Effects of Alkalization Therapy on Chemotherapy Outcomes in Advanced Pancreatic Cancer: A Retrospective Case-Control Study

Hamaguchi, Reo; Ito, Takashi; Narui, Ryoko; Morikawa, Hiromasa; Üemoto, Shinji; Wada, Hiromi

doi:10.21873/invivo.12080

Cited by 18 publications

(20 citation statements)

References 34 publications

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“…An animal study has shown that there is a correlation between changes in pH of the TME and changes in urine pH induced by alkalizing agents (30). Alkalization therapy tended to be more effective in patients with a higher urine pH in our clinical studies described above (50,(53)(54)(55), suggesting that urine pH may be an alternative indicator of the pH around cancer cells. It should be noted that these studies have not demonstrated the association between urine pH and tumor pHe/pHi ratio.…”

Section: Future Directions Of Alkalization Therapymentioning

confidence: 62%

“…A significantly prolonged median OS was observed in patients with a urine pH of higher than 7.0, compared with patients with a urine pH of 7.0 or lower (n = 28, 16.1 vs. 4.7 months; p < 0.05). Moreover, a retrospective case-control study was conducted to investigate the effects of alkalization therapy on chemotherapy outcomes in recurrent or metastatic pancreatic cancer patients ( 54 ). Patients in the alkalization group (alkalization therapy plus chemotherapy, n = 36), which included patients from the above retrospective study, were compared with patients in the control group (chemotherapy only, n = 89).…”

Section: Clinical Reports Of Alkalization Therapy For Cancermentioning

confidence: 99%

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Clinical review of alkalization therapy in cancer treatment

et al. 2022

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One of the most unique characteristics of cancer metabolism is activated aerobic glycolysis, which is called the “Warburg effect”, and is a hallmark of cancer. An acidic tumor microenvironment (TME) resulting from activated anaerobic glycolysis is associated with cancer progression, multi-drug resistance, and immune escape. Several in vitro and in vivo studies reported that neutralization of the acidic TME by alkalizing agents, such as bicarbonate, resulted in the suppression of cancer progression and a potential benefit for anti-cancer drug responses. In clinical settings, alkalizing effects were achieved not only by alkalizing agents, but also by a following a particular diet. An epidemiological study demonstrated that more fruits and vegetables and less meat and dairy products are associated with an increase in urine pH, which may reflect the alkalizing effect on the body. However, it remains unclear whether alkaline dietary intervention improves the effects of cancer treatment. Moreover, there are few clinical reports to date regarding cancer treatments being performed on patients together with alkalization therapy. In this review, we investigated whether alkalization therapy, which includes an alkaline diet and/or alkalizing agents, improves cancer treatment.

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Section: Future Directions Of Alkalization Therapymentioning

confidence: 62%

Section: Clinical Reports Of Alkalization Therapy For Cancermentioning

confidence: 99%

Clinical review of alkalization therapy in cancer treatment

et al. 2022

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“…However, the measurement of the acid-alkaline level of the microenvironment surrounding the cancer is not available in current clinical practice ( 12 , 66 , 67 ). We found that in all cases where various cancer treatments were effective using our ‘alkalization therapy’, the urine pH became alkaline ( 19 – 21 , 68 , 69 ). Due to the impossibility of measuring the pH of the microenvironment surrounding the cancer, we use the patient’s urine pH as a surrogate indicator to practice alkalization of it.…”

Section: Discussionmentioning

confidence: 89%

“…This means that it is possible to reduce the entropy of the body. It is our experience that alkalization of the TME enables various treatments to become more effective, and with the future collaboration of many researchers, we hope that it will soon become possible to treat intractable cancers using standard treatments combined with alkalization therapy (19,21,21,68,69,77,78).…”

Section: Discussionmentioning

confidence: 99%

Meaning and Significance of “Alkalization Therapy for Cancer”

et al. 2022

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Objectives of the StudyOur research aims to answer the following questions. Can cancer progression be stopped by changing the body condition of person with cancer? Can cancer be cured?If cancer progression can be stopped, what is the underlying mechanism?Theoretical Rationale for Alkalization TherapyAlmost 70 years ago, Goldblatt H. & Cameron G. reported on the idea of alkalization therapy. Before that, Otto Warburg had been studying the metabolism of cancer and had discovered the essential nature of cancer. He published a review in Science in 1956 under the title “On the origin of cancer cells”. From his phenomena described above, we established the theoretical rationale for alkalization therapy, based on the question of “How does cancer form and what is its nature”?Limitations of Deductive Methods and Inductive ApproachesIn this paper, we describe a method to reconstruct the limitations and weaknesses of modern cancer medicine as Science-based Medicine using an inductive method, and to present a new vision of cancer therapy. How should we treat cancer? (Case presentation): Using a specific clinical case, we present patients in whom were successfully treated with no or few anticancer drugs.SummaryThe biggest weakness of current cancer treatments is that they only treat the cancer and not the actual patient. The “alkalization therapy” that we advocate does not compete with any of the current standard treatments, but improves the effectiveness of standard treatments, reduces side effects, and lowers medical costs.

