This week I will be meeting with Richard Linchitz, MD to discuss insulin potentiated chemotherapy instead of the standard treatment, which I am thinking of putting on hold as it is so toxic and negates effect of so many standard therapies. By using insulin with chemo, Dr. Linchitz and others have found the tumors take up the chemo more, and you only need to use 10% of the dose to get the same if not better results--so I am told. I will go down and have a 2 hour visit with him this week. He seems really sharp nutritionally and overall.
Had 800,000 IU shot of vitamin D today and other intravenous nutrients through my port. I feel more energized because of it.
Now decompressing, and grateful to be outside all day driving around on such a beautiful April day. Thank you Jonathan for driving me around all day and being such a great friend.
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Dear Robert,
ReplyDeleteI am glad you are feeling a little better and doing intensive treatments. High dose vitamin D is great as it slows down cell proliferation but I hope you are taking high does vitamin K with it because it enhances apoptosis of cancer cells and it is very safe in high doses.
There is some good data on it for liver cancer breast and prostate cancer.
You just need to make sure you are absorbing it.
The easiest to absorb for you may be liquid K1 and K2 at 5mg each every 3 hrs because it clears out of the bloodstream fast.
Japanese studies have used 90mg/day for osteoporosis for 10yrs with no problems, and it will work in synergy with the vitamin D.
Take it sublingually and maybe someone out there can do vit K intravenous?
There is no risk for extra clotting once clotting factors are saturated at 2-300mcg.
Some do IV Vitamin K3 for cancer but that caused RBCs lysis and so I am not sure if the benefit risk ratio is worth it.
Anybody out there know more about IV vitamin K?
Cristiana Paul
Dear Robert,
ReplyDeleteIf I were you I would explore Max Wicha's approach to target the cancer stem cells:
"A recent experimental trial with advanced breast cancer patients at the University of Michigan, Baylor University in Texas and the Dana-Farber Cancer Institute at Harvard University used standard chemotherapy along with a substance designed to block one of the biochemical pathways of stem cells"
"There is still a long road ahead, he said, and "my feeling is, to really knock these stem cells out, we're probably going to have to use multiple inhibitors."
http://www.post-gazette.com/pg/10055/1038056-114.stm
Cristiana Paul
Pharm Res. 2008 Feb;25(2):387-99. Epub 2007 Jul 27.
ReplyDeleteSynergistic effects of a combination of dietary factors sulforaphane and (-) epigallocatechin-3-gallate in HT-29 AP-1 human colon carcinoma cells.
Nair S, Hebbar V, Shen G, Gopalakrishnan A, Khor TO, Yu S, Xu C, Kong AN.
Graduate Program in Pharmaceutical Science, Department of Pharmaceutics, Ernest Mario School of Pharmacy, Rutgers, The State University of New Jersey, Piscataway, New Jersey 08854, USA.
Abstract
PURPOSE: The objective of this study was to investigate combinations of two chemopreventive dietary factors: EGCG 20 microM (or 100 microM) and SFN (25 microM) in HT-29 AP-1 human colon carcinoma cells. METHODS: After exposure of HT-29 AP-1 cells to SFN and EGCG, individually or in combination, we performed AP-1 luciferase reporter assays, cell viability assays, isobologram analyses, senescence staining, quantitative real-time PCR (qRT-PCR) assays, Western blotting, and assays for HDAC activity and hydrogen peroxide. In some experiments, we exposed cells to superoxide dismutase (SOD) or Trichostatin A (TSA) in addition to the treatment with dietary factors. RESULTS: The combinations of SFN and EGCG dramatically enhanced transcriptional activation of AP-1 reporter in HT-29 cells (46-fold with 25 microM SFN and 20 microM EGCG; and 175-fold with 25 microM SFN and 100 microM EGCG). Isobologram analysis showed synergistic activation for the combinations with combination index, CI < 1. Interestingly, co-treatment with 20units/ml of SOD, a free radical scavenger, attenuated the synergism elicited by the combinations (2-fold with 25 muM SFN and 20 muM EGCG; and 15-fold with 25 microM SFN and 100 microM EGCG). Cell viability assays showed that the low-dose combination decreased cell viability to 70% whereas the high-dose combination decreased cell viability to 40% at 48 h, with no significant change in