a45Tumor Treatment

There are many cancer patients in our lives. Everyone thinks that once they have a cancer, they have a terminal illness. In fact, this disease can be treated. No matter whether it is benign or malignant, as long as the tumor is removed, it will get better after a period of recuperation. Now medicine has developed a new method for treating tumors called a45 tumor treatment, which is a treatment method that combines dynamics and characteristic immunity. So how is a45 tumor treatment treated?

Step 1: Oral or injection of photosensitizing drugs

Patients need to take photosensitizing drugs orally and inject catalytic substrates before treatment. Photosensitizing drugs have been used in the clinical diagnosis and treatment of malignant tumors for more than 20 years. They have selective affinity for cancer cells and can remain in them.

There are certain physiological differences between tumor tissue and normal tissue, such as larger interstitial spaces within tumor tissue and a higher proportion of macrophages. The absorption of photosensitizing drugs by tumor tissue can be 10 times or more higher than that by normal tissue, and the excretion of photosensitizing drugs by tumor tissue will be 72 hours later than that by normal tissue.

No obvious toxic side effects were found in the photosensitizing drug ingredients themselves or the intermediates involved in human metabolism. Normal human tissues that have taken in drugs will not trigger photodynamic reactions and produce cytotoxic substances if they are not irradiated by light.

Even if exposed to natural light, the cells will not be seriously damaged because the wavelength and irradiance of natural light do not meet the requirements for producing photodynamic reactions.

A45 is a new type of photosensitizer used in tumor treatment. It has the advantages of higher selective uptake rate in tumor tissue, stronger photosensitization effect and lower toxicity. It plays an excellent role in positioning tumor tissue and cancer cells. On this basis, precise treatment of tumors can be achieved.

Step 2: Radiation activates photosensitizer

The 45MV high-energy, low-dose rays emitted by the LA45 medical electron linear accelerator are used to irradiate the patient locally and throughout the body.

Photosensitizing drugs have photochemical properties. When irradiated by light of appropriate wavelength, photosensitizing drugs can absorb the energy of a photon to produce changes in molecular structure, from the ground state to the activated triplet state.

On the one hand, the excited triplet photosensitizer acts on tissue substrates or hydrogen atoms or electrons, and the products react with oxygen to form various oxides (reactive oxygen species, ROS). On the other hand, it directly transfers energy to oxygen to form singlet oxygen (1O2).

Both singlet oxygen and oxides have cytotoxic effects, especially singlet oxygen, which is the main form of damage that induces tumor necrosis in A45 tumor treatment. It can destroy the microvessels in the tumor, causing local ischemia and cell death. After a few days, the tissue in this area will necrotize and fall off, thereby achieving the purpose of local cancer treatment.

A45 tumor treatment uses 45MV high-energy, low-dose photon beams emitted by the LA45 medical electron linear accelerator as irradiation light. Its effective irradiation depth can penetrate 30cm into the human body, breaking through the limitations of traditional photodynamic therapy and having a good therapeutic effect on tumors located at both deep and shallow levels of the human body.

Step 3: Initiate cell apoptosis and necrosis

The singlet oxygen and oxides produced by the activation of photosensitizers can act on the mitochondria of tumor cells. Mitochondrial edema can cause rupture of the mitochondrial outer membrane, thereby initiating irreversible apoptosis and necrosis of tumor cells.

The mitochondrial membrane of a cell is composed of an inner and outer double membrane. Normally, the permeability of the inner mitochondrial membrane is very poor. During the treatment process, due to the damage and stress of the mitochondria of tumor cells, the permeability of the inner membrane suddenly increases, and a large amount of ions, water and other substances non-selectively enter the matrix, causing mitochondrial edema.

Mitochondrial edema can cause mitochondrial outer membrane rupture, and some pro-apoptotic substances in the membrane space, such as cytochrome C and apoptosis-inducing factor (apoptosis-inducing factor), can also cause mitochondrial edema.

factor, AIF), Smac/DIABLO, endonuclease G (endonuclease G, ends G), etc. are released into the cytoplasm.

The above substances that enter the cytoplasm combine with apoptosis activation factor 1 and procaspase-9 to form apoptotic bodies. Caspase-9 is activated, and Caspase-9 activates Caspase-3, which activates the Caspase protease system, and then activates a series of hydrolases, ultimately leading to apoptosis of tumor cells.