American Association for Cancer Research

March 2008 Molecular Cancer Therapeutics Highlights

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Selected Articles from the March 1, 2008 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 March 2008 issue of Molecular Cancer Therapeutics


HER-2/neu Protein Expression May Impact Endogenous Immunity

Goodell et al.

Page 449

The relationship between protein overexpression and protein immunogenicity in human cancer has not been well-characterized. HER-2/neu protein expression is upregulated in breast cancer, and patients with HER-2/neu overexpressing tumors can have pre-existing immunity to HER-2/neu. Breast cancer patients with HER-2/neu overexpressing primary tumors were evaluated for antibody levels and T cell responses to HER-2/neu. Goodell and colleagues found that presence of HER-2/neu antibodies and T cells increased as level of HER-2/neu protein overexpression increased in primary tumors. The observed dose-dependent response suggests that a portion of the protein not normally available for immune recognition may become immunogenic when the protein is increasingly abundant in the cancer cell. 


Ellipticine Derivative Promising New Candidate for Treatment of Multiple Myeloma

Tian et al.

Page 500

In most cases, molecularly defined high-risk multiple myeloma receives no tangible benefits from all currently employed therapeutic strategies. Overexpression of the cell cycle regulator gene CKS1B is known to be associated with rapid failure of current therapies. Tian and colleagues correlated gene expression levels of CKS1B with the IC50 of over 40,000 anticancer compounds tested against the NCI-60 panel. This strategy identified the ellipticine derivative EPED3 (NSC 338258) as a potent new agent targeting mitochondrial function to rapidly deplete cellular energy resulting in massive and rapid killing of myeloma cells without harming non-tumor stromal cells. 


Mesothelioma Cells Killed by Targeted Drug Delivery

An et al.

Page 569

Current treatments for mesothelioma are generally ineffective; however, one promising area of anti-cancer drug development is tumor susceptibility to targeted therapy. To achieve efficient, targeted intracellular delivery of therapeutic agents to mesothelioma cells, An and colleagues selected a naïve human single chain (scFv) phage antibody display library directly on the surface of live mesothelioma cells to identify internalizing antibodies that target mesothelioma-associated cell surface antigens. The authors showed that scFv-targeted immunoliposomes were efficiently and specifically taken up by both epithelioid and sarcomatous mesothelioma cells, but not control cells, and immunoliposomes encapsulating the small molecule drug topotecan caused targeted killing of both types of mesothelioma cells in vitro


It is well established that mitogen activated protein kinase kinase (MKK) pathways promote the growth and metastasis of human tumors. However, little is known about the role of MKK signaling in soft tissue sarcomas. Lethal Toxin (LeTx) is a bacterial toxin that inactivates MKKs by proteolysis. Ding and colleagues found that LeTx substantially inhibited MKK activity and fibrosarcoma growth in mouse xenograft models. Ultrasound imaging revealed that LeTx caused a rapid and marked decrease in perfusion of tumor but not normal tissues. These results indicate LeTx may be a broadly effective strategy for targeting MKK signaling and neovascularization in sarcomas. 


ATFs Map Drug Resistance Phenotypes

Blancafort et al.

Page 688

Cancer cells develop drug resistance through dysregulation of one or more genes or cellular pathways. In order to isolate efficient regulators of drug resistance in tumor cells, Blancafort and colleagues have adopted a genome-wide scanning approach based on the screening of large libraries of artificial transcription factors (ATFs) made of three and six randomly assembled zinc finger (ZF) domains. ZF libraries were linked to a VP64 activation domain and delivered into a paclitaxel-sensitive tumor cell line. Several ATFs were isolated that promoted drug resistance. Furthermore, the authors demonstrated that a number of ATFs up-regulated targets of p53and genes participating in the p14ARF-MDM2-p53 tumor suppressor pathway. Thus, ATFs can be used to map genes and pathways involved in drug resistance phenotypes and have potential as novel therapeutic agents to inhibit drug resistance.


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