External Hyperthermia

Hyperthermia Cancer Institute- Los Angeles

external thermal therapy
Hyperthermia increases the treatment response rate for some previously irradiated tumors by 44 percent more than radiation alone(2).

External hyperthermia has been successfully used to improve the response rate of radiation or chemotherapy. Many randomized and scientifically conducted research by respected scientists have shown that the response rate can be doubled when hyperthermia is combined with external beam radiation. External hyperthermia is generally used for superficial tumors that do not exceed 4 to 5 centimeter in depth.

Hyperthermia uses an external applicator, which is applied to the outside of patient’s body on or near the tumor. The applicator looks like a box and has a plastic water-filled bag at the bottom which will lie next to patient. In a typical external treatment, the patient lays on a therapy table so that he or she can be comfortably positioned for treatment. A physicist or therapists monitors the temperature to make sure the temperature of the tumor reaches the therapeutic temperature (106º to 110º Fahrenheit).

Scientists attribute the death of cancer cells at hyperthermic temperature to damage of the plasma membrane, the cell skeleton, and the cell nucleus. Cancer cells are particularly susceptible to hyperthermia treatment due to their high acidity. Hyperthermia works synergistically with radiation to induce an increase in cell killing. (2) Jones et al. J. Clin. Oncolo. 23, 3079-3085, 2005.

hyperthermia chart

sonotherm 2

Therapeutic gains from hyperthermia

In summary, clinical studies and experience have shown the following therapeutic gains from hyperthermia:

  • Improvement in survival rates
  • Improvement in local tumor control and the duration of local tumor control
  • