American Association for Cancer Research

November 2007 MCT Highlights

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Selected Articles from the November, 2007 Issue

The articles referenced in this Highlights section will be available online in HTML and PDF formats to all interested users at no charge until the next issue of Molecular Cancer Therapeutics is published. Click on the article title to view the complete article.

View the Table of Contents for the November 2007 issue of Molecular Cancer Therapeutics


Exemestane Conserves Bone Loss

Ariazi et al.

Page 2817

Selection of a non-steroidal aromatase inhibitor (AI) versus the steroidal AI exemestane for long-term use in adjuvant therapy and chemoprevention of breast cancer may be decided by which promotes the least detrimental side effects such as bone mineral density loss. Ariazi and colleagues demonstrated that exemestane’s primary metabolite 17-hydroexemestane bound the androgen receptor (AR) with high affinity, and regulated AR-dependent proliferation, transcription, and AR protein accumulation in T47D breast cancer cells. Molecular modeling indicated that 17-hydroexemestane interacted with AR’s Asn705, a conserved recognition motif. Since androgens exert beneficial effects on bone, these results may have important implications for long-term use of AIs. 
 

EGFR Tracked in Early Breast Cancer Development

Choong et al.

Page 2828

Understanding the molecular etiology of cancer has a direct impact on target-directed therapeutics. Using phosphoproteomics on the MCF10AT model comprising isogenic xenograft-derived cell lines, Choong and colleagues observed a marked reduction of EGFR expression during breast cancer progression. Further analysis of matched normal and cancer breast samples revealed that diminished EGFR expression as a result of gene deletion could be detected in pre-neoplastic lesions. Although many studies of EGFR expression have been conducted, this study tracked its expression developmentally from normal through disease states using in vitro, animal and clinical models. The findings are likely to influence the design of clinical trials targeting EGFR family members in breast cancer. 


Cyclophosphamide Collaboration Reduces Collateral Damage

Ma and Waxman

Page 2879

The effectiveness of cancer chemotherapeutic drugs is often limited by the collateral damage caused when the drugs are administered at their maximum tolerated doses. Ma and Waxman investigated the mechanisms whereby intratumoral expression of a cyclophosphamide (CPA)-activating hepatic cytochrome P450 gene enhances therapeutic activity when CPA is given on an every 6-day (metronomic) schedule. The authors concluded that metronomic CPA regresses P450-expressing tumors by two independent but complementary mechanisms: increased tumor cell killing via intratumoral P450-catalyzed prodrug activation, coupled with strong anti-angiogenic activity, which is primarily associated with hepatic prodrug activation.


With the advent of hypoxia targeted therapies in combination with hepatic artery ligation, the need for noninvasive hypoxia monitoring and therapeutic efficacy will become necessary. Brader and colleagues developed an orthotopic liver tumor model with a hypoxia-sensitive reporter system to monitor tumor hypoxia by noninvasive imaging. Their results demonstrated that the orthotopic reporter-transduced RH7777 Morris hepatomas are natively hypoxic and poorly perfused in this animal model, and that the magnitude of moderately severe hypoxia can be monitored using a HRE-responsive reporter system for both bioluminescence and PET imaging. 


Activation Loop of AKT/PKB Targeted

Toral-Barza et al.

Page 3028

Extensive conservation of the ATP-binding sites of AGC kinases presents an impediment to the development of selective inhibitors. Lactoquinomycin and related pyranonaphthoquinones were found as a new class of potent and selective inhibitors of AKT/PKB. Through biochemical studies and enzyme mutagenesis, Toral-Barza and colleagues showed that these inhibitors targeted AKT via a novel allosteric mechanism that involves Cys-296 and Cys-310 residues of the T-loop. Lactoquinomycin inhibited cellular AKT substrate phosphorylation induced by growth factors, loss of PTEN, and myristoylated AKT. Co-expression of the AKT mutant C296A/C310A attenuated inhibitor-induced substrate dephosphorylation. These findings identified T-loop targeting as a new strategy to target AKT.