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"December 17, 2009 (San Antonio) - A new targeted cancer drug has been shown to shrink tumors in women with metastatic breast cancer after an average of seven other drugs, including Herceptin, failed. The new drug, called T-DM1, combines Herceptin with a potent chemotherapy drug. It's a Trojan horse approach, where Herceptin homes in on cancer cells and delivers the cancer-killing agent directly to its target. Tumors shrank in one-third of women with metastatic breast cancer given T-DM1, says Ian Krop, MD, of the Dana-Farber Cancer Institute in Boston. In another 12%, tumors stopped growing for at least six months. The women remained cancer-free for an average of seven months -- results unheard of in patients this sick, he says. All the women, who had breast tumors for an average of three years, had cancer that had metastasized, or spread to other parts of the body. They had been treated with an average of seven different therapies, including Herceptin, Tykerb, and Xeloda, and each had failed."

Dichloroacetate (DCA) as a potential metabolic-targeting therapy for cancer.\nMichelakis ED, Webster L, Mackey JR.\nBr J Cancer. 2008 Oct 7;99(7):989-94. Epub 2008 Sep 2. Review.\nPMID: 18766181 \ndoi:10.1038/sj.bjc.6604554 \n

Specenier P, Vermorken JB. The role of taxanes and targeted therapies in locally advanced head and neck cancer. Curr Opin Oncol. 2007 May;19(3):195-201. PMID: 17414636 [PubMed - in process]

Dichloroacetate (DCA) as a potential metabolic-targeting therapy for cancer. Michelakis ED, Webster L, Mackey JR. Br J Cancer. 2008 Oct 7;99(7):989-94. Epub 2008 Sep 2. Review. PMID: 18766181 doi:10.1038/sj.bjc.6604554 The unique metabolism of most solid tumours (aerobic glycolysis, i.e., Warburg effect) is not only the basis of diagnosing cancer with metabolic imaging but might also be associated with the resistance to apoptosis that characterises cancer. The glycolytic phenotype in cancer appears to be the common denominator of diverse molecular abnormalities in cancer and may be associated with a (potentially reversible) suppression of mitochondrial function. The generic drug dichloroacetate is an orally available small molecule that, by inhibiting the pyruvate dehydrogenase kinase, increases the flux of pyruvate into the mitochondria, promoting glucose oxidation over glycolysis. This reverses the suppressed mitochondrial apoptosis in cancer and results in suppression of tumour growth in vitro and in vivo. Here, we review the scientific and clinical rationale supporting the rapid translation of this promising metabolic modulator in early-phase cancer clinical trials More than 40 nonrandomised trials of DCA in small cohorts of patients have been reported, but the first two randomised control trials of chronic oral therapy with DCA in congenital mitochondrial diseases were reported in 2006. In the first, a blinded placebo-controlled study was performed with oral DCA administered at 25 mg kg-1 day-1 in 30 patients with MELAS syndrome (mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes) (Kaufmann et al, 2006). Most patients enrolled in the DCA arm developed symptomatic peripheral neuropathy, compared with 4 out of 15 in the placebo arm, leading to the termination of the study. Seventeen out of 19 patients had at least partial resolution of peripheral neurological symptoms by 9 months after discontinuation of DCA. This neurotoxicity res

"Worcester, MA - Current research suggests that TNF-receptor associated protein-1 (TRAP-1) may prevent cancer cell death. The related report by Leav et al, "Cytoprotective Mitochondrial Chaperone TRAP-1 as a Novel Molecular Target in Localized and Metastatic Prostate Cancer," appears in the January 2010 issue of the American Journal of Pathology. Prostate cancer cells are often resistant to cell death. Researchers led by Dr. Dario C. Altieri of the University of Massachusetts Medical School, therefore, explored the role of TRAP-1, a protein thought to regulate cell death, in prostate cancer survival. TRAP-1 was highly expressed in both high-grade human prostate cancer lesions and mouse models of prostate cancer, but not in benign or normal prostate tissue. In addition, TRAP-1 overexpression in non-cancer prostate cells inhibited cell death, whereas TRAP-1-deficient prostate cancer cells had enhanced levels of cell death. Moreover, treatment with Gamitrinib, which inhibits TRAP-1, resulted in prostate cancer cell death, but not death of non-cancerous prostate cells. Therefore, targeting TRAP-1 via Gamitrinib treatment may be a viable therapeutic strategy for patients with advanced prostate cancer."

Multi-targeted therapy of cancer by omega-3 fatty acids. Berquin IM, Edwards IJ, Chen YQ. Cancer Lett. 2008 Oct 8;269(2):363-77. Epub 2008 May 13. Review. PMID: 18479809 doi:10.1016/j.canlet.2008.03.044

Arginine deprivation as a targeted therapy for cancer. Feun L, You M, Wu CJ, Kuo MT, Wangpaichitr M, Spector S, Savaraj N. Curr Pharm Des. 2008;14(11):1049-57. Review. PMID: 18473854

Simultaneously targeting epidermal growth factor receptor tyrosine kinase and cyclooxygenase-2, an efficient approach to inhibition of squamous cell carcinoma of the head and neck. Chen Z, Zhang X, Li M, Wang Z, Wieand HS, Grandis JR, Shin DM. Clin Cancer Res. 2004 Sep 1;10(17):5930-9. PMID: 15355926

