Skip to main content

Targeting NF-κB in Anticancer Adjunctive Chemotherapy

  • Chapter
The Link Between Inflammation and Cancer

Part of the book series: Cancer Treatment and Research ((CTAR,volume 130))

Abstract

After more than three decades of its declaration, the war against cancer still appears far from being won. Although there have been decisive victories in a few battles, such as the one against testicular cancer, the overall result is sobering. Hopes for an imminent cure had been raised among the public by the promises of molecular biology, combinatorial chemistry and high-throughput screening. These promises have manifested themselves in the widely proclaimed strategy of rationally targeted anticancer drug discovery, which may be summarized as the ‘one-gene-one target-one drug’ approach. Over the years, however, it has gradually become clear that, in most cases, treatment of cancer with a single drug may at best delay progression of the disease but is unlikely to lead to a cure. Thus, it appears that rationally targeted monotherapy will have to be replaced by rationally targeted combination therapy. Inhibitors of NF-κB look likely to become an important weapon in the anticancer combination therapy arsenal.

This is a preview of subscription content, log in via an institution to check access.

Access this chapter

Chapter
USD 29.95
Price excludes VAT (USA)
  • Available as PDF
  • Read on any device
  • Instant download
  • Own it forever
eBook
USD 89.00
Price excludes VAT (USA)
  • Available as PDF
  • Read on any device
  • Instant download
  • Own it forever
Softcover Book
USD 119.99
Price excludes VAT (USA)
  • Compact, lightweight edition
  • Dispatched in 3 to 5 business days
  • Free shipping worldwide - see info
Hardcover Book
USD 169.99
Price excludes VAT (USA)
  • Durable hardcover edition
  • Dispatched in 3 to 5 business days
  • Free shipping worldwide - see info

Tax calculation will be finalised at checkout

Purchases are for personal use only

Institutional subscriptions

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

9. References

  • Adams, J. (2003). Potential for proteasome inhibition in the treatment of cancer. Drug. Discov. Today 8: 307–315.

    PubMed  CAS  Google Scholar 

  • Aggarwal, B.B. (2004). Nuclear factor-κB: the enemy within. Cancer Cell 6: 203–208.

    PubMed  CAS  Google Scholar 

  • Amit, S. and Ben-Neriah, Y. (2003). NF-κB activation in cancer: a challenge for ubiquitination-and proteasome-based therapeutic approaches. Semin. Cancer Biol. 13: 15–28.

    PubMed  CAS  Google Scholar 

  • Arts, J. et al. (2003). Histone deacetylase inhibitors: from chromatin remodeling to experimental cancer therapeutics. Curr. Med. Chem. 10: 2343–2350.

    PubMed  CAS  Google Scholar 

  • Azam, M. et al. (2003). Mechanisms of autoinhibition and STI-571/imatinib resistance revealed by mutagenesis of Bcr-Abl. Cell 112: 831–843.

    PubMed  CAS  Google Scholar 

  • Baum, M. (2002). A new strategy for cancer. Prospect February: 44–48.

    Google Scholar 

  • Beinke, S. and Ley, S.C. (2004). Functions of NF-κB and NF-κB2 in immune cell biology. Biochem. J. 382: 393–409.

    PubMed  CAS  Google Scholar 

  • Bhalla, U.S. (2004). Models of cell signaling pathways. Curr. Opin. Genet. Dev. 14: 375–381.

    PubMed  CAS  Google Scholar 

  • Bhojani, M.S. et al. (2003). TRAIL and anti-tumor responses. Cancer Biol. Ther. 2(4 Suppl. 1): S71–S78.

    PubMed  CAS  Google Scholar 

  • Bohuslav, J. et al. (2004). p53 induces NF-κB activation by an IκB kinase-independent mechanism involving phosphorylation of p65 by ribosomal S6 kinase 1. J. Biol. Chem. 279: 26115–26125.

