM, Yamada D, Kobayashi M, Kohno S, Ueno M, Ali MA, et al. Therapeutic strategy for targeting aggressive malignant gliomas by disrupting their energy balance. J Biol Chem. 2016; doi: 10.​1074/​jbc.​M116.​734756.
63.
go back to reference Wick W, Gorlia T, Bady P, Platten M, van den Bent MJ, Taphoorn MJ, et al. Phase II study of radiotherapy and Temsirolimus versus Radiochemotherapy with Temozolomide in patients with newly diagnosed glioblastoma without MGMT promoter Hypermethylation (EORTC 26082). Clin Cancer Res. 2016;22(19):4797–806. doi: 10.1158/1078-0432.CCR-15-3153.PubMedCrossRef Wick W, Gorlia T, Bady P, Platten M, van den Bent MJ, Taphoorn MJ, et al. Phase II study of radiotherapy and Temsirolimus versus Radiochemotherapy with Temozolomide in patients with newly diagnosed glioblastoma without MGMT promoter Hypermethylation (EORTC 26082). Clin Cancer Res. 2016;22(19):4797–806. doi: 10.​1158/​1078-0432.​CCR-15-3153.PubMedCrossRef
70.
go back to reference Strong R, Miller RA, Antebi A, Astle CM, Bogue M, Denzel MS, et al. Longer lifespan in male mice treated with a weakly estrogenic agonist, an antioxidant, an alpha-glucosidase inhibitor or a Nrf2-inducer. Aging Cell. 2016; doi: 10.1111/acel.12496. Strong R, Miller RA, Antebi A, Astle CM, Bogue M, Denzel MS, et al. Longer lifespan in male mice treated with a weakly estrogenic agonist, an antioxidant, an alpha-glucosidase inhibitor or a Nrf2-inducer. Aging Cell. 2016; doi: 10.​1111/​acel.​12496.
72.
go back to reference Coulston F, Dougherty WJ, LeFevre R, Abraham R, Silvestrini B. Reversible inhibition of spermatogenesis in rats and monkeys with a new class of indazol-carboxylic acids. Exp Mol Pathol. 1975;23(2):357–66.PubMedCrossRef Coulston F, Dougherty WJ, LeFevre R, Abraham R, Silvestrini B. Reversible inhibition of spermatogenesis in rats and monkeys with a new class of indazol-carboxylic acids. Exp Mol Pathol. 1975;23(2):357–66.PubMedCrossRef
74.
go back to reference Magno L, Terraneo F, Bertoni F, Tordiglione M, Bardelli D, Rosignoli MT, et al. Double-blind randomized study of lonidamine and radiotherapy in head and neck cancer. Int J Radiat Oncol Biol Phys. 1994;29(1):45–55.PubMedCrossRef Magno L, Terraneo F, Bertoni F, Tordiglione M, Bardelli D, Rosignoli MT, et al. Double-blind randomized study of lonidamine and radiotherapy in head and neck cancer. Int J Radiat Oncol Biol Phys. 1994;29(1):45–55.PubMedCrossRef
75.
go back to reference Carapella CM, Paggi MG, Calvosa F, Cattani F, Jandolo B, Mastrostefano R, et al. Lonidamine in the combined treatment of malignant gliomas. A randomized study. J Neurosurg Sci. 1990;34(3–4):261–4.PubMed Carapella CM, Paggi MG, Calvosa F, Cattani F, Jandolo B, Mastrostefano R, et al. Lonidamine in the combined treatment of malignant gliomas. A randomized study. J Neurosurg Sci. 1990;34(3–4):261–4.PubMed
76.
go back to reference Schiffer D, Sales S, Soffietti R. Lonidamine in malignant brain tumors. Semin Oncol. 1991;18(2 Suppl 4):38–41.PubMed Schiffer D, Sales S, Soffietti R. Lonidamine in malignant brain tumors. Semin Oncol. 1991;18(2 Suppl 4):38–41.PubMed
78.
go back to reference Nancolas B, Guo L, Zhou R, Nath K, Nelson DS, Leeper DB, et al. The anti-tumour agent lonidamine is a potent inhibitor of the mitochondrial pyruvate carrier and plasma membrane monocarboxylate transporters. Biochem J. 2016;473(7):929–36. doi: 10.1042/BJ20151120.PubMedPubMedCentralCrossRef Nancolas B, Guo L, Zhou R, Nath K, Nelson DS, Leeper DB, et al. The anti-tumour agent lonidamine is a potent inhibitor of the mitochondrial pyruvate carrier and plasma membrane monocarboxylate transporters. Biochem J. 2016;473(7):929–36. doi: 10.​1042/​BJ20151120.PubMedPubMedCentralCrossRef
79.
