Since She Came Back And Posted Again...I'd Like To Say Hi To Mrs. Edwards

[THUNDER HANDS]

Hi Mrs. Rightful Vice President! (or Rightful Second Lady, I'm not sure what you call a vice presidential wife)

You'll always be my favorite political spouse. I loved every moment you appeared on tv these past two years.

I hope your kids grow up and have the same success in life that both you and your husband did. And I know they will because their parents ROCK!

:loveya:

[GOPisEvil]

1. Kick cancer's butt, too!

:hi:

[GalleryGod]

2. I RARELY Disagree with THAT Texan! Kick butt, EE!

:grouphug:

[Career Prole]

4. Ditto from the Hamel family!

:hi:

[graywarrior]

3. Eat miso soup, Elizabeth

It will cleanse you while you go through treatment.

[LoZoccolo]

5. Where did she post? n/t

[THUNDER HANDS]

7. GD

she had like, just the one post after her initial thread. Then she came back recently and posted EIGHT more.

Wow. She'll have more than Matcom in a few weeks. :D

[Misunderestimator]

9. Here:

http://www.democraticunderground.com/discuss/duboard.php?az=view_all&address=104x2604461

[Maat]

6. As a 45-year-old mom, whose becoming a lawyer...

well, I'm her greatest fan. She's so articulate, well-educated, and classy.

Mrs. Edwards, our thoughts and prayers are with you and your family.

Thanks for all of your effort.

I hope that every vote is counted. I hope that if and when they discover that something dishonest and criminal occurred, with respect to this election and the voting and tallying of results, I pray and affirm that the perpetrators will get exactly what is coming to them (a great amount of really negative energy - heck on earth).

My conscience is clean, and I'm glad of it.

Success and health to the Edwards family!

[Blue Gardener]

8. She Posted Again?

And I missed it?

[Misunderestimator]

10. She replied to some of the messages on the original thread.

[HysteryDiagnosis]

11. I would like to say something as well..... and it concerns ALL WOMEN

who post here so listen up.

I have read and studied about natural interventions for illness for over 10 years. I have no degree... but I do know what I have seen.

There is an extract of CABBAGE, believe it or not... that has been studied to the tune of I think it was 2 million dollars.... to find out how in the heck this extract "Indole-3-Carbinol" could TURN OFF THE CANCER PROCESS AT THE DNA LEVEL.

The product is sold as Indole 3 Carbinol and the best one comes with something called DIM.

The magic amount women can take for prevention is 300mg/day and it has been shown to be equal if not superior to Tamoxifen.

Let me see what I can dig up..... there are DOZENS more papers at the NIH... I suggest women who are at increased risk for breast cancer dig into this... learn about it... see that it is real... and act on it.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9589355&dopt=Abstract

1: J Cell Biochem Suppl. 1997;28-29:111-6. Related Articles, Links

Dose-ranging study of indole-3-carbinol for breast cancer prevention.

Wong GY, Bradlow L, Sepkovic D, Mehl S, Mailman J, Osborne MP.

Strang Cancer Prevention Center, New York, New York 10021, USA.

Sixty women at increased risk for breast cancer were enrolled in a placebo-controlled, double-blind dose-ranging chemoprevention study of indole-3-carbinol (I3C). Fifty-seven of these women with a mean age of 47 years (range 22-74) completed the study. Each woman took a placebo capsule or an I3C capsule daily for a total of 4 weeks; none of the women experienced any significant toxicity effects. The urinary estrogen metabolite ratio of 2-hydroxyestrone to 16 alpha-hydroxyestrone, as determined by an ELISA assay, served as the surrogate endpoint biomarker (SEB). Perturbation in the levels of SEB from baseline was comparable among women in the control (C) group and the 50, 100, and 200 mg low-dose (LD) group. Similarly, it was comparable among women in the 300 and 400 mg high-dose (HD) group. Regression analysis showed that peak relative change of SEB for women in the HD group was significantly greater than that for women in the C and LD groups by an amount that was inversely related to baseline ratio; the difference at the median baseline ratio was 0.48 with 95% confidence interval (0.30, 0.67). No other factors, such as age and menopausal status, were found to be significant in the regression analysis. The results in this study suggest that I3C at a minimum effective dose schedule of 300 mg per day is a promising chemopreventive agent for breast cancer prevention. A larger study to validate these results and to identify an optimal effective dose schedule of I3C for long-term breast cancer chemoprevention will be necessary.

Publication Types:

* Clinical Trial
* Controlled Clinical Trial


PMID: 9589355

1: Nutr Cancer. 2004;48(1):84-94. Related Articles, Links

Inactivation of akt and NF-kappaB play important roles during indole-3-carbinol-induced apoptosis in breast cancer cells.

Rahman KM, Li Y, Sarkar FH.

Department of Pathology, Karmanos Cancer Institute, Wayne State University School of Medicine, Detroit, MI 48201, USA.