    PubMed  CAS  Google Scholar 

  • Borisy, A.A. et al. (2003). Systematic discovery of multicomponent therapeutics. Proc. Natl Acad. Sci. USA 100: 7977–7982

    PubMed  CAS  Google Scholar 

  • Borst, P. et al. (1999). The multidrug resistance protein family. Biochem. Biophys. Acta 1461: 347–357.

    PubMed  CAS  Google Scholar 

  • Brahimi, F. et al. (2004). Multiple mechanisms of action of ZR2002 in human breast cancer cells: a novel combi-molecule designed to block signaling mediated by the Erb family of oncogenes and to damage genomic DNA. Int. J. Cancer 112: 484–491.

    PubMed  CAS  Google Scholar 

  • Burgess, M.R. et al. (2005). Comparative analysis of two clinically active Bcr-Abl kinase inhibitors reveals the role of conformation-specific binding in resistance. Proc. Natl Acad. Sci. USA 102: 3395–3400.

    PubMed  CAS  Google Scholar 

  • Butcher, E.C. et al. (2004). Systems biology in drug discovery. Nat. Biotechnol. 22:1253–1259.

    PubMed  CAS  Google Scholar 

  • Caffo, O. (2001). Radiosensitization with chemotherapeutic agents. Lung Cancer 34: S81–S90.

    PubMed  Google Scholar 

  • Campbell, K.J. et al. (2004). Active repression of antiapoptotic gene expression by RelA(p65) NF-κB. Mol. Cell 13: 853–865.

    PubMed  CAS  Google Scholar 

  • Cancer Facts and Figures 2004. American Cancer Society.

    Google Scholar 

  • Carr, K.M. et al. (2004). Genomic and proteomic approaches for studying human cancer: prospects for true patient-tailored therapy. Hum. Genomics 1: 134–140.

    PubMed  CAS  Google Scholar 

  • Castro, A.C. et al. (2003). Novel IKK inhibitors: β-carbolines. Bioorg. Med. Chem. Lett. 13: 2419–2422.

    PubMed  CAS  Google Scholar 

  • Cayrol, C. and Ducommun, B. (1998). Interaction with cyclin-dependent kinases and PCNA modulates proteasome-dependent degradation of p21. Oncogene 17: 2437–2444.

    PubMed  CAS  Google Scholar 

  • Chambon, P. and Beuzard, M. (2004). Cancer. Les varies raisons d’une epidemie. Science & Vie June: 46–69.

    Google Scholar 

  • Chauhan, D. et al. (2004). The bortezomib/proteasome inhibitor PS-341 and triterpenoid CDDO-Im induce synergistic anti-multiple myeloma (MM) activity and overcome bortezomibn resistance. Blood 103: 3158–3166.

    PubMed  CAS  Google Scholar 

  • Claudio, E. et al. (2002). BAFF-induced NEMO-independent processing of NF-κB2 in maturing B cells. Nat. Immunol. 3: 958–965.

    PubMed  CAS  Google Scholar 

  • Clemons, P.A. (2004). Complex phenotypic assays in high-throughput screening. Curr. Opin. Chem. Biol. 8: 334–338.

    PubMed  CAS  Google Scholar 

  • Constantinou, M. et al. (2003). Paclitaxel and concurrent radiation in upper gastrointestinal cancers. Cancer Invest. 21: 887–896.

    PubMed  CAS  Google Scholar 

  • Cools, J. et al. (2005). Resistance to tyrosine kinase inhibitors: calling on extra forces. Drug Resist. Updat. in press.

    Google Scholar 

  • Dajee, M. et al. (2003). NF-κB blockade and oncogenic Ras trigger invasive human epidermal neoplasia. Nature 421: 639–643.

    PubMed  CAS  Google Scholar 

  • Davidov, E. et al. (2003). Advancing drug discovery through systems biology. Drug Discov. Today 8: 175–183.

