Call us today! 1.800.923-7878
Sunridge Medical Logo

DCA Treatment and Cancer

It is noted that cancer cells thrive in a low oxygen environment with low pH values and that raising the cell pH makes it hard for cancer cells to survive. DCA (Dichloroacetic Acid) is believed to work by turning on the oxygen-generating energy systems within all cells. It increases the oxygenation within the cancer cell and disrupts intracellular anaerobic metabolism. In an oxygenated environment, cancerous cells can no longer survive.

DCA Treatment

DCA Cancer treatment at Sunridge Medical At Sunridge Medical, our highly-trained physicians are experts in providing an integrated approach to the treatment of cancer and chronic disease. Our treatment plans are individualized and involve both traditional and alternative medicines including DCA. The physicians at Sunridge Medical have found that symptoms frequently can be improved and even reversed with our natural treatments. We take a holistic approach to patient care and strive not only to treat the disease, but also to alleviate symptoms, increase the quality of life and, most importantly, address the underlying cause of disease.

References on DCA

Tataranni, T., & Piccoli, C. (2019). Dichloroacetate (DCA) and Cancer: An Overview towards Clinical Applications. Oxidative medicine and cellular longevity, 2019, 8201079.

An extensive body of literature describes anticancer properties of dichloroacetate (DCA), but its effective clinical administration in cancer therapy is still limited to clinical trials. The occurrence of side effects such as neurotoxicity as well as the suspicion of DCA carcinogenicity still restricts the clinical use of DCA. However, in the last years, the number of reports supporting DCA employment against cancer increased also because of the great interest in targeting metabolism of tumor cells.

Dissecting DCA mechanism of action helped to understand the bases of its selective efficacy against cancer cells. Successful coadministration of DCA with conventional chemotherapy, radiotherapy, other drugs, or natural compounds has been tested in several cancer models.

New drug delivery systems and multi-action compounds containing DCA and other drugs seem to ameliorate bioavailability and appear more efficient thanks to a synergistic action of multiple agents. The spread of reports supporting the efficiency of DCA in cancer therapy has prompted additional studies that led to find other potential molecular targets of DCA. Interestingly, DCA could significantly affect cancer stem cell fraction and contribute to cancer eradication. Collectively, these findings provide a strong rationale towards novel clinical translational studies of DCA in cancer therapy.

Wang, Y., Gao, F., Li, X., Niu, G., Yang, Y., Li, H., & Jiang, Y. (2022). Tumor microenvironment-responsive fenton nanocatalysts for intensified anticancer treatment. Journal of nanobiotechnology20(1), 69.

Chemodynamic therapy (CDT) based on Fenton or Fenton-like reactions is an emerging cancer treatment that can both effectively fight cancer and reduce side effects on normal cells and tissues, and it has made important progress in cancer treatment. The catalytic efficiency of Fenton nanocatalysts(F-NCs) directly determines the anticancer effect of CDT. To learn more about this new type of therapy, this review summarizes the recent development of F-NCs that are responsive to tumor microenvironment (TME), and introduces their material design and action mechanism.

Based on the deficiencies of them, some effective strategies to significantly improve the anticancer efficacy of F-NCs are highlighted, which mainly includes increasing the temperature and hydrogen peroxide concentration, reducing the pH, glutathione (GSH) content, and the dependence of F-NCs on acidic environment in the TME. It also discusses the differences between the effect of multi-mode therapy with external energy (light and ultrasound) and the single-mode therapy of CDT. Finally, the challenges encountered in the treatment process, the future development direction of F-NCs, and some suggestions are analyzed to promote CDT to enter the clinical stage in the near future.
Lee TG, Jeong EH, Min IJ, Kim SY, Kim HR, Kim CH. Altered expression of cellular proliferation, apoptosis and the cell cycle-related genes in lung cancer cells with acquired resistance to EGFR tyrosine kinase inhibitors. Oncol Lett. 2017 Aug;14(2):2191-2197. doi: 10.3892/ol.2017.6428. Epub 2017 Jun 20. PMID: 28781659; PMCID: PMC5530116.
Non-small cell lung cancers harboring somatic gain-of-function mutations in the epidermal growth factor receptor (EGFR) tyrosine kinase domain respond well to treatment with EGFR tyrosine kinase inhibitors (TKIs) including gefitinib and erlotinib. However, all patients who experience a marked improvement with these drugs eventually develop disease progression due to the acquisition of drug resistance. Approximately half of the cases with acquired resistance to EGFR TKIs can be accounted for by a second-site mutation in exon 20 of the EGFR kinase domain (T790M).
However, the changes of gene expression involved in EGFR TKI resistance due to the T790M mutation remain poorly defined. The present study established lung cancer cell lines that were resistant to gefitinib or erlotinib, and these cell lines were verified to contain the EGFR T790M mutation.
The differential expression of genes associated with acquired resistance was verified in the present study by mRNA microarray analysis. Among the genes whose expression was significantly altered, genes whose expression was altered in gefitinib- and erlotinib-resistant cells were focused on. Notably, a total of 1,617 genes were identified as being differentially expressed in gefitinib- and erlotinib-resistant cells.

Indeed, gene ontology analysis revealed altered expression of genes involved in the regulation of cellular proliferation, apoptosis, and the cell cycle in EGFR TKI-resistant cells. The present results demonstrate distinctive gene expression patterns of EGFR TKI-resistant lung cancer cells with the EGFR T790M mutation. The present study can provide key insights into gene expression profiles involved in conferring resistance to EGFR TKI therapy in lung cancer cells.

For answers or to make an appointment, call us toll-free at 800-923-7878 to speak with a Patient Care Team. Recover your vitality, reclaim your energy and rediscover your health.
Schedule Appointment
Contact Us Today.  Call 1.800.923.7878 to speak to our patient care team

Table of Contents

Helpful Links

  • About Us
  • Become A Patient
  • Contact Us
  • Frequently Asked Questions
  • Travelling to Sunridge
  • Maps and Directions
  • New Patient Form Download
How can we help you today?
Our Patient Care Team is always available to answer any of your questions. Get in touch with us today!
Call today
Have a Question or Share Feedback:
It's easy to get in touch with us