Salicinium Non-Toxic Anti-Cancer Agent by Jeffrey Dach MD
A few recent articles in Townsend Letter for Doctors discuss Salicinium as a non-toxic anticancer agent.(1-2) Salicinium was patented in 2011 by Joe Brown as a glyco-benzaldehyde, by adding glucose to benzaldehyde.(19)
Below image: Chemical structure of Glyco-Benzaldehyde (Salicinium) courtesy of Joe Brown Patent (19). Benzaldehyde (left) is attached to a glucose molecule(right)
See chemical formula at below (19):
Benzaldehyde is present in the plant world, as an extract from figs for example, and has been studied going back to the 1980’s as a potent anticancer agent.(7-14) In addition to direct cytotoxicity to cancer cells, a second benefit of benzaldehyde is the enhancement of the host immune system with increased numbers of Killer T Cells observed after treatment. (15)
Since cancer cells have increased glucose uptake to support fermentation (aerobic glycolysis, or Warburg Effect), it makes sense to conjugate the benzaldehyde to a glucose molecule, insuring avid uptake by the cancer cell, while sparing normal cells.
Previous work conjugating benzaldehyde to ascorbic acid was promising, “rapidly necrotized inoperable human lung cancer, and induced degeneration of rat hepatocellular carcinoma”.(12) Glucose and Ascorbate are very similar in molecular structure and both seen by the cancer cell as glucose with avid uptake. Previous work on Benzadehyde-Glucose conjugates showed promising results.(17-18)
Left Image: Two Basal Cell cancer Lesions of the EAR (dark areas) Before Treatment. Courtesy of Townsend Letter(2).
Nagalase is a cell surface protein secreted by cancer cells which allows immune evasion, preventing activation of MAF(Macrophage Activating Factor) . Recent studies measuring Nagalase levels before and after Salcinium reveals profound reduction in serum Nagalase in treated patients. This allows immune system to activate Macrophages which then attack the cancer cells.(2)
The routine protocol is a 15 session course of IV Salcinium infusions followed by Oral salicinium (Orasal). No toxicities have been reported (3)
Conclusion: Salicinium may represent a promising non-toxic anticancer agent.
Left Image , same lesions after 18 days Salicinium. Lesions are healing, smaller and less vascular. Courtesy of Townsend Letter (2)
Jeffrey Dach MD
7450 Griffin Road suite 190
Davie, Fl 33314
954-792-4663
Header Image: Salicinium Logo courtesy of Perfect Balance.
Links and References
Salicinium – glyco benzaldehyde
1) http://www.townsendletter.com/
http://www.townsendletter.com/
Salicinium – Disrupting Anaerobic Glycolosis and Improving GcMAF Immune Response
by Virginia Osborne, ND
2) http://www.townsendletter.com/
Salicinium: An Excellent Addition to My Armamentarium for Cancer Patients
by Carol M. Brown, DO, PhD, FAARFM’
3) http://www.naturodoc.com/
Guidelines for the Use of Salicinium (OraSal)
By Thomas S. Lee NMD, APH
free pdf
3) Matamoros, Morales Eric. “GcMAF: a polemic or a highly promising molecule?.” World Scientific News 65 (2017): 20-36.
4) https://www.erowid.org/
Darrell Lemaire In 2005, Joe Brown and Forrest Niccum hired Lemaire to help them with investigating the potential medicinal applications for some phytochemicals. Together they discovered that salicinium—a glucoside of 4-hydroxy-benzaldehyde, extracted from the plant Helicia nilagirica—shows great promise as a cancer treatment, with a survival rate in Stage 4 cancer patients of nearly 85%.
5) Orasal 250 http://forperfectbalance.com/
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benzaldehyde.
7) http://www.
Cancer Treat Rep. 1980 Jan;64(1):21-3.
Antitumor activity of benzaldehyde. Kochi M, Takeuchi S, Mizutani T, Mochizuki K, Matsumoto Y, Saito Y.
Ninety patients with inoperable carcinoma in the terminal stages and 12 patients in serious condition with other tumor types were given benzaldehyde in the form of beta-cyclodextrin benzaldehyde inclusion compound (CDBA) orally or rectally at a daily dose of 10 mg/kg divided in four doses. Toxic effects, including hematologic or biochemical disturbances, were not seen during long-term successive administration of CDBA. Fifty-seven of the patients treated were evaluable; 19 patients responded completely and ten patients responded partially (greater than 50% regression). For all responding patients longer response durations were associated with longer CDBA treatment periods. Treatment of squamous cell carcinoma induced the cancer cells to change into a conglomeration of pearls (the well-known product of differentiation) which consisted of keratinized normal squamous cells.
8) http://ar.iiarjournals.org/
Anticancer Res. 2010 Dec;30(12):5069-76.
Tumor-specific cytotoxicity and type of cell death induced by benzaldehyde.