    PubMed  CAS  Google Scholar 

  • Denlinger, C.E. et al. (2004). Modulation of antiapoptotic cell signaling pathways in non-small cell lung cancer: the role of NF-κB. Semin. Thorac. Cardiovasc. Surg. 16: 28–39.

    PubMed  Google Scholar 

  • Doggrell, S.A. (2005). BMS-354825: a novel drug with potential for the treatment of imatinib-resistant chronic myeloid leukaemia. Expert. Opin. Investig. Drugs 14: 89–91.

    PubMed  Google Scholar 

  • Donato, N.J. et al. (2003). Bcr-Abl independence and Lyn kinase overexpression in chronic myelogenous leukemia cells selected for resistance to STI571. Blood 101: 690–698.

    PubMed  CAS  Google Scholar 

  • Dvorak, H.F. (1986). Tumors: wounds that do not heal. Similarities between tumor stroma generation and wound healing. N. Engl. J. Med. 315: 1650–1659.

    PubMed  CAS  Google Scholar 

  • Eaton, D.L. (2002). ‘Americas epidemic of chemicals and cancer — myth or fact?’ in Chiras, D. Human Biology. Fourth Edition. Jones and Bartlett, Sudbury MA.

    Google Scholar 

  • Fisher, A.C. et al. (1995). Update: is there a cancer epidemic in the United States? American Council of Science and Health.

    Google Scholar 

  • French, L.E. and Tschopp, J. (2003). Protein-based therapeutic approaches targeting death receptors. Cell Death Differ. 10: 117–123.

    PubMed  CAS  Google Scholar 

  • Fujioka, S. et al. (2004a). Stabilization of p53 is a novel mechanism for proapoptotic function of NF-KB. J. Biol. Chem. 279: 27549–27559.

    PubMed  CAS  Google Scholar 

  • Fujioka, S. et al. (2004b). NF-KB and AP-1 connection: mechanism of NF-κB-dependent regulation of AP-1 activity. Mol. Cell. Biol. 24: 7806–7819.

    PubMed  CAS  Google Scholar 

  • Garber, K. (2002). Synthetic lethality: killing cancer with cancer. J. Natl Cancer Inst. 94: 1666–1668.

    PubMed  Google Scholar 

  • Garber, K. (2004). Running interference: pace picks up on synthetic lethality research. J. Natl Cancer Inst. 96: 982–983.

    PubMed  Google Scholar 

  • Gatto, S. et al. (2003). The proteasome inhibitor PS-341 inhibits growth and induces apoptosis in Bcr/Abl-positive cell lines sensitive and resistant to imatinib mesylate. Haematologica 88: 853–863.

    PubMed  CAS  Google Scholar 

  • Gumireddy, K. et al. (2005). A non-ATP-competitive inhibitor of Bcr-Abl overrides imatinib resistance. Proc. Natl Acad. Sci. USA 102: 1992–1997.

    PubMed  CAS  Google Scholar 

  • Haefner, B. (2005). The transcription factor NF-κB as drug target. Progress in Medicinal Chemistry 43: 137–188.

    PubMed  CAS  Google Scholar 

  • Hagemann, C. and Blank J.L. (2001). The ups and downs of MEK kinase interactions. Cell. Signal. 13, 863–875.

    PubMed  CAS  Google Scholar 

  • Han, Y. et al. (1999). Tumor necrosis factor-α-inducible IκBα proteolysis mediated by cytosolic m-calpain. A mechanism parallel to the ubiquitin-proteasome pathway of nuclear factor-κB activation. J. Biol. Chem. 274: 787–794.

    PubMed  CAS  Google Scholar 

  • Hanahan, D. and Weinberg, R.A. (2000). The hallmarks of cancer. Cell 100: 57–70.

    PubMed  CAS  Google Scholar 

  • Hideshima et al. (2002). NF-κB as a therapeutic target in multiple myeloma. J. Biol. Chem. 277: 16639–16647.

