protocel לטיפול ב - aml

לאבי יש לוקמיה ונעשה לו נסיון של השתלה שלא הצליחה ועכשיו נתוני הדם שלו על הפנים. מישהו המליץ לנו לנסות את תוסף המזון הזה. האם הוא מתאים למצב הזה? האם יש רעיונות אחרים?

1: Carcinogenesis. 2007 May 3 Dietary flavonoids induce MLL translocations in primary human CD34+ cells. Barjesteh van Waalwijk van Doorn-Khosrovani S, Janssen J, Maas LM, Godschalk RW, Nijhuis JG, van Schooten FJ. Department of Health Risk Analysis AND Toxicology, Nutrition AND Toxicology Research Institute Maastricht (NUTRIM), Maastricht University, the Netherlands. Genetic abnormalities leading to infant leukemias already occur during fetal development AND often involve rearrangements of the mixed-lineage-leukemia (MLL) gene. These rearrangements resemble the aberrations observed in therapy-related leukemias following treatment with topoisomerase II-inhibiting agents such as etoposide. Since flavonoids are potent topoisomerase II inhibitors, we examined the role of three widely consumed dietary flavonoids (quercetin, genistein AND kaempferol) on the development of MLL rearrangements in primary human CD34(+) cells. Using the neutral Comet assay we demonstrated a dose-dependent double-strand break formation after exposure to flavonoids. An incorrect repair of these double-strand breaks resulted in chromosomal translocations that co-localized with those identified in infant leukemias. Most of these translocations were formed by microhomology-mediated end joining. Moreover, in all but one translocation, SINE/Alu OR LINE/L1 repetitive elements were present in at least one side of the breakpoint junction. Beside MLL translocations, Fluorescence In Situ Hybridization analysis demonstrated monosomy OR trisomy of MLL in 8-10% of the quercetin-exposed CD34(+) cells. Our study demonstrates that biologically relevant concentrations of flavonoids can induce MLL abnormalities in primary hematopoietic progenitor cells. This is particularly alarming knowing that the differences in metabolism AND excretion rate between mother AND fetus can lead to a higher flavonoid-concentration on the fetal side. Therefore it is important to raise public awareness AND set guidelines for marketing flavonoid supplements to reduce the risk of infant leukemias.

J Am Diet Assoc. 2003 Aug;103(8):982-90. The association between vitamin C AND vitamin E supplement use before hematopoietic stem cell transplant AND outcomes to two years. Bruemmer B, Patterson RE, Cheney C, Aker SN, Witherspoon RP. Department of Epidemiology, Nutritional Sciences Program, University of Washington, Box 353410, 305-M Raitt Hall, Seattle, WA 98105, USA. [email protected] OBJECTIVE: To examine the prevalence of supplement use in persons before receiving hematopoietic stem cell transplant (HSCT) AND the association of select supplements with outcomes. DESIGN: This observational cohort study included a questionnaire on supplement use before HSCT. Nonrelapse mortality, recurrence/relapse, AND mortality OR relapse (the inverse of disease-free survival) were followed to two years. Subjects/Setting Persons receiving HSCT at the Fred Hutchinson Cancer Research Center between September 1994 AND December 1997 were eligible (N=1,182). Statistical Analyses Performed Descriptive statistics AND univariate AND Cox regression analyses were conducted. RESULTS: Sixty-six percent of patients used supplements (31% vitamin C, 19% vitamin E, AND 20% herbs OR others preparations). Vitamin C at > OR =500 mg/day was inversely associated with recurrence among persons with breast cancer (RR=0.11; 95% CI, 0.02-0.89; P=.03). However, among persons with acute leukemia, vitamin C at > OR =500 mg/day was positively associated with nonrelapse mortality (RR=2.25; 95% CI, 1.33-3.83; P=.01) AND mortality OR relapse (RR=1.63; 95% CI, 1.09-2.44; P=.01), respectively. Vitamin E at > OR =400 IU/day was positively associated with mortality OR relapse (RR=1.77; 95% CI, 1.06 -2.96; P=.02). Applications/Conclusions Though this work was observational, the results suggest supplemental vitamin C before therapy may be beneficial in persons with breast cancer but both vitamin C AND vitamin E may increase risk in persons with acute leukemia receiving HSCT. Practitioners should document supplement use in subjects receiving therapy for cancer.