cell viability at 24 h as compared to control cells. In addition, 20 microM and 100 microM EGCG, but not 25 microM SFN, showed induction of senescence in the HT-29 AP-1 cells subjected to senescence staining. However, both low- and high-dose combinations of SFN and EGCG attenuated the cellular senescence induced by EGCG alone. There was no significant change in the protein levels of phosphorylated forms of ERK, JNK, p38, and Akt-Ser473 or Akt-Thr308. Besides, qRT-PCR assays corroborated the induction of the luciferase gene seen with the combinations in the reporter assay. Relative expression levels of transcripts of many other genes known to be either under the control of the AP-1 promoter or involved in cell cycle regulation or cellular influx-efflux such as cyclin D1, cMyc, ATF-2, Elk-1, SRF, CREB5, SLCO1B3, MRP1, MRP2 and MRP3 were also quantified by qRT-PCR in the presence and absence of SOD at both 6 and 10 h. In addition, pre-treatment with 100 ng/ml TSA, a potent HDAC inhibitor, potentiated (88-fold) the synergism seen with the low-dose combination on the AP-1 reporter transcriptional activation. Cytoplasmic and nuclear fractions of treated cells were tested for HDAC activity at 2 and 12 h both in the presence and absence of TSA, however, there was no significant change in their HDAC activity. In addition, the H2O2 produced in the cell system was about 2 microM for the low-dose combination which was scavenged to about 1 microM in the presence of SOD. CONCLUSION: Taken together, the synergistic activation of AP-1 by the combination of SFN and EGCG that was potentiated by HDAC inhibitor TSA and attenuated by free radical scavenger SOD point to a possible multifactorial control of colon carcinoma that may involve a role for HDACs, inhibition of cellular senescence, and SOD signaling.
Cristiana Paul
Zhonghua Er Bi Yan Hou Tou Jing Wai Ke Za Zhi. 2009 Jan;44(1):63-8.
ReplyDeleteRelated Articles, Links
[Reversal effect of resveratrol on chemotherapy resistance in KBv200 cell line and underlying mechanisms]
[Article in Chinese]
Quan F, Pan CE, Zhang SQ, Yan LY, Yu L.
Department of Otorhinolaryngology Head and Neck Surgery, First Affiliated Hospital, Xi'an Jiaotong University, Xi'an 710061, China. quanfang2008@sina.com.cn
OBJECTIVE: To explore the reversal effect and potential mechanism of resveratrol on multidrug resistance of human oral epidermoid carcinoma KBv200 cells. METHODS: MTT assay was used to investigate reversal index of resveratrol to vincristine, adriamycin and paclitaxel. Cell apoptosis were measured by flow cytometry. RT-PCR and Western blot were used to detect mRNA and protein expression of multidrug resistant 1 (MDR1) and B cell lymphoma leukemia-2 (Bcl-2). RESULTS: Resveratrol produced a synergistic effect with chemotherapeutics and obviously reversed the multidrug resistant phenotype of KBv200 cells. The reversal fold (RF) of 200 micromol/L resveratrol to vincristine, paclitaxel and adriamycin were 77.1, 61.3 and 5.9, respectively. The gene array results showed that resveratrol greatly downregulated expression levels of Bcl-2 and MDR1. After treated with 100 micromol/L, 200 micromol/L resveratrol, the expression level of Bcl-2 and MDR1 in KBv200 cells were markedly decreased in comparison with those untreated (t were 2.98, 3.51 and 3.12, 4.56, P < 0.05). CONCLUSIONS: Resveratrol can efficiently reverse multidrug resistance in KBv200 cells. The potential mechanism may be via inhibiting the multidrug resistant gene expressions and/or promoting cell apoptosis.
Biochem Pharmacol. 2006 Feb 23; Aggarwal BB, Shishodia S
ReplyDeleteMolecular targets of dietary agents for prevention and therapy of cancer..
Cytokine Research Laboratory, Department of Experimental Therapeutics, The University of Texas M.D. Anderson Cancer Center, Box 143, 1515 Holcombe Boulevard, Houston, TX 77030, USA.
While fruits and vegetables are recommended for prevention of cancer and other diseases, their active ingredients (at the molecular level) and their mechanisms of action less well understood. Extensive research during the last half century has identified various molecular targets that can potentially be used not only for the prevention of cancer but also for treatment. However, lack of success with targeted monotherapy resulting from bypass mechanisms has forced researchers to employ either combination therapy or agents that interfere with multiple cell-signaling pathways.
