Salicinium and the Immune System
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)
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)
Nagalase & Cancer Immunology
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)
Links and References
Salicinium – glyco benzaldehyde
Salicinium – Disrupting Anaerobic Glycolosis and Improving GcMAF Immune Response
by Virginia Osborne, ND
Salicinium: An Excellent Addition to My Armamentarium for Cancer Patients
by Carol M. Brown, DO, PhD, FAARFM’
Guidelines for the Use of Salicinium (OraSal)
By Thomas S. Lee NMD, APH
3) Matamoros, Morales Eric. “GcMAF: a polemic or a highly promising molecule?.” World Scientific News 65 (2017): 20-36.
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/order-now/
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.
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.
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.
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-dimethylaminoazobenzene-induced rat hepatocellular carcinoma (vacuolar, eosinophilic degeneration, nuclear debris) without affecting the serum glutamic oxaloacetic transaminase, gamma-glutamyl transpeptidase and total protein levels. Cultured normal human lung and skin fibroblasts, and human glioma and glioblastoma cell lines were relatively resistant to SBA, when compared to human myelogenous leukemic cell lines. SBA had no apparent host immunopotentiation activity such as stimulation of cytokine action or production; activation of monocyte or polymorphonuclear cells; or modulation of poly (ADP-ribose) glycohydrolase activity. The data suggest that the antitumor activity of SBA might be produced by direct action of authentic SBA or its metabolized form(s), rather than by immunopotentiation of the hosts.
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.
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-benzaldehyde.
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.
J Cancer Res Clin Oncol. 1991;117(2):109-14.
Augmentation of murine lymphokine-activated killer cell cytotoxicity by beta-cyclodextrin-benzaldehyde. Kuroki Y1, Ochiai H, Kurokawa M, Niwayama S, Kishimoto C, Tazawa K, Fujimaki M.
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.
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.
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-glucose (BG), was given iv at a daily dose of 720-1800 mg/m2 to 65 patients with inoperable carcinoma in the advanced stages. The overall objective response rate was 55%; seven patients achieved complete response, 29 achieved partial response, 24 remained stable, and five showed progressive disease. Response was seen in various cell types. Prolongation of survival was apparent for the patients. Toxic reactions were not observed during long-term injection with BG.
Br J Cancer. 1990 Sep;62(3):436-9. 4, 6-0-benzylidene-D-glucopyranose (BG) in the treatment of solid malignant tumours, an extended phase I study. Tatsumura T1, Tsujimoto M, Koyama S, Furuno T, Komori Y, Sato H, Yamamoto K, Kitagawa M, Kagamimori S.
4, 6-0-Benzylidene-D-glucopyranose (BG), a derivative of benzaldehyde (BA), whose anti-tumour action has often been reported, showed responses in 10 out of 24 patients (41.7%). These patients consisted of 11 cases of primary lung cancer, 4 of metastatic lung cancer, 5 of gastric cancer, and one each of cancer of the sigmoid colon, liver, pancreas and prostate. There were two complete responses (one each of ipsilateral lung metastasis from breast cancer and metastatic liver lesions due to gastric cancer). The mean total dose of BG was 392.6 g, given by intravenous infusion of 1.2 g BG in 100 ml saline twice daily. The treatment was discontinued when no response was observed after two months. Careful monitoring showed no toxic action of BG at these large doses. Complete necrotic liquefaction of tumour, without any damage to surrounding tissue, was seen in 2 of 3 cases in which histological examination was feasible. It is apparent that BG, like BA, is not a cytotoxic agent in the ordinary sense, but its mechanism of action is still unknown.
US 20110311477 A1 Publication date Dec 22, 2011 Inventors Joe Ernest BROWN
In 1931 a German physician/scientist, Otto Warburg MD, PhD, received a Nobel prize for proving that all cancer cells use anaerobic metabolism (burn sugar without using oxygen) to produce energy. The problem (for the cancer cell) is that this mechanism is 18 timesless efficient than the aerobic (oxygen utilizing) metabolism that our normal cells use. That means the cancer cells need 18 times more sugar than normal cells to grow and prosper. n
Text under construction
Salicinium is a natural plant based extract, a complexed sugar molecule that is harmless to normal cells in the body because they cannot absorb a “complex glycome”. Because this extract is a complexed molecule and not a “free” glucose, it has no impact on the patients’ blood sugar.
Salicinium targets anaerobic cancer cells
The composite Salicinium molecule will only affect anaerobic (cancer) cells destroying the enzymatic “cloak” which allows them to hide from the immune system.
Circulating tumor cells are at the forefront of an ongoing or escalading malignant process. Salicinium affects these cells first, therefore, contributing to halting the spread of malignancy.
- Continued use of Salicinium will allow the immune system to steadily attack remaining malignant cells.
- This therapy, whether I.V. or oral, should be continued without interruption until testing shows no further indicators of cancer.