go back to reference Paggi MG, Zupi G, Fanciulli M, Del Carlo C, Giorno S, Laudonio N, et al. Effect of lonidamine on the utilization of 14C-labeled glucose by human astrocytoma cells. Exp Mol Pathol. 1987;47(2):154–65.PubMedCrossRef Paggi MG, Zupi G, Fanciulli M, Del Carlo C, Giorno S, Laudonio N, et al. Effect of lonidamine on the utilization of 14C-labeled glucose by human astrocytoma cells. Exp Mol Pathol. 1987;47(2):154–65.PubMedCrossRef
80.
go back to reference Floridi A, Lehninger AL. Action of the antitumor and antispermatogenic agent lonidamine on electron transport in Ehrlich ascites tumor mitochondria. Arch Biochem Biophys. 1983;226(1):73–83.PubMedCrossRef Floridi A, Lehninger AL. Action of the antitumor and antispermatogenic agent lonidamine on electron transport in Ehrlich ascites tumor mitochondria. Arch Biochem Biophys. 1983;226(1):73–83.PubMedCrossRef
81.
go back to reference Davidescu M, Macchioni L, Scaramozzino G, Cristina Marchetti M, Migliorati G, Vitale R, et al. The energy blockers bromopyruvate and lonidamine lead GL15 glioblastoma cells to death by different p53-dependent routes. Sci Rep. 2015;5:14343. doi: 10.1038/srep14343.PubMedPubMedCentralCrossRef Davidescu M, Macchioni L, Scaramozzino G, Cristina Marchetti M, Migliorati G, Vitale R, et al. The energy blockers bromopyruvate and lonidamine lead GL15 glioblastoma cells to death by different p53-dependent routes. Sci Rep. 2015;5:14343. doi: 10.​1038/​srep14343.PubMedPubMedCentralCrossRef
82.
go back to reference Nath K, Nelson DS, Heitjan DF, Leeper DB, Zhou R, Glickson JD. Lonidamine induces intracellular tumor acidification and ATP depletion in breast, prostate and ovarian cancer xenografts and potentiates response to doxorubicin. NMR Biomed. 2015;28(3):281–90. doi: 10.1002/nbm.3240.PubMedCrossRef Nath K, Nelson DS, Heitjan DF, Leeper DB, Zhou R, Glickson JD. Lonidamine induces intracellular tumor acidification and ATP depletion in breast, prostate and ovarian cancer xenografts and potentiates response to doxorubicin. NMR Biomed. 2015;28(3):281–90. doi: 10.​1002/​nbm.​3240.PubMedCrossRef
83.
go back to reference Schmeisser S, Zarse K, Ristow M. Lonidamine extends lifespan of adult Caenorhabditis Elegans by increasing the formation of mitochondrial reactive oxygen species. Horm Metab Res. 2011;43(10):687–92. doi: 10.1055/s-0031-1286308.PubMedCrossRef Schmeisser S, Zarse K, Ristow M. Lonidamine extends lifespan of adult Caenorhabditis Elegans by increasing the formation of mitochondrial reactive oxygen species. Horm Metab Res. 2011;43(10):687–92. doi: 10.​1055/​s-0031-1286308.PubMedCrossRef
86.
go back to reference Wang Z, Liu P, Chen Q, Deng S, Liu X, Situ H, et al. Targeting AMPK signaling pathway to overcome drug resistance for cancer therapy. Curr Drug Targets. 2016;17(8):853–64.PubMedCrossRef Wang Z, Liu P, Chen Q, Deng S, Liu X, Situ H, et al. Targeting AMPK signaling pathway to overcome drug resistance for cancer therapy. Curr Drug Targets. 2016;17(8):853–64.PubMedCrossRef
90.
go back to reference Li C, Liu Y, Liu H, Zhang W, Shen C, Cho K, et al. Impact of autophagy inhibition at different stages on cytotoxic effect of autophagy inducer in glioblastoma cells. Cell Physiol Biochem. 2015;35(4):1303–16. doi: 10.1159/000373952.PubMedCrossRef Li C, Liu Y, Liu H, Zhang W, Shen C, Cho K, et al. Impact of autophagy inhibition at different stages on cytotoxic effect of autophagy inducer in glioblastoma cells. Cell Physiol Biochem. 2015;35(4):1303–16. doi: 10.​1159/​000373952.PubMedCrossRef
94.