    PubMed  CAS  Google Scholar 

  • Higashitsuji, H. et al. (2002). A novel protein overexpressed in hepatoma accelerates export of NF-κB from the nucleus and inhibits p53-dependent apoptosis. Cancer Cell 2: 335–346.

    PubMed  CAS  Google Scholar 

  • Hu, Y. et al. (2004). Requirement of Src kinases Lyn, Hck and Fgr for Bcr-Abl 1-induced Blymphoblastic leukemia but not chronic myeloid leukemia. Nat. Genet. 36: 453–461.

    PubMed  CAS  Google Scholar 

  • Investigational Drugs database (www.iddb3.com).

    Google Scholar 

  • Kalled, S.L. et al. (2003). BAFF: B cell survival factor and emerging therapeutic target for autoimmune disorders. Expert Opin. Ther. Targets 7: 115–123.

    PubMed  CAS  Google Scholar 

  • Karin, M. et al. (2002). NF-κB in cancer: from innocent bystander to major culprit. Nat. Rev. Cancer 2: 301–310.

    PubMed  CAS  Google Scholar 

  • Kitano, H. (2004). Cancer as a robust system: implications for anticancer therapy. Nat. Rev. Cancer 4: 227–235.

    PubMed  CAS  Google Scholar 

  • Kucharczak, J. et al. (2003). To be, or not to be: NF-κB is the answer — role of Rel/NF-κB in the regulation of apoptosis. Oncogene 22: 8961–8982.

    PubMed  CAS  Google Scholar 

  • Kuo, M.T. et al. (2002). Induction of human MDR1 gene expression by 2-acetylaminofluorene is mediated by effectors of the phosphoinositide 3-kinase pathway that activate NF-κB signaling. Oncogene 21: 1945–1954.

    PubMed  CAS  Google Scholar 

  • Lashinger, L.M. et al. (2005). Bortezomib abolishes tumor necrosis factor-related apoptosis-inducing ligand resistance via a p21-dependent mechanism in human bladder and prostate cancer cells. Cancer Res. 65: 4902–4908.

    PubMed  CAS  Google Scholar 

  • Leaf, C. (2004). Why we’re losing the war on cancer (and how to win it) Fortune March 22: 77–92.

    Google Scholar 

  • Levesque, H. and Lafont, O. (2000). L’aspirine a travers les siecles: rappel historique. Rev. Med. Interne 21Suppl. 1: 8s–17s.

    PubMed  Google Scholar 

  • Li, Q. et al. (2005). Inflammation-associated cancer: NF-κB is the lynchpin. Trends Immunol. 26: 318–325.

    PubMed  Google Scholar 

  • Lombardo, L.J. et al. (2004). Discovery of N-(2-chloro-6-methyl-phenyl)-2-(6-(4-(2-hydroxyethyl)-piperazin-1-yl)-2-methylpyrimidin-4-ylamino)thiazole-5-carboxamide (BMS-354825), a dual Src/Abl kinase inhibitor with potent antitumor activity in preclinical assays. J. Med. Chem. 47: 6658–6661.

    PubMed  CAS  Google Scholar 

  • Loop, T. and Pahl, H.L. (2003). ‘Activators and target genes of Rel/ NF-κB transcription factors — from bench to bedside.’ in Nuclear factor κB. Regulation and role in disease. Rudi Beyaert (ed.). Kluwer Academic Publishers. Dordrecht. The Netherlands.

    Google Scholar 

  • Losi, L. et al. (2005). Evolution of intratumoral genetic heterogeneity during colorectal cancer progression. Carcinogenesis 26: 916–922.

    PubMed  CAS  Google Scholar 

  • Markmann, M. (2003). Are we winning or losing the war on cancer? Cleveland Clin. J. Med 70: 632–633.

    Google Scholar 

  • Mayo, M.W. et al. (2003). Ineffectiveness of histone deacetylase inhibitors to induce apoptosis involves the transcriptional activation of NF-κB through the Akt pathway. J. Biol Chem. 278: 18980–18989.