האם תרופה בשם PROTOCELאינה מוכרת לך? האם היא אינה מתאימה ללוקמיה?

שלום יוסי, חשוב לי שתתיחס לתוכן הודעתי כאל מידע בלבד ולא כאל עצות. אני לא מכיר את המקרה של אביך מקרוב. protocel/cancell יכולים להיות יעילים בשורה ארוכה של סרטנים. אני כותב על התוסף בספרי. עם זאת, למיטב ידיעתי התוסף יעיל יותר בלויקמיה מסוג ALL ופחות בלויקמיה מסוג AML. דברים שעשויים אולי לעזור ב- AML (קשה ביותר לטיפול) הם: 1. methylprednisolone http://www.ncbi.nlm.nih.gov/entrez/queryd.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=15979702&itool=pubmed_docsum החוקרים התורכים במחקר הנ"ל ניסו במשך 17 שנים גלוקוסטרואידים שונים לטיפול ב-AML. הם לאחרונה פרסמו את תוצאותיהם עם השימוש ב- methylprednisolone והתוצאות הן די מדהימות. השימוש בסטרואיד הנ"ל בשילוב עם מינונים נמוכים של כימותרפיה הצליח להשיג רמיסיות ב-87-89%. רמיסיה מוחלטת בהקשר של AML היא דבר יחסית נדיר. 2. התרופות להורדת כולסטרול לובסטטין או סימבסטטין (יתכן שאפילו טוב יותר לשלב עם מעכבי COX2 ו- phenylacetate או phenylbutyrate) Blood 1999 Feb 15;93(4):1308-18 Increased sensitivity of acute myeloid leukemias to lovastatin-induced apoptosis: A potential therapeutic approach. Dimitroulakos J, Nohynek D, Backway KL, Hedley DW, Yeger H, Freedman MH, Minden MD, Penn LZ Department of Cellular AND Molecular Biology, Ontario Cancer Institute, Toronto, Ontario, Canada. We recently demonstrated that 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, the rate-limiting enzyme of de novo cholesterol synthesis, was a potential mediator of the biological effects of retinoic acid on human neuroblastoma cells. The HMG-CoA reductase inhibitor, lovastatin, which is used extensively in the treatment of hypercholesterolemia, induced a potent apoptotic response in human neuroblastoma cells. This apoptotic response was triggered at lower concentrations AND occurred more rapidly than had been previously reported in other tumor-derived cell lines, including breast AND prostate carcinomas. Because of the increased sensitivity of neuroblastoma cells to lovastatin-induced apoptosis, we examined the effect of this agent on a variety of tumor cells, including leukemic cell lines AND primary patient samples. Based on a variety of cytotoxicity AND apoptosis assays, the 6 acute lymphocytic leukemia cell lines tested displayed a weak apoptotic response to lovastatin. In contrast, the majority of the acute myeloid leukemic cell lines (6/7) AND primary cell cultures (13/22) showed significant sensitivity to lovastatin-induced apoptosis, similar to the neuroblastoma cell response. Of significance, in the acute myeloid leukemia, but not the acute lymphocytic leukemia cell lines, lovastatin-induced cytotoxicity was pronounced even at the physiological relevant concentrations of this agent. Therefore, our study suggests the evaluation of HMG-CoA reductase inhibitors as a therapeutic approach in the treatment of acute myeloid leukemia. 3. ויטמין D3 Antiproliferative Effect of Vitamin D3 Anlaog in Hematologic Malignancies Hematologic malignancy including acute myelogenous leukemia (AML) represents a hemtopoietic stem cell disorder representing a block in differentiation into mature cells. High-dose chemotherapy has improved survival of patients with hematologic malignant disease, but severe bone marrow suppression limits its clinical use. An alternative therapy for these patients is to induce differentiation and/or inhibit clonla proliferation of malignant cells without toxic effects on their normal hematopoietic stem cells. The seco-steroid hormone, 1,25 dihydroxyvitamin D3 [1,25(OH)2D3], has an inportant role in the maintenance of calcium homeostasis through binding to specific intracellular receptors. The classical target organs of this seco-steroid are the interstine, bone AND kieney. A variety of tissues that do not participate in mineral AND bone metabolism also possess specific receptors for AND respond to 1,25(OH)2D3 including normal AND neoplastic hematopoietic cells. The 1,25(OH)2D3 induces AML cell lines as