American Association for Cancer Research

June 15 Clinical Cancer Research Highlights

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Selected Articles from the June 15, 2006 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 Clinical Cancer Research is published. Click on the article title to view the complete article.

View the Table of Contents for the June 15 issue of Clinical Cancer Research.


Fas Acts Out of Character in Thyroid Cancer Cells

Mitsiades et al.
Page 3705

The death receptor Fas is present in thyroid carcinomas, yet fails to trigger apoptosis. Mitsiades et al. found that crosslinking of Fas in thyroid carcinoma cells in vitro induced recruitment of the apoptosis-inhibitor FLIP instead of procaspase-8. Fas cross-linking promoted BrdU incorporation and activated the MEK/ERK, NF-κB, and AP-1 pathways. They concluded that, in thyroid carcinomas, the proteolytic cleavage and activation of caspase-8 depends on the balance between expression levels for procaspase-8 and FLIP. Fas may actually stimulate proliferation and confer a survival advantage to thyroid cancer cells.

 


Novel Reagent Targets, Disrupts Drug-Resistant Microtubules Networks

Gururaja et al.
Page 3831

Loss of clinical efficacy of many useful microtubule targeting drugs because of resistance and undesired side effects necessitates development of new tubulin-binding chemical entities that are devoid of such activities. Gururaja et al. used a proprietary high-content cell-based screen of a compound library to identify R-253 [N-cyclopropyl-2-(6-(3,5-dimethylphenyl)thieno[3,2-d]pyrimidin-4-yl)hydrazine carbothioamide], a potent anti-proliferative agent (average EC50 = 20 mol/L). R-253 emerged from the library as effective when assessed for growth, cytotoxicity, apoptosis, and cell cycle progression in a spectrum of tumor cell lines, including cells that were resistant to known microtubule inhibitors. Both biochemical and cellular mechanistic studies indicate that R-253 could become a promising new tubulin-binding drug candidate for treating various malignancies.


Progress in Chemoprevention Drug Development

Kelloff et al.
Page 3661

This article from the AACR Cancer Prevention Task Force reviews emerging concepts in chemopreventive drug development. Molecular biomarker expressions in carcinogenesis and genetic progression models of intraepithelial neoplasia are emphasized. Their roles in mechanism-based, molecular-targeted drug development, risk stratification, and cohort and endpoint selection for clinical trials are analyzed. Updates on ten clinical target organs include new data on molecular progression, significant trials, agents, and promising directions for future studies. Strategies for accelerating chemopreventive drug development are discussed, such as integrating new science into clinical development planning and regulatory policy, providing industry incentives, fostering multisector cooperation, and educating the public.


Gliomas Respond to Targeted Radiotherapy Plus Peptide Vectors

Kneifel et al.

Page 3843

CCR 06-15-06 Kneifel 3843The substance P receptor neurokinin type 1 is overexpressed in the vast majority of malignant glial brain tumors. Kneifel et al. developed a new 1806 Da targeting vector by conjugating the chelator DOTAGA to substance P, which specifically targets tumor cells. In a pilot study, feasibility, biodistribution, and early and long-term toxicity were assessed in 20 brain tumor patients following direct intratumoral administration. Disease was stabilized and neurologic status improved in 13 of 20 patients. Secondary resection disclosed widespread radiation necrosis with improved demarcation. Targeted radiotherapy using diffusible peptidic vectors represents an innovative strategy for local control of malignant gliomas.