Ariyoshi-Kishino K1, Hashimoto K, Amano O, Saitoh J, Kochi M, Sakagami H.
We have previously reported that sodium 5,6-benzylidene-L-ascorbate (SBA) induced dramatic antitumor activity in inoperable cancer patients, but induced only marginal tumor specificity in vitro. Here the tumor specificity and type of cell death induced by benzaldehyde (BA), a degradation product of SBA, was investigated, using human tumor cell lines (oral squamous cell carcinoma [OSCC], glioblastoma, myelogenous leukemia) and human normal oral cells (gingival fibroblast, pulp cell, periodontal ligament fibroblast). BA showed much higher tumor-specific cytotoxicity than SBA. BA induced the formation of autophagosomes, the destruction of mitochondrial structure and digestion of broken organelles, without any apparent induction of internucleosomal DNA fragmentation and caspase activation in an OSCC cell line HSC-2, in a similar manner to SBA. However, pretreatment with 3-methyladenine or bafilomycin A(1), autophagy inhibitors, did not completely rescue the cells from the cytotoxicity induced by BA. The study suggests that BA may play an important role in the induction of antitumor activity of SBA in vivo, although the autophagic phenotypes induced by BA may be involved in both cell death and survival.
9) http://cancerres.aacrjournals.
Abstract 4758: Benzaldehyde suppresses multiple signal pathways in cancer cells by regulating 14-3-3ζ-mediated protein-protein interactions Jun Saitoh and Hideyuki Saya
DOI: 10.1158/1538-7445.AM2016-4758 Published July 2016
Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA
Abstract Benzaldehyde is the simplest aromatic aldehyde constituent of almonds and many fruits. Anticancer effect of Benzaldehyde was first reported in 1980, and multi-institutional clinical trials were performed in those days in Japan. However trial was over without determination of effectiveness, only its safety was confirmed. The underlying mechanism why Benzaldehyde specifically suppresses growth of some particular cancer cells but not that of normal cells has not been elucidated. Therefore, we attempted to clarify the mechanism of anticancer effect of Benzaldehyde. In pancreatic cancer cell BxPC3 and in non-small cell lung cancer cell A549, we found that Benzaldehyde inhibits PI3K/AKT/mTOR, STAT3, NFκB and ERK pathways, those are major signaling pathways activated in cancer cells. Effects of Benzaldehyde on multiple signaling pathways are found to be derived from regulation of 14-3-3 family proteins which interact with phosphorylation sites of various proteins of multiple signals. In BxPC3 cells, Benzaldehyde treatment reduced the phosphorylation levels of 14-3-3-binding sites. Furthermore, we ectopically expressed seven isoforms of 14-3-3 in HEK293T cells and found that Benzaldehyde treatment significantly suppressed association of 14-3-3ζ with client proteins such as mTOR, Rictor, cRaf, STAT3 and FOXOs. The interaction of other isoforms of 14-3-3 with their client proteins was also partially reduced. But, the expression levels of those seven 14-3-3 isoforms were not significantly changed. Those data indicate that Benzaldehyde suppresses the interaction of 14-3-3ζ with its client proteins. Recent reports have shown that 14-3-3ζ is overexpressed in many cancers and acts as a signaling hub controlling the network of oncogenic pathways, suggesting that 14-3-3ζ associates with carcinogenesis, metastasis and resistance for chemotherapy and radiation. Hence, Benzaldehyde is considered to be a new class of anti-cancer agent inhibiting 14-3-3ζ-mediated tumor promoting and/or maintaining signals.
Citation Format: Jun Saitoh, Hideyuki Saya. Benzaldehyde suppresses multiple signal pathways in cancer cells by regulating 14-3-3ζ-mediated protein-protein interactions. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 4758.
Benzaldehyde
full pdf
10) Takeuchi, Setsuo, et al. “Benzaldehyde as a carcinostatic principle in figs.” Agricultural and Biological Chemistry 42.7 (1978): 1449-1451.
11) Kochi, Mutsuyuki, et al. “Antitumor activity of a benzaldehyde derivative.” Cancer treatment reports 69.5 (1985): 533-537.
12) Sakagami, H., et al. “Induction of tumor degeneration by sodium benzylideneascorbate.” Anticancer research 11.4 (1991): 1533-1538.
Anticancer Res. 1991 Jul-Aug;11(4):1533-8.
Induction of tumor degeneration by sodium benzylideneascorbate.
Sakagami H1, Asano K, Fukuchi K, Gomi K, Ota H, Kazama K, Tanuma S, Kochi M.
Intravenous administration of sodium benzylideneascorbate (SBA) rapidly necrotized inoperable human lung cancer, and induced degeneration of 3′-methyl-4-
13) http://journals.sagepub.com/
Chieco, P. A. S. Q. U. A. L. E., et al. “Quantitative histochemistry of benzaldehyde dehydrogenase in hepatocellular carcinomas of vinyl chloride-treated rats.” Journal of Histochemistry & Cytochemistry 34.2 (1986): 151-158.