well as blast cells from AML patients to differentiate into mature cells AND inhibits their proliferation in vitro AND in vivo without suppression of normal granulocyte-monocyte committed stem cells. However, it can not be used in clinical trial because of development of major side effects, hypercalcemia. Therefore, research activities have been directed at finding potent analogs of 1,25(OH)2D3 with a more favorable therapeutic profile. We have examined more than 200 analogs to find potent viatmain D3 analogs. EB1089 is a novel 1,25(OH)2D3 analog that has more potent antitumor properties with reduced hypercalcemic effects in vitro AND in vivo. Antitumor effects of EB1089 has been proven in a vareity of solid tumors including prostate cancer AND breast cancer. We have extented our experiments to its antiproliferative AND bilogical effects on hematologic malignancies, especially AML AND multiple myeloma. In addition to antiproliferative effects, we have investigated its mechamisms regardign cell cycle AND apoptosis. Finally, we will try this analog in hematopoietic stem cell transplantation. Antitumoral Effect of Heavy Metal in Malignant Diseases Very recently, we have interested in antitumoral effect of heavy metal on malignant diseases. In vito AND in vivo studies have been done, AND we have examined mechanisms on antitumoral effect regarding apoptosis AND cell cycle, AND looked for target molecules. Effect of a vitamin D3 analoge, EB1089, on hematopoietic stem cells from normal AND myeloid leukemia blasts (Leukemia 1996;10,1751-1757) The sero-steroid 1,25 dihydroxyvitamin D3 (1,25(OH)2D3) induces differentiation AND inhibitor clonal proliferation of HL-60 cells. We analyzed the effect of a noval vitamin D3 analog, EB1089, on normal myeloid AND leukemic cells as well as CD34+ cells. EB1089 showed an extraodinary inhibition of clonal growth of HL-60 cells(ED50=5x10-11M) AND AML blast cells (ED50=9x10-10M) compared to 1,25(OH)2D3 without suppression of growth of normal human bone marrow CFU-GM. The CD34 cells from acute myeloid leukemia(AML) blasts were inhibited in a dose-dependent fashion by 1,25(OH)2D3 with an ED50 of 1.2x10-9M; AND even more strikingly, 10-10M of EB1089 inhibited all clonal growth of human CD34+ leukemic clony-forming cells. In contrast, both EB1089 AND 1,25(OH)2D3 (10-8M) showed little per only mild inhibition of CD34+ clongenic hematopoietic cells from normal human peripheral blood(PB); AND in liquid culture, EB1089 stimulated the proliferation of normal human CD34+ cells about 2.5 times as compared to control cultures. In order to evaluate the potential use of EB1089 for purging leukemic cells from normal CD34+ progenitor cells for PB stem cells transplantation (PBSCT), normal human PB mononuclear cells(PBMNC) were contaminated with HL-60 cells, AND then CD34+ cells purified AND treated with EB1089. We found that CD34+ purificated AND EB1089 purging was able to eliminate approximately 100% of HL-60 leukemic cells with no toxicity to normal CD34+ hematopoietic progenitor cells. These data suggested that purification of CD34+ cells AND ex vivo treatment with EB1089 might provide an effective therapeutic approach for PBSCT. Telomerase activity in acute myelogenous leukemia:clinical AND biological implications (British Journal of Haematology 1998. 100, 156-165) We examined telomerase activity in myeloid leukaemic cell lines, normal haemopoietic cells, AND leukaemic blasts from acute myelogenous leukaema (AML) patients. Normal bone marrow mononuclear (BMNC) cells expressed low telomerase activity was detected in 10 myeloid leukaemic cell lines compared to normal BMNC cells. Treatment with 1,25(OH)2D3, AND vitamin D3 analogues, EB1089 AND KH1060, reduced telomerase activity in vitamin D3-sensitive HL-60 cells. whereas vitamin D3 insensitive K562 cells did not change its activity. This down-regulation of telomerase activity by EB1089 was associated with induced of p21 protein. The rank order