In this review, we present evidence that numerous agents identified from fruits and vegetables can interfere with several cell-signaling pathways. The agents include curcumin (turmeric), resveratrol (red grapes, peanuts and berries), genistein (soybean), diallyl sulfide (allium-onion family), S-allyl cysteine (allium-onion family), allicin (garlic), lycopene (tomato), capsaicin (red chilli), diosgenin (fenugreek), 6-gingerol (ginger), ellagic acid (pomegranate), ursolic acid (apple, pears, prunes), silymarin (milk thistle), anethol (anise, camphor, and fennel), catechins (green tea), eugenol (cloves), indole-3-carbinol (cruciferous vegetables), limonene (citrus fruits), carotenes (carrots), and dietary fiber. For instance, the cell-signaling pathways inhibited by curcumin alone include NF-kappaB, AP-1, STAT3, Akt, Bcl-2, Bcl-X(L), caspases, PARP, IKK, EGFR, HER2, JNK, MAPK, COX2, and 5-LOX. The active principle identified in fruit and vegetables and the molecular targets modulated may be the basis for how these dietary agents not only prevent but also treat cancer and other diseases. This work reaffirms what Hippocrates said 25 centuries ago, let food be thy medicine and medicine be thy food.
Greetings from Boulder, Robert! The promise of spring hangs in the air here, ready to be snatched away by the winter weary. All around town, lucious buds are appearing on trees, yellow flowers push up through the remaining snow and in the distance the peaks, still dusted in white, create a backdrop along with the Maxfield Parish blue sky. Boulder misses you and thinks about you. I run into people who ask about your well being, who are sending you prayers and good thoughts. You are a New Yorker, but you are a member of this community too, your quirkiness ever a part of what makes Boulder a strange and wonderful place. Dean and I send you lots of love. I want you to know that you are loved by many people here and I pray that the power of that love reaches you and becomes part of your healing process. Hugs across the miles. May this be a good day for you, one that reveals the wonder of spring where you are...new beginnings.
ReplyDeleteHey Robert-
ReplyDeleteI tried calling the hospital last week but couldn't round you up. I would love to see you in human form. Do you want visitors?
Lots of love and healing warm fuzzies!
Wendy
917-733-5915
joe@joesgrille.com
Continue your search and be smart (like you always are). Get a third, fourth, fifth and sixth opinion. Don't act on fear. You know all of this stuff!
ReplyDeleteSheri Gruener
A fan of yours for only 6 years.
Hi Robert,
ReplyDeleteI'm glad we have gotten to talk a few times lately. I have always admired the easeful and brilliant way you have about you. Whether I was listening to you speak, experiencing the true pleasure of being interviewed by you, or sharing our takes on spirit or the challenges of healing childhood wounds, I have loved being with you. You have added so much to my life and the lives of so many others. Thank you.
Today is my 59th birthday and it seems that life goes so much faster as we age. Remember in grade school how the second hand on those big clunky school clocks seem to refuse to move during that last school hour between 2 and 3 pm? Now the months go by like the weeks used to and none of know how long we might live in these miraculous and all too fragile bodies.
I do my best to try to remember that we are spirit having a human experience, not humans trying to have a spiritual experience. I know you do too. Very challenging times can seduce us into forgetting. So try not forget my friend.
I deeply hope that you live for many more years. But if it happens that you don't, I pray that you don't fall prey to the New Age narcissism that can make one wonder
"How did I create this?" or to the terrible ifs..."if I had just gotten more rest, eaten better, gotten to the doctor quicker. dealt with my emotions better, drunk less soda, eaten less sugar blah, blah blah. We all die of something including the saints and gurus(the false and true).
What I know about you Robert is that you always have given your all and you have enhanced the lives of so many doctors and their patients that you probably will not be able to see the awesome ripple effects of your passionate giving and contributions until you pass over into the non-physical.
So I hope that you can deeply take in the love, admiration, appreciation from all of us who have had the priviledge of knowing you(warts and all :)and to realize that even if you didn't live another day, the service that you have already rendered has been more than enough and has truly enhanced our lives.
That being said, I hope your days will be many.
Your friend,
Dean Raffelock
The article have a helpful massage for others.I would love to see you in human form. Thanks a lot.......................
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