Targeting tumor stroma and exploiting mature tumor vasculature to improve anti-cancer drug delivery

Bouzin, Caroline; Feron, Olivier

doi:10.1016/j.drup.2007.03.001

Cited by 89 publications

(66 citation statements)

References 62 publications

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“…Strategies targeting the tumor stroma (Bouzin and Feron, 2007;Hofmeister et al, 2008) also should be beneficial to prostate cancer patients, as exemplified by the better treatment efficacy of combining therapy with ADT and anti-angiogenic agents targeting the stromalderived vascular factors (Johansson et al, 2007) in the rat Dunning prostate cancer model. Similarly, combining ADT with Trk tyrosine kinase inhibitors targeting the receptor for stroma-derived AR-independent nerve growth factor was reported to prolong tumor regression in the rat prostate cancer model (George et al, 1999).…”

Section: The Impact Of Ar Dual Functions On Current Clinical Adtmentioning

confidence: 99%

Differential androgen receptor signals in different cells explain why androgen-deprivation therapy of prostate cancer fails

et al. 2010

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Prostate cancer is one of the major causes of cancerrelated death in the western world. Androgen-deprivation therapy (ADT) for the suppression of androgens binding to the androgen receptor (AR) has been the norm of prostate cancer treatment. Despite early success to suppress prostate tumor growth, ADT eventually fails leading to recurrent tumor growth in a hormonerefractory manner, even though AR remains to function in hormone-refractory prostate cancer. Interestingly, some prostate cancer survivors who received androgen replacement therapy had improved quality of life without adverse effect on their cancer progression. These contrasting clinical data suggest that differential androgen/ AR signals in individual cells of prostate tumors can exist in the same or different patients, and may be used to explain why ADT of prostate cancer fails. Such a hypothesis is supported by the results obtained from transgenic mice with selective knockout of AR in prostatic stromal vs epithelial cells and orthotopic transplants of various human prostate cancer cell lines with AR overexpression or knockout. These studies concluded that AR functions as a stimulator for prostate cancer proliferation and metastasis in stromal cells, as a survival factor of prostatic cancer epithelial luminal cells, and as a suppressor for prostate cancer basal intermediate cell growth and metastasis. These dual yet opposite functions of the stromal and epithelial AR may challenge the current ADT to battle prostate cancer and should be taken into consideration when developing new AR-targeting therapies in selective prostate cancer cells.

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Section: The Impact Of Ar Dual Functions On Current Clinical Adtmentioning

confidence: 99%

Differential androgen receptor signals in different cells explain why androgen-deprivation therapy of prostate cancer fails

et al. 2010

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“…However, nanoparticles of greater size (larger than 10 kDa) have been shown to be less affected by an increase in interstitial fluid pressure and are able to successfully overcome this barrier to accumulate within tumors (Heldin et al, 2004;Bouzin and Feron, 2007). This is a result of their size as well as the high magnitude of microvasculature pressure, which facilitates the extravasation of nanoparticles into tumors (Jain, 1987;Heldin et al, 2004;Bouzin and Feron, 2007).…”

Section: A Passive Targetingmentioning

confidence: 99%

Lipid-Based Drug Delivery Systems in Cancer Therapy: What Is Available and What Is Yet to Come

2016

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“…With the development of new technologies in combination of bioinformatics, more and more genes related to drug resistance are discovered or predicted (Potti et al, 2006;Raguz et al, 2008;Crijns et al, 2009;Etemadmoghadam et al, 2009). Drug resistance results from diverse factors, including individual variations in patients, genetic and epigenetic changes within tumors (Roberti et al, 2006;Tan et al, 2010) such as mutations, translocations, deletions and amplifications of coding genes or promoter regions, gene rearrangement (Fojo T, 2007), alteration of tumor microenvironment and tumor stromal cell components (Bouzin et al, 2007), self-protection of cancer stem cells (Rosen et al, 2009), epithelial-mesenchymal transition (Han et al, 2014), energy metabolism and hypoxia (Broxterman et al, 1991;Robey et al, 2009;Ruan et al, 2009). In addition, other reasons like classical drug efflux (Gottesman et al, 2006), acceleration of drug metabolism and decreasing sensitivity to induction of apoptosis (Janne et al, 2009;Coley, 2010) also result in drug resistance.…”

Section: Introductionmentioning

confidence: 99%

Long Non-coding RNAs and Drug Resistance

Pan

Xie²,

Xu³

et al. 2016

Asian Pacific Journal of Cancer Prevention

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Background: Long non-coding RNAs (lncRNAs) are emerging as key players in gene expression that govern cell developmental processes, and thus contributing to diseases, especially cancers. Many studies have suggested that aberrant expression of lncRNAs is responsible for drug resistance, a substantial obstacle for cancer therapy. Drug resistance not only results from individual variations in patients, but also from genetic and epigenetic differences in tumors. It is reported that drug resistance is tightly modulated by lncRNAs which change the stability and translation of mRNAs encoding factors involved in cell survival, proliferation, and drug metabolism. In this review, we summarize recent advances in research on lncRNAs associated with drug resistance and underlying molecular or cellular mechanisms, which may contribute helpful approaches for the development of new therapeutic strategies to overcome treatment failure.

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Targeting tumor stroma and exploiting mature tumor vasculature to improve anti-cancer drug delivery

Cited by 89 publications

References 62 publications

Differential androgen receptor signals in different cells explain why androgen-deprivation therapy of prostate cancer fails

Differential androgen receptor signals in different cells explain why androgen-deprivation therapy of prostate cancer fails

Lipid-Based Drug Delivery Systems in Cancer Therapy: What Is Available and What Is Yet to Come

Long Non-coding RNAs and Drug Resistance

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