Despite significant advances in treatment, breast cancer is still the second leading cause of cancer-related deaths in women in the United States. Therefore, significant efforts are being given to develop novel strategies for the prevention of breast cancer in recent years. Our laboratory and others have been studying the effects of a potential chemopreventive agent, indole-3-carbinol (I3C), in breast cancer cells. We have previously shown that I3C induces apoptosis in breast cancer cells and found that the induction of apoptotic processes was partly mediated by dysregulation of anti- and pro-apoptotic molecules. However, the precise molecular mechanism(s) by which I3C induces apoptosis in breast cancer cells has not been fully elucidated. For the present study, we focused our investigation on important cell signaling molecules such as Akt and NF-kappaB during I3C-induced apoptosis in breast cancer cells. We found that I3C induces apoptotic processes in MCF10A-derived cell lines with premalignant (DCIS.com) and malignant (MCF10CA1a) phenotypes but not in nontumorigenic parental MCF10A cells. Immunoprecipitation, kinase assays, and Western blot analysis showed that I3C specifically inhibits Akt kinase activity and abrogates the EGF-induced activation of Akt in breast cancer cells. NF-kappaB DNA-binding analysis and transfection studies with Akt cDNA and NF-kappaB-Luc reporter constructs revealed that Akt gene transfection directly activates NF-kappaB, and this activation was completely abrogated by I3C treatment. In addition, I3C also abrogated the EGF-induced activation of NF-kappaB, which was mediated via the Akt signaling pathway. From these results, we conclude that there is a direct cross-talk between Akt and NF-kappaB pathways and that the inactivation of Akt and NF-kappaB activity plays important roles in mediating I3C-induced apoptosis in breast cancer cells. These results also suggest that I3C may be a potential chemopreventive agent by virtue of its selective apoptosis-inducing ability in premalignant and malignant breast epithelial cells. Copyright 2004 Lawrence Erlbaum Associates, Inc.

PMID: 15203382

1: J Nutr. 2003 Jul;133(7 Suppl):2470S-2475S. Related Articles, Links
Click here to read
Indole-3-carbinol is a negative regulator of estrogen.

Auborn KJ, Fan S, Rosen EM, Goodwin L, Chandraskaren A, Williams DE, Chen D, Carter TH.

North Shore-Long Island Jewish Research Institute, Manhasset, NY 11030, USA. [e-mail]

Studies increasingly indicate that dietary indole-3-carbinol (I3C) prevents the development of estrogen-enhanced cancers including breast, endometrial and cervical cancers. Epidemiological, laboratory, animal and translational studies support the efficacy of I3C. Whereas estrogen increases the growth and survival of tumors, I3C causes growth arrest and increased apoptosis and ameliorates the effects of estrogen. Our long-range goal is to best use I3C together with other nutrients to achieve maximum benefits for cancer prevention. This study examines the possibility that induction of growth arrest in response to DNA damage (GADD) in genes by diindolylmethane (DIM), which is the acid-catalyzed condensation product of I3C, promotes metabolically stressed cancer cells to undergo apoptosis. We evaluated whether genistein, which is the major isoflavonoid in soy, would alter the ability of I3C/DIM to cause apoptosis and decrease expression driven by the estrogen receptor (ER)-alpha. Expression of GADD was evaluated by real-time reverse transcription-polymerase chain reaction. Proliferation and apoptosis were measured by a mitochondrial function assay and by fluorescence-activated cell sorting analysis. The luciferase reporter assay was used to specifically evaluate expression driven by ER-alpha. The estrogen-sensitive MCF-7 breast cancer cell line was used for these studies. We show a synergistic effect of I3C and genistein for induction of GADD expression, thus increasing apoptosis, and for decrease of expression driven by ER-alpha. Because of the synergistic effect of I3C and genistein, the potential exists for prophylactic or therapeutic efficacy of lower concentrations of each phytochemical when used in combination.

Publication Types:

* Review
* Review, Tutorial


PMID: 12840226

1: Nutr Cancer. 2003;45(1):101-12. Related Articles, Links

Indole-3-carbinol (I3C) induces apoptosis in tumorigenic but not in nontumorigenic breast epithelial cells.

Rahman KM, Aranha O, Sarkar FH.

Department of Pathology, Karmanos Cancer Institute, Wayne State University School of Medicine, Detroit, MI 48201, USA.

Recent results from epidemiology, in vitro cell culture and in vivo (animal and human) studies have suggested the benefits of indole-3-carbinol (I3C) for the prevention of many types of cancer, including breast cancer. However, there are no reports, to the best of our knowledge, on the effect of I3C on isogenic nontumorigenic and tumorigenic breast epithelial cells, and there is a significant void in our understanding of the molecular mechanism(s) by which I3C induces apoptotic cell death in breast cancer cells. To fill this gap in our understanding, we conducted experiments to investigate the effects of I3C on an isogenic nontumorigenic (MCF10A) and tumorigenic (MCF10CA1a ) breast epithelial cells. Here we show that CA1a cells are more sensitive to low concentration of I3C in terms of cell growth inhibition compared to MCF10A cells. We further report that I3C upregulates Bax/Bcl-2 ratio and downregulates Bcl-xL expression in CA1a cells but not in MCF10A cells. We also report, for the first time, that I3C induces Bax translocation to the mitochondria, causing mitochondrial depolarization, resulting in the loss of mitochondrial potential leading to the release of cytochrome c and subsequent cell death in CA1a cells but not in MCF10A cells. From these results, we conclude that I3C selectively induces apoptosis in breast cancer cells, but not in nontumorigenic breast epithelial cells, suggesting the potential therapeutic benefit of I3C against breast cancer.

PMID: 12791510