of telomerase activity was leukaemic CD34- cells> leukaemic CD34+ cells> normal CD34- cells> normal CD34+ cells. Telomerase activity was posotive in all of the AML patients tested: however, heterogeneity of telomerase activity was found amongst this group. Therefore we compared telomerase activity with clinical response. Unexpectedly, we found that a higher rate of complete remission was noted in AML patients with higher telomerase activity. No associated between telomerase activity AND biological parameters including percentage of S-phase, cytotoxicity to cytosine arabinoside AND percentage of CD34+ cells in AML blasts was found. These results suggest that telomerase activity in AML patients is detected with high frequency, but is heterogenous. Expression level of telomerase activity may have a clinical implication in AML patients regarding clinical response. Research Group Members Byoung Kook Kim, M.D., Ph.D. Professor Chul Won Jung, M.D. Assistant Professor Eun Shil Kim, Master Graduate Student Jae Goo Seol, Master Graduate Student Woo Hyun Park, Master Graduate Student Mee Jung Hyun, Graduate Student Invited Presentations "Effect of a vitamin D3 analog on perepheral blood stem cells transplantation" The 1st Korea-Japan Kematology Joint Symposium, Seoul, May 10, 1996 "Differentiating AND antileukemic effect of vitamin D3 on myeloid leukemia" The 1st Chemoprevention Course of Seoul National University Hospital, Seoul, Oct. 27, 1996 "Clinicl manifestations in multiple myeloma" The Multipel Myeloma Course of KSH, Seoul, Nov. 7, 1996 :"Vitamin D3 AND hematopoieis" The Cancer Research Center Symposium of Kyoung Sang University, Jin Ju, June 28, 1996 "Telomerase activity in acute myelogenous leukemia" The 24th Annual Congress of Korean Cancer Association Symposium, Seoul, June 12, 1998 Publications Lee YY, Kim ES, Seol JG, Kim BK, Bindrup L, Elstner E, DJ Park, Koeffler HP. Effect of a vitamin D3 analoge, EB1089, on hematopoietic stem cells from normal AND myeloid leukemic blasts. Leukemia 1996; 10: 1751-1757 Kim ES, Seol JG, Lee YY, Kim BK, Lee HH. Identification of granulocyte-macrophage colony stimulating factor receptor assay on leukemic cells. Kor J BRM 1996; 6: 193-203 Hatta Y, Wada M, Takeuchi S, Tasaka T, Lee E, Lee YY, Kim BK, Bang YJ, Lee S, Yamada Y, Tomonaga M, WIlczinski SP, Sais JW, Koeffler HP. Mutational analysis of the hMSH2 gene in a wide variety of tumors. Int J Oncol 1997; 11: 465-469 Lee YY, Kang SH, Seo JY, Jung CW, Lee KU, Choe KJ, Kim BK, Kim NK, Koeffler HP, Bang YJ. Alteration of p16 AND p15 genes in gastric carcinomas. Cancer 1997; 80: 1889-1896 Jung CW, Lee SJ, Ahn MJ, Chung TJ, Kim IS, Choi IY, Seol JG, Kim ES, Kim BK, Lee YY. Study on the growth suppression effect of vitamin D3 mediated by transforming growth factor-b1(TGF-b1) in acute myelogenous leukemia. J Kor Cancer Assoc 1998; 30: 827-841 Jung CW, Lee SJ, Kim WS, Ahn MJ, Chung TJ, Kim IS Choi IY, Kim SY, Yoon WJ, Cho KS, Kim BK, Lee YY. Mutation of the p53 gene in acute myelogenous leukemia. Kor J Hematol 1998; 33: 303-310 Seol JG, Kim ES, Park WH, Jung CW, Kim BK, Lee YY. Telomerase activity in acute myelogenous leukemia: clinical AND biological implications. Br J Haematol 1998; 100: 156-165 4. PARTHENOLIDE מצמח ה-FEVERFEW Guzman ML, Rossi RM, Karnischky L, et al. The sesquiterpene lactone parthenolide induces apoptosis of human acute myelogenous leukemia stem AND progenitor cells. Blood. 