95.
go back to reference Hori YS, Hosoda R, Akiyama Y, Sebori R, Wanibuchi M, Mikami T, et al. Chloroquine potentiates temozolomide cytotoxicity by inhibiting mitochondrial autophagy in glioma cells. J Neuro-Oncol. 2015;122(1):11–20. doi: 10.1007/s11060-014-1686-9.CrossRef Hori YS, Hosoda R, Akiyama Y, Sebori R, Wanibuchi M, Mikami T, et al. Chloroquine potentiates temozolomide cytotoxicity by inhibiting mitochondrial autophagy in glioma cells. J Neuro-Oncol. 2015;122(1):11–20. doi: 10.​1007/​s11060-014-1686-9.CrossRef
96.
go back to reference Rosenfeld MR, Ye X, Supko JG, Desideri S, Grossman SA, Brem S, et al. A phase I/II trial of hydroxychloroquine in conjunction with radiation therapy and concurrent and adjuvant temozolomide in patients with newly diagnosed glioblastoma multiforme. Autophagy. 2014;10(8):1359–68. doi: 10.4161/auto.28984.PubMedPubMedCentralCrossRef Rosenfeld MR, Ye X, Supko JG, Desideri S, Grossman SA, Brem S, et al. A phase I/II trial of hydroxychloroquine in conjunction with radiation therapy and concurrent and adjuvant temozolomide in patients with newly diagnosed glioblastoma multiforme. Autophagy. 2014;10(8):1359–68. doi: 10.​4161/​auto.​28984.PubMedPubMedCentralCrossRef
97.
go back to reference Briceno E, Reyes S, Sotelo J. Therapy of glioblastoma multiforme improved by the antimutagenic chloroquine. Neurosurg Focus. 2003;14(2):e3.PubMedCrossRef Briceno E, Reyes S, Sotelo J. Therapy of glioblastoma multiforme improved by the antimutagenic chloroquine. Neurosurg Focus. 2003;14(2):e3.PubMedCrossRef
98.
go back to reference Sotelo J, Briceno E, Lopez-Gonzalez MA. Adding chloroquine to conventional treatment for glioblastoma multiforme: a randomized, double-blind, placebo-controlled trial. Ann Intern Med. 2006;144(5):337–43.PubMedCrossRef Sotelo J, Briceno E, Lopez-Gonzalez MA. Adding chloroquine to conventional treatment for glioblastoma multiforme: a randomized, double-blind, placebo-controlled trial. Ann Intern Med. 2006;144(5):337–43.PubMedCrossRef
101.
go back to reference Lee MS, Johansen L, Zhang Y, Wilson A, Keegan M, Avery W, et al. The novel combination of chlorpromazine and pentamidine exerts synergistic antiproliferative effects through dual mitotic action. Cancer Res. 2007;67(23):11359–67. doi: 10.1158/0008-5472.CAN-07-2235.PubMedCrossRef Lee MS, Johansen L, Zhang Y, Wilson A, Keegan M, Avery W, et al. The novel combination of chlorpromazine and pentamidine exerts synergistic antiproliferative effects through dual mitotic action. Cancer Res. 2007;67(23):11359–67. doi: 10.​1158/​0008-5472.​CAN-07-2235.PubMedCrossRef
107.
go back to reference Cairns RA, Harris IS, Mak TW. Regulation of cancer cell metabolism. NatRevCancer. 2011;11(2):85–95. doi:nrc2981 [pii];doi: 10.1038/nrc2981 [doi]. Cairns RA, Harris IS, Mak TW. Regulation of cancer cell metabolism. NatRevCancer. 2011;11(2):85–95. doi:nrc2981 [pii];doi: 10.​1038/​nrc2981 [doi].