Yeudall WA, Miyazaki H. Chemokines and squamous cancer of the head and neck: targets for therapeutic intervention? Expert Rev Anticancer Ther. 2007 Mar;7(3):351-60. PMID: 17338654 [PubMed - in process]

Awada A, Ismael G. The challenging integration of platinum compounds, taxanes, and molecular-targeted therapies in the multidisciplinary treatment of squamous cell carcinoma of the head and neck. Curr Opin Oncol. 2007 May;19(3):177-9. PMID: 17414633 [

CD40L - a multipotent molecule for tumor therapy. Loskog A, Tötterman TH. Endocr Metab Immune Disord Drug Targets. 2007 Mar;7(1):23-8. Review. PMID: 17346201

Neotropix™ Inc. develops and commercializes systemically deliverable oncolytic viruses for the treatment of solid tumors. Capitalizing on its unique sources of naturally occurring viruses that selectively target tumors, the Company has the knowledge and skills to translate these discoveries into commercial products. Neotropix is committed to making a difference in the lives of cancer patients.

Mitochondrially targeted effects of berberine [Natural Yellow 18, 5,6-dihydro-9,10-dimethoxybenzo(g)-1,3-benzodioxolo(5,6-a) quinolizinium] on K1735-M2 mouse melanoma cells: comparison with direct effects on isolated mitochondrial fractions. Pereira GC, Branco AF, Matos JA, Pereira SL, Parke D, Perkins EL, Serafim TL, Sardão VA, Santos MS, Moreno AJ, Holy J, Oliveira PJ. J Pharmacol Exp Ther. 2007 Nov;323(2):636-49. Epub 2007 Aug 17. PMID: 17704354 doi: 10.1124/jpet.107.128017 The present work shows that berberine is accumulated by mitochondria of a mouse melanoma cell line, leading to mitochondrial fragmentation and dysfunction, accompanied by decreased cellular energy charge. When the effect was compared with the results obtained on isolated mitochondrial fractions, it is observed that regardless of the system used, berberine is toxic for mitochondria. One major limitation of the present study (as in many others) is the lack of knowledge of the real concentration of berberine that reaches mitochondria in intact cells. Although we do not possess data regarding this aspect, it is wise to speculate that mitochondrial berberine concentrations will be much higher than in the bulk cytosol due to electrophoretic accumulation. We believe that the range of berberine concentrations accumulated by mitochondria in intact cells is within the range of concentrations used on isolated mitochondrial fractions in the present study. The present work not only provides insights on the mechanism by which berberine interferes with tumor cell proliferation, demonstrating previously unknown effects on mitochondrial physiology, but also raises a note of caution on the use of berberine as a nontoxic "natural" over-the-counter medication.

Berberine inhibits metastasis of nasopharyngeal carcinoma 5-8F cells by targeting Rho kinase-mediated Ezrin phosphorylation at threonine 567. Tang F, Wang D, Duan C, Huang D, Wu Y, Chen Y, Wang W, Xie C, Meng J, Wang L, Wu B, Liu S, Tian D, Zhu F, He Z, Deng F, Cao Y. J Biol Chem. 2009 Oct 2;284(40):27456-66. Epub 2009 Aug 3. PMID: 19651779

ScienceDaily (Dec. 25, 2007) - Researchers from the Universities of Warwick, Edinburgh, Dundee and the Czech Republic's Institute of Biophysics have discovered a new light-activated platinum-based compound that is up to 80 times more powerful than other platinum-based anti-cancer drugs and which can use "light activation" to kill cancer cells in much more targeted way than similar treatment

February 14, 2009 - (BRONX, NY) - Scientists at Albert Einstein College of Medicine of Yeshiva University have piggybacked antibodies onto radioactive payloads to deliver doses of radiation that selectively target and destroy microbial and HIV-infected cells. The experimental treatment - called radioimmunotherapy, or RIT - holds promise for treating various infectious diseases, including HIV and cancers caused by viruses. The research was presented today at the annual meeting of the American Association for the Advancement of Science (AAAS), the world's largest general scientific society and the publishers of the journal Science.

Singh RP, Agarwal R. Prostate cancer prevention by silibinin. Curr Cancer Drug Targets. 2004 Feb;4(1):1-11. Review. PMID: 14965263 [PubMed - indexed for MEDLINE]

"Cancer lies dormant in all of us," he wrote in his new book, "Anticancer: A New Way of Life" (Viking, $25.95). "But our bodies are also equipped with a number of mechanisms that detect and keep such (defective) cells in check." Cancer rears its ugly head when things get out of balance, Servan-Schreiber said in an interview. And that can happen if the bad guys that promote the growth of cancer cells (tobacco, excessive alcohol, excessive sugar, hydrogenated fats, environmental pollutants) outnumber the good guys that support our natural defenses (cancer-fighting phytochemicals found in fruits, vegetables, herbs and teas; physical activity; and stress management techniques). But conventional treatment, while indispensable, focuses on a single target: destroying cancer cells. Doctors rarely address the other side: teaching patients how to fortify themselves using nutrition, exercise and stress-management techniques to create an inhospitable environment for cancer.