    PubMed  CAS  Google Scholar 

  • McCarty, M.F. (2004). Targeting multiple signaling pathways as a strategy for managing prostate cancer: multifocal signal modulation therapy. Integr. Cancer Ther. 3: 349–380.

    PubMed  CAS  Google Scholar 

  • Mercurio F. et al. (1997). IKK-1 and IKK-2: cytokine-activated IκB kinases essential for NF-κB activation. Science 278: 860–866.

    PubMed  CAS  Google Scholar 

  • Mitsiades, N. et al. (2003). The proteasome inhibitor PS-341 potentiates sensitivity of multiple myeloma cells to conventional chemotherapeutic agents: therapeutic applications. Blood 101: 2377–2380.

    PubMed  CAS  Google Scholar 

  • Munshi et al. (2004). Inhibition of constitutively activated nuclear factor-κB radiosensitizes human melanoma cells. Mol Cancer Ther. 3: 985–992.

    PubMed  CAS  Google Scholar 

  • Nakano, H. et al. (1998). Differential regulation of IκBkinase alpha and beta by two upstream kinases, NF-κB-inducing kinase and mitogen-activated protein kinase/ERK kinase kinase-1. Proc. Natl Acad. Sci USA 95: 3537–3542.

    PubMed  CAS  Google Scholar 

  • Nencioni, A. et al. (2005). Cooperative cytotoxicity of proteasome inhibitors and tumor necrosis factor-related apoptosis-inducing ligand in chemoresistant Bcl-2-overexpressing cells. Clin. Cancer Res. 11: 4259–4265.

    PubMed  CAS  Google Scholar 

  • Neshat, M.S. et al. (2001). Enhanced sensitivity of PTEN-deficient tumors to inhibition of FRAP/mTOR. Proc. Natl Acad. Sci USA 98: 10314–10319.

    PubMed  CAS  Google Scholar 

  • Nimmanapalli, R. and Bhalla, K. (2002). Mechanisms of resistance to imatinib mesylate in Bcr-Abl-positive leukemias. Curr. Opin. Oncol. 14: 616–620.

    PubMed  CAS  Google Scholar 

  • Nutton, V. (2004). Ancient Medicine. Routledge, London.

    Google Scholar 

  • O’Hare, T. et al. (2005). In vitro activity of Bcr-Abl inhibitors AMN107 and BMS-354825 against clinically relevant imatinib-resistant Abl kinase domain mutants. Cancer Res. 65: 4500–4505.

    PubMed  Google Scholar 

  • Orlowski, R.Z. and Baldwin Jr., A.S. (2002). NF-κB as a therapeutic target in cancer. Trends Mol. Med. 8: 385–389.

    PubMed  CAS  Google Scholar 

  • Palanki M.S. et al. (2003). The design and synthesis of novel orally active inhibitors of AP-1 and NF-κB mediated transcriptional activation. SAR of in vitro and in vivo studies. Bioorg. Med. Chem. Lett. 13: 4077–4080.

    PubMed  CAS  Google Scholar 

  • Perkins, N.D. (2004). NF-κB: tumor promoter or suppressor? Trends Cell Biol. 14: 64–69.

    PubMed  CAS  Google Scholar 

  • Porter, R. (1997). The greatest benefit to mankind. A medical history of humanity from antiquity to the present. Fontana Press, London.

    Google Scholar 

  • Pukac et al. (2005). HGS-ETR1, a fully human TRAIL-receptor 1 monoclonal antibody, induces cell death in multiple tumour types in vitro and in vivo. Br. J. Cancer 92: 1430–1441.

    PubMed  CAS  Google Scholar 

  • Rachid, Z. et al. (2005). Synthesis of half-mustard combi-molecules with fluorescence properties: correlation with EGFR status. Bioorg. Med. Chem. Lett. 15: 1135–1138.

    PubMed  CAS  Google Scholar 

  • Rayet, B. and Gelinas, C. (1999). Aberrant rel/nfkb genes and activity in human cancer. Oncogene 18: 6938–6947.