108.
go back to reference Pedersen PL. Warburg, me and hexokinase 2: multiple discoveries of key molecular events underlying one of cancers' most common phenotypes, the "Warburg effect", i.E., elevated glycolysis in the presence of oxygen. J Bioenerg Biomembr. 2007;39(3):211–22. doi: 10.1007/s10863-007-9094-x.PubMedCrossRef Pedersen PL. Warburg, me and hexokinase 2: multiple discoveries of key molecular events underlying one of cancers' most common phenotypes, the "Warburg effect", i.E., elevated glycolysis in the presence of oxygen. J Bioenerg Biomembr. 2007;39(3):211–22. doi: 10.​1007/​s10863-007-9094-x.PubMedCrossRef
109.
go back to reference Floridi A, Paggi MG, Fanciulli M. Modulation of glycolysis in neuroepithelial tumors. J Neurosurg Sci. 1989;33(1):55–64.PubMed Floridi A, Paggi MG, Fanciulli M. Modulation of glycolysis in neuroepithelial tumors. J Neurosurg Sci. 1989;33(1):55–64.PubMed
110.
go back to reference Paggi MG, Fanciulli M, Del Carlo C, Citro G, Carapella CM, Floridi A. The membrane-bound hexokinase as a potential marker for malignancy in human gliomas. J Neurosurg Sci. 1990;34:209–13.PubMed Paggi MG, Fanciulli M, Del Carlo C, Citro G, Carapella CM, Floridi A. The membrane-bound hexokinase as a potential marker for malignancy in human gliomas. J Neurosurg Sci. 1990;34:209–13.PubMed
114.
115.
go back to reference YL H, DeLay M, Jahangiri A, Molinaro AM, Rose SD, Carbonell WS, et al. Hypoxia-induced autophagy promotes tumor cell survival and adaptation to antiangiogenic treatment in glioblastoma. Cancer Res. 2012;72(7):1773–83. doi: 10.1158/0008-5472.CAN-11-3831.CrossRef YL H, DeLay M, Jahangiri A, Molinaro AM, Rose SD, Carbonell WS, et al. Hypoxia-induced autophagy promotes tumor cell survival and adaptation to antiangiogenic treatment in glioblastoma. Cancer Res. 2012;72(7):1773–83. doi: 10.​1158/​0008-5472.​CAN-11-3831.CrossRef
116.
go back to reference Talarico C, Dattilo V, D'Antona L, Menniti M, Bianco C, Ortuso F, et al. SGK1, the new player in the game of resistance: chemo-radio molecular target and strategy for inhibition. Cell Physiol Biochem. 2016;39(5):1863–76. doi: 10.1159/000447885.PubMedCrossRef Talarico C, Dattilo V, D'Antona L, Menniti M, Bianco C, Ortuso F, et al. SGK1, the new player in the game of resistance: chemo-radio molecular target and strategy for inhibition. Cell Physiol Biochem. 2016;39(5):1863–76. doi: 10.​1159/​000447885.PubMedCrossRef
117.
go back to reference D'Antona L, Amato R, Talarico C, Ortuso F, Menniti M, Dattilo V, et al. SI113, a specific inhibitor of the Sgk1 kinase activity that counteracts cancer cell proliferation. Cell Physiol Biochem. 2015;35(5):2006–18. doi: 10.1159/000374008.PubMedCrossRef D'Antona L, Amato R, Talarico C, Ortuso F, Menniti M, Dattilo V, et al. SI113, a specific inhibitor of the Sgk1 kinase activity that counteracts cancer cell proliferation. Cell Physiol Biochem. 2015;35(5):2006–18. doi: 10.​1159/​000374008.PubMedCrossRef
Metadata
Title
Drug repurposing for the treatment of glioblastoma multiforme
Authors
Claudia Abbruzzese
Silvia Matteoni
Michele Signore
Luca Cardone
Kavindra Nath
Jerry D. Glickson
Marco G. Paggi
Publication date
01-12-2017
Publisher
BioMed Central
Published in
Journal of Experimental & Clinical Cancer Research / Issue 1/2017
Electronic ISSN: 1756-9966
DOI
https://doi.org/10.1186/s13046-017-0642-x

Other articles of this Issue 1/2017

Journal of Experimental & Clinical Cancer Research 1/2017 Go to the issue
Webinar | 19-02-2024 | 17:30 (CET)

Keynote webinar | Spotlight on antibody–drug conjugates in cancer

Antibody–drug conjugates (ADCs) are novel agents that have shown promise across multiple tumor types. Explore the current landscape of ADCs in breast and lung cancer with our experts, and gain insights into the mechanism of action, key clinical trials data, existing challenges, and future directions.

Dr. Véronique Diéras
Prof. Fabrice Barlesi
Developed by: Springer Medicine