The mission of Nanothermia, or modulated electro-hyperthermia (mEHT), is to heal cancer, increase life expectancy and improve the quality of life of the patients with cancer. Modulated electro-hyperthermia (mEHT) is a complementary antitumor therapy applying capacitive radiofrequency at 13.56 MHz. It is a personalized, non-toxic therapy using an electric field and promoting the body’s natural regulatory processes.
Unlike conventional HT, however, mEHT does more than simply warm deep layers of tissue or function solely via certain thermodynamic parameters like temperature, it also combines such warming with a modulated electric field, generated by two active electrodes. Micro-biological tests have proven that malignant tissue has higher conductivity than healthy human tissue.
As a result, mEHT selectively destroys malignant cells by applying the required specific energy dose, inhibiting the natural activity of malignant cells, as well as triggering and supporting the body‘s immune response. When this therapy is combined with dendritic cell therapy (DCT), the effect of both improves considerably, since their effects are mutually beneficial.
The special feature of mEHT is that it promotes the renewal of cell junctions (e.g. E-cadherin and βß-catenin junctions), thereby facilitating the natural cell death process (apoptosis). Apoptosis is an orderly process in which the cell’s contents are packaged into small packets of membrane for “garbage collection” by immune cells.
mEHT selects at the cellular level, being malignant cells selectively destroyed. The selection occurs as a result of special metabolic characteristics of malignant cells. The special feature of mEHT is that it promotes renewed formation of cell connections (E-cadherin and βß-catenin junctions), thereby facilitating the apoptosis. Cell scattering is reduced, and apoptosis is initiated via delocalization of β-catenin and activation of the tumour-suppressor protein p53.
The tumour suppressor p53 protein plays an important role in cell-cycle regulation, and its inactivating mutations are pivotal to tumorigenesis in many human malignancies.