garden as well as these.... I recently gave some Bio Greens and glyconutrients to a family member who was facing surgery for breast cancer. She started only a few weeks prior to surgery... tumor mass had shrunk by the day of the surgery.
In Vivo. 2008 Jul-Aug;22(4):441-5.
Review. Indole-3-carbinol as a chemoprotective agent in breast and prostate cancer.
Bradlow HL.
David and Alice Jurist Institute for Medical Research, Hackensack University Medical Center Hackensack, NJ 07601, USA. bradlowhl@gmail.com
Assessment of the oral use of indole-3-carbinol (I3C) as a chemoprotective compound has not sufficiently considered the chemical instability of I3C. This review addresses the question of whether I3C is directly active in its own right or only serves as a precursor, with all of the biological responses coming from reaction products arising in culture media and in the presence of stomach acid. Because of the rapid conversion of I3C into its dimer. diindolylmethane (DIM), and trimers very little circulating I3C is present following oral use to effect a biological response. Reports of toxicity associated with oral use of I3C relate to unfavorable enzyme induction, which can be attributed to non-DIM reaction products. Because DIM provides a predictable, safer response than the mélange of compounds derived from I3C DIM should be regarded as the chemoprotective compound of choice.
PMID: 18712169
Publication Types, MeSH Terms, Substances
Biochem Pharmacol. 2006 Dec 15;72(12):1714-23. Epub 2006 Sep 12.
Indole-3-carbinol mediated cell cycle arrest of LNCaP human prostate cancer cells requires the induced production of activated p53 tumor suppressor protein.
Hsu JC, Dev A, Wing A, Brew CT, Bjeldanes LF, Firestone GL.
Department of Molecular and Cell Biology and The Cancer Research Laboratory, The University of California at Berkeley, Berkeley, CA 94720, USA.
Indole-3-carbinol (I3C), a dietary compound found naturally in cruciferous vegetables of the Brassica genus such as broccoli and brussels sprouts, induces a G1 growth arrest of human reproductive cancer cells. We previously reported that in LNCaP prostate cancer cells, I3C down-regulated cyclin-dependent kinase (CDK) 2 activity. In our current study, Western blotting and quantitative RT-PCR demonstrated that I3C treatment increased both the transcripts and protein levels of the CDK2 inhibitor p21(waf1/cip1) (p21). Transfection of luciferase reporter plasmids containing wild-type and mutated p21 promoter fragments revealed that I3C induced p21 gene transcription through a p53 DNA binding element. Oligonucleotide precipitation showed that I3C increased the level of activated p53 nuclear protein that is competent to bind its DNA target site on the p21 promoter. Ablation of p53 production using short interfering RNA (siRNA) prevented that the I3C induced G1 arrest and up-regulation of p21 expression. Western blots using p53 phospho-specific antibodies revealed that I3C treatment increased the levels of three phosphorylated forms of p53 (Ser15, Ser37, Ser392) that are known to contribute to p53 protein stability and greater transactivation potential. Taken together, our results establish that the I3C induced G1 arrest of human prostate cancer cells requires the induced production of the activated phosphorylated forms of p53, which stimulate transcription of the CDK2 inhibitor p21.
PMID: 16970927