A study by I. Baghli et al titled “Targeting the Mitochondrial-Stem Cell Connection in Cancer Treatment: A Hybrid Orthomolecular Protocol” published on 19 September 2024 discusses what has been, in some cases, known for decades: relatively cheap drugs can be repurposed for cancer treatment.
The paper is short at 16 pages. The main text is about eight pages, the remaining are references. Below is part of the abstract:
The mitochondrial-stem cell connection (MSCC) theory suggests that cancer originates from chronic oxidative phosphorylation (OxPhos) insufficiency in stem cells. This OxPhos insufficiency leads to the formation of cancer stem cells (CSCs) and abnormal energy metabolism, ultimately resulting in malignancy. This concept integrates two well-established theories: the cancer stem cell theory and the metabolic theory. … The aim of this hybrid orthomolecular protocol is to achieve additive and synergistic effects to enhance OxPhos, inhibit the primary fuels of cancer cells (glucose and glutamine), target CSCs and metastasis. …
The paper is essentially a review of other studies and discusses the effect of certain drugs and their possible mechanisms. This is followed by the actual protocol. It is probably easier to read the paper but extracts are reproduced below. This is not intended to be a summary and the protocol itself is not reproduced.
Vitamin C has been known for decades to have anti-cancer properties.
Vitamin C can target and eradicate CSCs (Bonuccelli, et al., 2017; Lee, 2023; Satheesh, et al., 2020), and protect against hypoxia and inflammation (Luo, et al., 2022). It can induce apoptosis in drug-resistant cancer cells, and inhibit uncontrolled proliferation of cancer cells and metastatic spread (Butt, et al., 2020). Vitamin C can also cause a polarization of M2 macrophages into M1 macrophages. This could be particularly relevant for inhibiting metastatic spread because M2 macrophages are implicated in metastases (Ma, et al., 2022). … In normal cells, vitamin C enters mitochondria in its oxidized form via glucose receptors (Glut1) and protects mitochondria from oxidative injury (Kc, et al., 2005). Thus, vitamin C can directly compete with glucose for cellular entry by glucose receptor.
Vitamin D has been shown to act against cancer of all types. Although it can reduce total cancer mortality, “this has not been observed for infrequent large bolus doses (Keum, et al., 2022)”.
Chandler et al. showed a preventive effect of vitamin D supplementation in patients with a normal body mass index (BMI), demonstrating a 37% reduction in the incidence of metastatic cancer (24 cancers in the vitamin D group and 39 cancers in the placebo group) leading to a reduction in cancer mortality of 42% (38 people in the Vitamin D group and 68 people in the placebo group). The dose utilized was 2000 IU/day, which is the recommended daily intake for a healthy individual (Chandler, et al., 2020).
Zinc deficiency has been linked to cancer.
In human ovarian cancer cells, zinc induces degradation of mitochondria, and restores apoptosis, especially if introduced together with zinc ionophores (Chen, et al., 2020). Zinc can suppress cancer stem cell-like properties of oral cancer and breast cancer cells in vitro (Chu, et al., 2023; Xu, et al., 2022), reduce the expression of markers of cancer cell stemness, and enhance sensitivity to chemotherapy in colorectal cancer cells (Ye, et al., 2022). Excess zinc can irreversibly block energy production of cancer cells, cause NAD+ loss, and inhibit cellular glycolysis (Wu, et al., 2022).
Ivermectin is an anti-parasitic drug derived from the bacteria Streptomyces avermitilis.
Ivermectin has shown a significant impact on various cancer cell lines (Juarez, et al., 2020), inducing apoptosis in cancer cells in vivo (Sharmeen, et al., 2010) and significantly reducing tumor volume compared to a control (Juarez, et al., 2020). … In vivo, Ivermectin alone is more effective than standard chemotherapy (gemcitabine) alone at reducing tumor weight and volume in pancreatic cancer (Lee, et al., 2022).
Benzimidazoles is a family of drugs used to treat worm infections in humans and animals. Mentioned in this paper are Mebendazole and Fenbendazole although only the former is FDA-approved for human use.
Benzimidazoles have anticancer effects through microtubule polymerization, induction of apoptosis, cell cycle arrest (G2/M), anti-angiogenesis, blocking glucose (Son, et al., 2020) and glutamine pathways (Mukherjee, et al., 2023). Apoptosis is induced by mitochondrial injury and mediated by p53 expression (Mukhopadhyay, et al., 2002; Park, et al., 2022). Benzimidazoles also target CSCs and metastases (Son, et al., 2020; Song, et al., 2022) and, thus, the chemoresistant (cisplatin) cancer cells (Huang, et al., 2021). Mebendazole was more potent against gastric cancer cell lines than other wellknown chemotherapeutic drugs (5-fluorouracil, oxaliplatin, gemcitabine, irinotecan, paclitaxel, cisplatin, etoposide and doxorubicin) in vitro (Pinto, et al., 2015).
DON (6-diazo-5-oxo-L-norleucine) is a glutamine antagonist.
It specifically targets glutamine and also affects glucose uptake (Leone, et al., 2019). DON can specifically induce apoptosis in CSCs (Jariyal, et al., 2021), and target metastases (Shelton, et al., 2010).
As for non-pharmaceutical considerations, fasting, ketogenic diet and ketone metabolic therapy (KMT), physical activity, hyperbaric oxygen therapy (HBOT) and press-pulse therapy (which is basically a combination of the aforementioned) may be helpful.
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