Encyclopedia of Cancer

Living Edition
| Editors: Manfred Schwab

Combinatorial Cancer Therapy

Living reference work entry
DOI: https://doi.org/10.1007/978-3-642-27841-9_7158-7

Synonyms

Definition

The evidence-based combination of therapeutic interventions to optimize the mechanistic spectrum and specificity of cancer therapy to achieve effective tumor clearance, prevent recurrence and minimize off-target cytotoxicity.

Characteristics

Introduction

A tumor in any part of the body can be characterized by six classical hallmarks.
  • Self-sufficiency in growth signals

  • Insensitivity to antigrowth signals

  • Limitless potential for cell division

  • Evasion of apoptosis or resistance to cell death

  • Sustained angiogenesis or the ability to form blood vessels

  • Tissue invasion and metastasis, or distant spread

These hallmark features collectively differentiate the tumor from its normal surrounding tissues. Hence, the initial interventional approaches were aimed at targeting these hallmarks in cancers or inhibiting the expression and activity of individual molecules that contribute to acquisition and maintenance of one or more of these six hallmarks in...

Keywords

Chemotherapy Drug Combine Modality Therapy Advanced Nasopharyngeal Carcinoma Multiple Tyrosine Kinase Complete Tumor Clearance 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.
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References

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  3. Bonadonna G et al (1995) Sequential or alternating doxorubicin and CMF regimens in breast cancer with more than three positive nodes. Ten-year results. JAMA 273:542–547CrossRefPubMedGoogle Scholar
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  5. Goudar RK et al (2005) Combination therapy of inhibitors of epidermal growth factor receptor/vascular endothelial growth factor receptor 2 (AEE788) and the mammalian target of rapamycin (RAD001) offers improved glioblastoma tumor growth inhibition. Mol Cancer Ther 4:101–112PubMedGoogle Scholar
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  7. Paternot S, Roger PP (2009) Combined inhibition of MEK and mammalian target of rapamycin abolishes phosphorylation of cyclin-dependent kinase 4 in glioblastoma cell lines and prevents their proliferation. Cancer Res 69:4577–4581CrossRefPubMedGoogle Scholar

See Also

  1. (2012) Cell Death. In: Schwab M (ed) Encyclopedia of Cancer, 3rd edn. Springer Berlin Heidelberg, p 737. doi: 10.1007/978-3-642-16483-5_6724Google Scholar

Copyright information

© Springer-Verlag Berlin Heidelberg 2014

Authors and Affiliations

  1. 1.City of Hope National Medical CenterDuarteUSA