2005 Feb 1; [Epub ahead of print] 5. Brusatol http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&list_uids=12399973&cmd=Retrieve&indexed=google 6. Sutton's Colloidal Silver Solutions. Allan Sutton האיש העומד מאחורי השם והמוצר מתאר במילותיו הוא את חוויות הבריאות הטראגיות שחווה, ואשר בסופו של דבר הובילו ליצור המוצר: I was hospitalised in Perth - Western Australia, on Valentine's Day, 14th February, 1995 with an acute high temperature AND rigours. After 3 days of extensive tests AND liberal doses of pethadine, my doctor presented himself at the side of my hospital bed AND said, "Mr Sutton, we have some bad news, we have finally found out what is wrong with you". He informed me that I had 'Acute Myloid Leukaemia' AND that there was an Oncologist waiting outside my room whom he wished me to speak with. The Oncologist explained to me that there were two types of Leukaemia AND I unfortunately, was diagnosed with the worst one. He told me in his opinion, I had 4 -6 weeks left to live AND chances of my surviving were 15% - 20%, only if chemotherapy was started immediately. Steps were immediatley taken in preparation of locating a bone-marrow donor. After sedation a bone-marrow sample was removed to match, initially against close family. I awoke from this procedure with numerous tubes hanging out of me AND my mind swirling with black thoughts about the implications of my situation AND demise. Six hours later, a doctor entered my room AND informed me that he had some good news. "You don't have Acute Myloid Leukaemia, Mr Sutton". Stunned, numb AND in a state of utter shock I asked him what I had? He could not tell me, saying the doctor's did not know. What should have provided me immense relief, was exchanged by fear ridden thoughts that raged through my head "how could they be sure that I didnt have Leukaemia if they didnt know what I HAD?!!!!! I discussed these fears with him of which his candid reply was simply that, they had mixed up my blood slides with another patient. I couldn't grasp the fact, another patient was about to receive the same death sentence, I had earlier received. Unable to comprehend the acceptance of what I had been told, I went into a state of deep shock AND was sedated as a result. Not only was I now suffering an unknown malady, I had a deep, psychological trauma to deal with as well. The following day I was discharged from the public hospital AND taken to a private hospital where it took 3 weeks to find the cause of my illness. The diagnosis was Epstein Barr virus (commonly known to cause Glandular fever AND Chronic fatigue syndrome) along with a few other pathogentic ills, thrown in for good measure!!!. I ended up at the psychiatrist in an attempt to deal with the trauma AND due to my run-down immune system, suffered from numerous illnesses for a number of months ie; flu's, stomach bugs etc. It was a visit at a friend, (Klaus's) home one day that changed my life. I remember him taking one look at me when he opened the door AND saying, "What is wrong with you today?" I replied that I had the throat from hell!!, to which he replied, "I have been meaning to tell you, I have something for you". He opened an unlabelled bottle of liquid AND told me take a big mouthful and gargle, ensuring that I made it hot AND gooey with my saliva. He insisted that I keep the solution in my mouth for about 5 minutes before swallowing. After this he made me lie down on his couch for 1/2 an hour, having had nothing to drink OR eat. I awoke an hour later AND to my utter astonishment, the raging throat from hell was gone!! That was my introduction to Colloidal Silver AND from that day on, my immune system improved AND has continued to do so, to the point that, I have not experienced a days illness for the past 6 years. Allan Sutton http://www.suttonssolutions.com/suttons.html>http://www.suttonssolutions.com/suttons.html 7. דיאטת באדוויג יכולה בהחלט לתרום. לויקמיה מגיבה היטב לדיאטה זו. 8. השיטה המטאבולית של Dr. William Donald Kelly יכולה גם כן לעזור. בברכה, גובי www.cure-cancer-naturally.com

מכוון שיש רבים המששתמשים במיצים סטטינים ואשכוליות/או מיץ אשכוליות גורם לעיתים תוך זמן קצר להרס הכליות ציטוט קצר אכילת אשכוליות כגורם לרבדומיוליזיס (Rhabdomyolysis) בחולה המטופל בסטטין Rhabdomyolysis (פירוק שריר,שתוצרי פירוקו (מיוגלובין) מופרשים בכיליה וגורמים לפגיעה ואי ספיקת כליות) ,נחשב לתופעת לוואי נדירה אך מסוכנת, כתוצאה מטיפול בסטטינים. חב' באייר נאלצה באוגוסט 2001 להפסיק לשווק את ה- Cerivastatin, כתוצאה מריבוי מקרים של רבדומיוליזיס, כולל 100 מקרי מוות.