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14) Ochiai, Hiroshi, Seihachiro Niwayama, and Kiichi Masuyama. “Inhibition of experimental pulmonary metastasis in mice by β-cyclodextrin-benzaldehyde.” Journal of cancer research and clinical oncology 112.3 (1986): 216-220. J Cancer Res Clin Oncol. 1986;112(3):216-20.
Inhibition of experimental pulmonary metastasis in mice by beta-cyclodextrin-
Ochiai H, Niwayama S, Masuyama K.
The effect of beta-cyclodextrin-benzaldehyde (CDBA) on experimental pulmonary metastasis in C3H/He mice was examined. In an in vitro assay, the growth of RCT(+) cells was inhibited by 1200 micrograms/ml CDBA using unrenewed media, and by 600 micrograms/ml CDBA in that using daily renewed media. When mice were treated daily with CDBA, 3 weeks later the number of lung nodules developing after i.v. injection of 1 X 10(6) RCT(+) cells was significantly decreased in a dose-dependent manner, i.e., 73.8%, 85.6%, and 95.7% inhibition was observed following 0.5, 5, and 25 mg CDBA/mouse per day p.o. administration, respectively. The same mice showed almost as much natural killer (NK) activity as normal mice. Therefore, experiments were designed to evaluate the effect of CDBA on the NK activity of tumor-free mice whose immunity had been suppressed by 5-fluorouracil (5FU). Injections of 5FU only suppressed this activity to about 50% of normal mice, but the combined treatment with CDBA negated the suppressive effect of 5FU on NK activity. The results suggested that the inhibition of experimental pulmonary metastasis might be induced by the possible combined effects of CDBA; that is, the direct inhibition of tumors and the augmentation of NK cell activity.
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15) https://www.ncbi.nlm.nih.gov/
J Cancer Res Clin Oncol. 1991;117(2):109-14.
Augmentation of murine lymphokine-activated killer cell cytotoxicity by beta-cyclodextrin-
We investigated the effect of beta-cyclodextrin-benzaldehyde (CDBA) on lymphokine-activated killer (LAK) cell activity of spleen cells from normal or RCT(+)H-2(+)-sarcoma-bearing C3H/He mice. CDBA augmented the induction of LAK cytotoxicity in vitro against RCT(+)H-2+ tumor cells by IL-2, whereas the culture with CDBA alone did not. In a LAK cytotoxicity assay in vitro, the augmentative effect of CDBA was strongly exerted against spleen cells originating from 2-week-tumor-bearing mice, rather than those from normal mice or mice that had born tumors for 5 weeks. Such an augmentative effect was not observed against other tumor cells (YAC-1, D-6, Colon-26 and EL-4 cells) non-specifically. When the intravenous adoptive transfer of LAK cells was carried out in the mice, LAK cells from tumor-bearing mice induced by combined culture with interleukin-2 (IL-2) and CDBA markedly inhibited the pulmonary metastases of RCT(+)H-2+ tumor, while neither LAK cells from the same tumor-bearing mice induced by only IL-2 nor those from normal mice inhibited the pulmonary metastasis. The majority of LAK cells induced either by IL-2 plus CDBA or by IL-2 alone were found to be Thy1.2+ and asialoGM1+ cells by flow-cytometric analysis, but no obvious phenotypical difference was observed between them. However, the most significant effect of CDBA might be the maintenance of the Lyt-2+ cell level in the spleen cells from tumor-bearing mice. These results suggested that the costimulation of spleen cells with IL-2 and CDBA might induce cytotoxic T cells specific for syngeneic tumor cells.
16) http://www.bloodjournal.org/
Reittie, Joyce E., et al. “Endogenously generated activated killer cells circulate after autologous and allogeneic marrow transplantation but not after chemotherapy.” Blood 73.5 (1989): 1351-1358.
17) https://www.ncbi.nlm.nih.gov/
Cancer Treat Rep. 1985 May;69(5):533-7. Antitumor activity of a benzaldehyde derivative.
Kochi M, Isono N, Niwayama M, Shirakabe K.
Benzaldehyde, in the form of 4,6-benzylidene-alpha-D-
18) https://www.ncbi.nlm.nih.gov/
Br J Cancer. 1990 Sep;62(3):436-9. 4, 6-0-benzylidene-D-
4, 6-0-Benzylidene-D-
19) Infusion Treatment Methods And Compositions Using Salicinium For Treating Cellular Proliferative Disorders And Immune Deficiencies
US 20110311477 A1 Publication date Dec 22, 2011 Inventors Joe Ernest BROWN
Chemical Structure of Salicinium
Link to this article: http://wp.me/p3gFbV-5bQ
Jeffrey Dach MD
7450 Griffin Road, Suite 190
Davie, Fl 33314
954-792-4663
www.jeffreydachmd.com
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