- Salicinium is completely targeted- it will only enter anaerobic cells.
- Salicinium allows GcMAF to resume operation, greatly increasing the effectiveness of the immune system.
- Salicinium does not kill the malignant cells- the immune system does.
- As tissue levels of Salicinium build up more and more cancer cells die.
- Salicinium is used in the context of an integrative protocol to enhance the effectiveness of other therapies.
Salicinium is a prospective adjunt to orthodox chemotherapy, as neither interferes with function of the other. However, by using Salicinium, the dosage of the chemotherapy can be reduced to a fraction (10%-15%) of the full dose. This is especially true when the chemo drugs are administered in the setting of IPT therapy. This combined type of therapy is dictated by the seriousness and stage of the malignancy.
For more information, got to:
Every normal cell in our body takes in oxygen from our blood to perform its function; this is called respiration or an aerobic process and this process takes place in the mitochondria. Cells take in oxygen and perform their functions by producing a chemical called Adenosine tri-phosphate or ATP for short, which is the vital energy that runs our entire body.
Nobel Laureate Dr. Otto Warburg published in 1926 that by placing normal cells in a vacuum chamber and lowering oxygen content by 35%, normal cells had the ability to continue living without respiration: it is a survival process that every single cell in our body has the ability to do. This is called an anaerobic process meaning without oxygen or respiration.
Every cell in our body has a completely different set of enzymes and a completely different way of living than by respiration which is quiescent until needed. We experience this every time we work or exercise too hard and our oxygen starved muscles become sore. The soreness is caused by the formation of Lactic Acid as some of our cells live anaerobically while returning to respiration. Dr. Warburg realized that after a short time in hours, one could add oxygen back and those cells would return to aerobic activity. However, if held in a reduced oxygen state long enough they become committed to being anaerobic cells. If oxygen is depleted long enough, cells lose their RNA and DNA identity and are permanently obligated anaerobic cells reproducing only other anaerobic cells.
This new way of living for the formerly normal aerobic cell is called anaerobiasis and is accomplished by a process of fermentation. These cells now produce only five percent as much ATP or energy as formerly. They now ferment simple sugars—any sugar; it makes no difference to a fermenting cell what type of sugar. It is believed they have the ability to develop 19 times the number of sugar receptors on their surface as normal cells. If it weren’t for this low-energy phenomenon cancer would grow at the same rate as our normal cells and we would die very quickly. All dedicated or obligated fermenting cells have a universal co-enzyme called NAD+ and its function is very simple. Anaerobic or fermenting cells which include malignant cells all have a very acidic outside environment and an alkaline inside environment.
The NAD+ coenzyme travels the inside of the cell attaching itself to a hydrogen atom becoming NADH- and then transferring the hydrogen through the Trans Golgi Network to the outside by way of lactate and into the bloodstream. Taking the hydrogen from inside the cell to the outside, repeating this simple cycle of dismutation over and over again. A lack of hydrogen is alkaline and an abundance is acid. Medical science says there are 210 different types of cells. This means there are 210 different places – or different tissues – in the human body for anaerobic malignant or cancerous) cells to grow but the one function of the NAD+ co-enzyme is universal to all of those 210 different fermenting cells.
Glycome means sugar. Salicinium is a Glycome; a complexed molecule, the active ingredient being attached to a glycome. The sugar hungry malignant cell sees the glycome passing by in the blood, takes it in and very quickly another enzyme universal only to fermenting cells, beta-Glucosidase splits the sugar from the combined molecule. The NON-glycome material in Salicinium upon being released, attaches to the NAD+co-enzyme and disrupts the fermentation process by stopping dismutation. This is now the crux or turning point in the life of a fermenting cell.When a person first learns they have cancer their first question usually is: “How did I get it, where did it come from?
Salicinium changes the way the macrophage of the immune system recognizes diseased cells through immune modulation. The Nagalase enzyme produced by anaerobic cells shuts down the natural function of the immune system providing safety for these diseased cells.
The composite Salicinium molecule will only affect anaerobic cells destroying the enzymatic “cloak” which allows them to hide from the immune system’s NK cells. Salicinium stops the production of Nagalase and lactate removing their protection while simultaneously stimulating the the innate immune macrophage to eliminate these diseased cells. Circulating tumor cells are at the forefront of an ongoing or escalating malignant process. CTC testing has shown Salicinium affects these cells first therefore halting the spread of malignancy. Continued use of Salicinium will allow the immune system to steadily attack remaining malignant cells. The same testing also induces the death of cancer stem cells and Salicinium therapy, whether I.V. or oral, should be continued without interruption until testing shows no further indicators of malignancy.
and here is MORE science
Salicinium – Disrupting Anaerobic Glycolosis and Improving GcMAF Immune Response
by Virginia Osborne, ND
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