    PubMed  CAS  Google Scholar 

  • Regenstein, L.G. (2002). Are we facing an epidemic of cancer? in Chiras, D. Human Biology. Fourth Edition. Jones and Bartlett, Sudbury MA.

    Google Scholar 

  • Reuther, J.Y. et al. (1998). A requirement for NF-κB activation in Bcr-Abl-mediated transformation. Genes Dev. 12: 968–981.

    PubMed  CAS  Google Scholar 

  • Rocha, S. et al. (2003). p53 represses cyclin D1 transcription through downregulation of Bcl-3 and inducing increased association of the p52 NF-κB subunit with histone deacetylase 1. Mol. Cell Biol. 23: 4713–4727.

    PubMed  CAS  Google Scholar 

  • Rundall, B.K. et al. (2004). Combined histone deacetylase and NF-κB inhibition sensitizes non-small cell lung cancer to cell death. Surgery 136: 416–425.

    PubMed  Google Scholar 

  • Russo, S.M. et al. (2001). Enhancement of radiosensitivity by proteasome inhibition: implications for a role of NF-κB. Int. J. Radiat. Oncol. Biol. Phys. 50: 183–193.

    PubMed  CAS  Google Scholar 

  • Ryan, K.M. et al. (2000). Role of NF-κB in p53-mediated programmed cell death. Nature 404: 892–897.

    PubMed  CAS  Google Scholar 

  • Sayers, T.J. and Murphy, W.J. (2005). Combining proteasome inhibition with TNF-related apoptosis-inducing ligand (Apo2L/TRAIL) for cancer therapy. Cancer Immunol. Immunother. in press.

    Google Scholar 

  • Schmidt, C. et al. (2003). Mechanisms of proinflammatory cytokine-induced biphasic NF-κB activation. Mol. Cell 12: 1287–300.

    PubMed  CAS  Google Scholar 

  • Senftleben, U. et al. (2001). Activation by IKKα of a second, evolutionary conserved, NF-κB signaling pathway. Science 293: 1495–1499.

    PubMed  CAS  Google Scholar 

  • Shah, N.P. et al. (2004). Overriding imatinib resistance with a novel Abl kinase inhibitor. Science 305: 399–401.

    PubMed  CAS  Google Scholar 

  • Shi, Y. et al. (2002). Enhanced sensitivity of multiple myeloma cells containing PTEN mutations to CCI-779. Cancer Res. 62: 5027–5034.

    PubMed  CAS  Google Scholar 

  • Shishodia, S. and Aggarwal, B.B. (2004). Nuclear factor-κB: a friend or foe in cancer? Biochem. Pharmacol. 68: 1071–1080.

    PubMed  CAS  Google Scholar 

  • Smith, C. et al. (2001). NF-κB inducing kinase is dispensable for activation of NF-κB in inflammatory settings but essential for lymphotoxin β receptor activation of NF-κB in primary human fibroblasts. J. Immunol. 167: 5895–5903.

    PubMed  CAS  Google Scholar 

  • Sorlie, T. (2004). Molecular portraits of breast cancer: tumour subtypes as distinct disease entities. Eur. J. Cancer 40: 2667–2675.

    PubMed  CAS  Google Scholar 

  • Stewart, B.W. and Kleihues, P. (2003). World Cancer Report. ARC Press, Lyon, France.

    Google Scholar 

  • Strausberg, R.L. and Schreiber, S.L. (2003). From knowing to controlling: a path from genomics to drugs using small molecule probes. Science 300: 294–295.

    PubMed  CAS  Google Scholar 

  • The History of Cancer. American Cancer Society (www.cancer.org/docroot/cri/content/cri_2_6x_the_history_of_cancer_72.asp?sitearea=cri).

    Google Scholar 

  • Thevenod, F. et al. (2000). Up-regulation of multidrug resistance P-glycoprotein via nuclear factor-κB activation protects kidney proximal tubule cells from cadmium-and reactive oxygen species-induced apoptosis. J. Biol. Chem. 275: 1887–1896.