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“…First, the Warburg effect is not necessarily a function of faulty mitochondria, but one of its main purposes is to sustain tumor microenvironment acidity (33), which is paramount to invasive metastasis, chemo resistance and immune escape (34,35). Secondly, while the mitochondrial electron transport chain (ETC) and OXPHOS is required to sustain tumor growth and ATP production when needed (33,36,37), high levels of either oxygen and/or greater mitochondrial biogenesis will drive tumorigenic processes as evidenced by perioperative surgical, experimental models (6-8) and investigation of stem cell metabolism (9, 10). While previous therapeutic attempts have involved experimenting with glycolytic inhibitors (38), a fairly new area of anti-cancer therapy now includes deployment of mitochondria-targeted therapeutics, however challenges in using classical inhibitors of OXPHOS are not without counter-indication, as mitochondrial inhibitors have a long history of contributing to degenerative diseases such as Parkinson's or Alzheimer's disease (39,40).…”

Section: Discussionmentioning

confidence: 99%

Metabolic Response to the Mitochondrial Toxin 1-Methyl-4-phenylpyridinium (MPP+) in LDH-A/B Double-knockout LS174T Colon Cancer Cells

Mack

Mazzio

Badisa

et al. 2021

Cancer Genomics Proteomics

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Background/Aim: Rapid glycolytic substrate-level phosphorylation (SLP) and accumulation of lactic acid are characteristics of diverse cancers. Recent advances in drug discovery have included the use of glycolytic inhibitors with mitochondrial targeting drugs to attempt to invoke an energy crisis in aggressive metabolically active chemo-resistant cancers. In this work, we examine the consequences of inhibiting mitochondrial oxidative phosphorylation (OXPHOS) with 1-methyl-4-phenylpyridinium (MPP+) in LS14T colon cancer cells containing a genetic double knock out (DKO) of lactic acid dehydrogenase (LDHA and LDHB). Materials and Methods: Several metabolic parameters were evaluated concomitant to whole transcriptomic (WT) mRNA, microRNA, and long intergenic non-coding RNAs using Affymetrix 2.1 human ST arrays. Results: MPP+ effectively blocked OXPHOS where a compensatory shift toward anaerobic SLP was only observed in the control vector (CV), and not observed in the LDH-A/B DKOs (lacking the ability to produce lactic acid). Despite this, there was an unexpected resilience to MPP+ in the latter in terms of energy, which displayed significantly higher resting baseline respiratory OXPHOS capacity relative to controls. At the transcriptome level, MPP+ invoked 1738 differential expressed genes (DEGs) out of 48,226; LDH-A/B DKO resulted in 855 DEGs while 349 DEGs were found to be overlapping in both groups versus respective controls, including loss of mitochondrial complex I (subunits 3 and 6), cell cycle transcripts and fluctuations in epigenetic chromatin remodeling systems. In terms of energy, the effects of MPP+ in the CV transcripts reflect the funneling of carbon intermediates toward glycolysis. The LDH-A/B DKO transcripts reflect a flow of carbons away from glycolysis toward the production of acetyl-CoA. Conclusion: The findings from this study suggest a metabolic resilience to MPP+ in cancer cells devoid of LDH-A/B, explainable in-part by higher baseline OXPHOS respiratory ATP production, necessitating more toxin to suppress the electron transport chain.

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Effects of Alkalization Therapy on Chemotherapy Outcomes in Advanced Pancreatic Cancer: A Retrospective Case-Control Study

Cited by 18 publications

References 34 publications

Clinical review of alkalization therapy in cancer treatment

Clinical review of alkalization therapy in cancer treatment

Meaning and Significance of “Alkalization Therapy for Cancer”

Metabolic Response to the Mitochondrial Toxin 1-Methyl-4-phenylpyridinium (MPP+) in LDH-A/B Double-knockout LS174T Colon Cancer Cells

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