American Cancer Research Center and Foundation

RDA Is Not Enough
A superior multivitamin and mineral formulation should contain more than the RDA. For example, amounts higher than the RDA for the B-complex vitamins - in the presence of coenzyme Q10 and carnitine - are necessary to provide enough energy for people living in a fast-paced and stressful society.

From The Detox Revolution - pg. 81

Recent Research Developments

ACRCF is currently supporting research in the laboratory of Dr. Andres Klein-Szanto at the Fox Chase Cancer Center in Philadelphia, PA.

SUMMARY OF ACTIVITIES:
Tumor progression is a chain of cellular and molecular events that occur gradually during the development of neoplasia. We are studying the role of pro-protein convertases (PCs) such PACE-4 and furin during the early and late stages of tumor progression.

Over-expression of PCs correlates with an aggressive neoplastic phenotype both in mouse models and in human primary tumors. This has been demonstrated in our laboratory using tumor cells derived from lung, ovarian and oral malignant tumors.

Inhibition of PCs can be obtained by using competitive inhibitors such as chloro-methyl-ketone (CMK). This inhibitor decreases and even abolishes the invasive/malignant phenotype of tumor cells by inhibiting the activation of invasion and metastasis-associated gene products such as MT1-MMP, stromelysin 3, TGF-b and IGFR1.

CMK was also used in vivo by topical skin administration. Using this modality we were able to decrease 40% the number of chemically-induced mouse skin cancers as well as diminish 60% the respective tumor volumes.

Another unrelated gene, discovered during differential display together with PCs is VILIP-1, a member of the neuronal Ca++ sensor protein family. VILIP-1 is able to act as a tumor suppressor in mouse skin squamous carcinoma cells inhibiting cell proliferation, adhesion and invasion by modulating cAMP levels as well as inactivating MMP-9 and RhoA activity.

ecently, we have found that this gene is silenced in human tumors due to epigenetic changes including promoter hypermethylation and histone modification.

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