    PubMed  CAS  Google Scholar 

  • Tergaonkar, V. et al. (2002). p53 stabilization is decreased upon NF-κB activation: a role for NF-κB in acquisition of resistance to chemotherapy. Cancer Cell 1: 493–503.

    PubMed  CAS  Google Scholar 

  • Tergaonkar, V. et al. (2003). IκB kinase-independent IκBα degradation pathway: functional NF-κB activity and implications for cancer therapy. Mol. Cell Biol. 23: 8070–8083.

    PubMed  CAS  Google Scholar 

  • Uetz, P. and Finley Jr., R.L. (2005). From protein networks to biological systems. FEBS Lett. 579: 1821–1827.

    PubMed  CAS  Google Scholar 

  • Velcade, new science and new hope: a case study. National Institutes of Health Office of Technology Transfer. September 2003.

    Google Scholar 

  • Vermeulen, L. et al. (2003). Transcriptional activation of the NF-κB p65 subunit by mitogen-and stress-activated protein kinase-1 (MSK1). EMBO J. 22: 1313–1324.

    PubMed  CAS  Google Scholar 

  • von Hoff, D.D. (2002). Patterns. Patterns. Patterns. The future of cancer research. Oncology Issues. November/December: 38–40.

    Google Scholar 

  • Voorhees, P.M. et al. (2003). The proteasome as a target for cancer therapy. Clin. Cancer Res. 9: 6316–6325.

    PubMed  CAS  Google Scholar 

  • Wang, Y. et al. (2004). Synthetic lethal targeting of Myc by activation of the DR5 death receptor pathway. Cancer Cell 5: 501–512.

    PubMed  CAS  Google Scholar 

  • Watters, J.W. and McLeod, H.L. (2003). Cancer pharmacogenomics: current and future applications. Biochim. Biophys. Acta 1603: 99–111.

    PubMed  CAS  Google Scholar 

  • Waxman, S. and Anderson, K.C. (2001). History of the development of arsenic derivatives in cancer therapy. Oncologist 6Suppl. 2: 3–10.

    PubMed  CAS  Google Scholar 

  • Wolmark, N. and Fisher, B. (1985). Adjuvant therapy in primary breast cancer. Surg. Clin. North Am. 65: 161–180.

    PubMed  CAS  Google Scholar 

  • Yin, M.J. et al. (1998). The anti-inflammatory agents aspirin and salicylate inhibit the activity of IκB kinase-beta. Nature 396: 77–80.

    PubMed  CAS  Google Scholar 

  • Yu, C. et al. (2003). The proteasome inhibitor bortezomib interacts synergistically with histone deacetylase inhibitors to induce apoptosis in Bcr/Abl+ cells sensitive and resistant to STI571. Blood 102: 3765–3774.

    PubMed  CAS  Google Scholar 

Download references

Author information

Authors and Affiliations

Authors

Editor information

Editors and Affiliations

Additional information

Dedicated to the memory of Valerie Fincham. Everything in the laboratory she touched turned into gold.

Rights and permissions

Reprints and permissions

Copyright information

© 2006 Springer Science+Business Media, Inc.

About this chapter

Cite this chapter

Haefner, B. (2006). Targeting NF-κB in Anticancer Adjunctive Chemotherapy. In: Dalgleish, A.G., Haefner, B. (eds) The Link Between Inflammation and Cancer. Cancer Treatment and Research, vol 130. Springer, Boston, MA. https://doi.org/10.1007/0-387-26283-0_10

Download citation

  • DOI: https://doi.org/10.1007/0-387-26283-0_10

  • Publisher Name: Springer, Boston, MA

  • Print ISBN: 978-0-387-26282-6

  • Online ISBN: 978-0-387-26283-3

  • eBook Packages: MedicineMedicine (R0)

Publish with us

Policies and ethics