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Challenging issues in molecular-targeted therapy.

Ezziane Z - Ther Clin Risk Manag (2009)

Bottom Line: There are variety of anticancer treatments including chemotherapeutic drugs, which are known to induce cell growth arrest and apoptosis through DNA damage and cytoskeleton toxicity.Meanwhile, histone deacetylase (HDAC) inhibitors could apply their antitumor activity through chromatin remodeling and gene expression modulation that affect the cell cycle and survival pathways.This paper proposes an anticancer three-drug compound and discusses several challenging issues in relation to designing multidrug compounds that could possibly lead to molecular-targeted therapies.

View Article: PubMed Central - PubMed

Affiliation: Applied Science and Technology, Higher Colleges of Technology, Al Ain, United Arab Emirates.

ABSTRACT
There are variety of anticancer treatments including chemotherapeutic drugs, which are known to induce cell growth arrest and apoptosis through DNA damage and cytoskeleton toxicity. Meanwhile, histone deacetylase (HDAC) inhibitors could apply their antitumor activity through chromatin remodeling and gene expression modulation that affect the cell cycle and survival pathways. This paper proposes an anticancer three-drug compound and discusses several challenging issues in relation to designing multidrug compounds that could possibly lead to molecular-targeted therapies.

No MeSH data available.


Related in: MedlinePlus

Representation of concomitant molecular changes after combination treatment with a potential compound: Combination therapies with agents that target endothelial cells to block angiogenesis, EGFR/ERBB2, and histone deacetylase inhibitors to prevent tumor adaptation in cancer treatment warrants experimental studies.Abbreviations: EGFR, epidermal growth factor receptor; ErbB2, epidermal receptor growth factor 2; VEGF, vascular endothelial growth factor.
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f1-tcrm-5-0239: Representation of concomitant molecular changes after combination treatment with a potential compound: Combination therapies with agents that target endothelial cells to block angiogenesis, EGFR/ERBB2, and histone deacetylase inhibitors to prevent tumor adaptation in cancer treatment warrants experimental studies.Abbreviations: EGFR, epidermal growth factor receptor; ErbB2, epidermal receptor growth factor 2; VEGF, vascular endothelial growth factor.

Mentions: The tangle of signaling pathways leading from the receptors to the cellular processes that actually cause a cell to divide or to resist suicide despite DNA damage is highly complex. As depicted in Figure 1, a potential drug compound may suppress the growth of cancer cells by inducing either G1 or G2 arrest, DNA synthesis, apoptosis, and should have antitumor activity against various types of cancer. Synergistic inhibition of cell proliferation and induction of apoptosis is an important factor towards effective combination therapy.


Challenging issues in molecular-targeted therapy.

Ezziane Z - Ther Clin Risk Manag (2009)

Representation of concomitant molecular changes after combination treatment with a potential compound: Combination therapies with agents that target endothelial cells to block angiogenesis, EGFR/ERBB2, and histone deacetylase inhibitors to prevent tumor adaptation in cancer treatment warrants experimental studies.Abbreviations: EGFR, epidermal growth factor receptor; ErbB2, epidermal receptor growth factor 2; VEGF, vascular endothelial growth factor.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2697511&req=5

f1-tcrm-5-0239: Representation of concomitant molecular changes after combination treatment with a potential compound: Combination therapies with agents that target endothelial cells to block angiogenesis, EGFR/ERBB2, and histone deacetylase inhibitors to prevent tumor adaptation in cancer treatment warrants experimental studies.Abbreviations: EGFR, epidermal growth factor receptor; ErbB2, epidermal receptor growth factor 2; VEGF, vascular endothelial growth factor.
Mentions: The tangle of signaling pathways leading from the receptors to the cellular processes that actually cause a cell to divide or to resist suicide despite DNA damage is highly complex. As depicted in Figure 1, a potential drug compound may suppress the growth of cancer cells by inducing either G1 or G2 arrest, DNA synthesis, apoptosis, and should have antitumor activity against various types of cancer. Synergistic inhibition of cell proliferation and induction of apoptosis is an important factor towards effective combination therapy.

Bottom Line: There are variety of anticancer treatments including chemotherapeutic drugs, which are known to induce cell growth arrest and apoptosis through DNA damage and cytoskeleton toxicity.Meanwhile, histone deacetylase (HDAC) inhibitors could apply their antitumor activity through chromatin remodeling and gene expression modulation that affect the cell cycle and survival pathways.This paper proposes an anticancer three-drug compound and discusses several challenging issues in relation to designing multidrug compounds that could possibly lead to molecular-targeted therapies.

View Article: PubMed Central - PubMed

Affiliation: Applied Science and Technology, Higher Colleges of Technology, Al Ain, United Arab Emirates.

ABSTRACT
There are variety of anticancer treatments including chemotherapeutic drugs, which are known to induce cell growth arrest and apoptosis through DNA damage and cytoskeleton toxicity. Meanwhile, histone deacetylase (HDAC) inhibitors could apply their antitumor activity through chromatin remodeling and gene expression modulation that affect the cell cycle and survival pathways. This paper proposes an anticancer three-drug compound and discusses several challenging issues in relation to designing multidrug compounds that could possibly lead to molecular-targeted therapies.

No MeSH data available.


Related in: MedlinePlus