Tumour-host interactions: Implications for developing anti-cancer therapies Journal Article


Authors: Gadea, B. B.; Joyce, J. A.
Article Title: Tumour-host interactions: Implications for developing anti-cancer therapies
Abstract: Cancers are a complex set of proliferative diseases that arise in most cases through multi-step pathways involving an accumulation of genetic and epigenetic changes. These steps include inactivation of tumour suppressor genes and activation of oncogenes. However, in addition to genetic mutations in the tumour cells themselves, the local host environment can act as a critical modulator of cancer progression, having either tumour-suppressive or tumour-promoting effects depending on the stage and site of cancer development. Because stromal cells can have these opposing functions during cancer development and progression, a recurring theme throughout this review will be that of balance: maintaining the normal functions of these co-opted cells, yet selectively inhibiting their pro-tumourigenic functions. To achieve this equilibrium, we need to understand the molecular mechanisms by which normal cells become modified by cancer cells before we can hope to target these functions selectively. Here, we will discuss recent efforts to address these key challenges and offer perspectives on the translation of discoveries made in model systems to the clinic. © 2006 Cambridge University Press.
Keywords: vasculotropin; gene mutation; lenalidomide; thalidomide; clinical trial; review; sorafenib; bevacizumab; erlotinib; sunitinib; cancer growth; cancer risk; monotherapy; nonhuman; solid tumor; unspecified side effect; drug targeting; alpha interferon; cancer staging; antineoplastic agent; neoplasms; colorectal cancer; tumor associated leukocyte; animals; bone marrow cells; imatinib; unindexed drug; inflammation; inflammation mediators; combination chemotherapy; antineoplastic activity; neovascularization, pathologic; cancer therapy; kidney carcinoma; carcinogenesis; molecular mechanics; cancer inhibition; tumor suppressor gene; gene activation; epigenetics; celecoxib; etanercept; tumor cell; 2,4 dimethyl 5 (2 oxo 1h indol 3 ylmethylene) 3 pyrrolepropionic acid; combretastatin a4; vandetanib; vatalanib; fibroblast; fibroblasts; innate immunity; gene inactivation; tumor promotion; taxane derivative; trabectedin; axitinib; tumor vascularization; enzastaurin; zoledronic acid; downstream processing; 2 methoxyestradiol; epothilone derivative; thrombocyte function; atrasentan; mast cell; pi 88; immunity, natural; macrophage function; ae 941; incb 3284; mk 0812; sibrotuzumab
Journal Title: Expert Reviews in Molecular Medicine
Volume: 8
Issue: 30
ISSN: 1462-3994
Publisher: Cambridge University Press  
Date Published: 2006-12-01
Start Page: 1
End Page: 32
Language: English
DOI: 10.1017/s1462399406000172
PUBMED: 17156575
PROVIDER: scopus
DOI/URL:
Notes: --- - "Cited By (since 1996): 7" - "Export Date: 4 June 2012" - "CODEN: ERMMF" - "Source: Scopus"
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  1. Bedrick B Gadea
    4 Gadea
  2. Johanna A Joyce
    67 Joyce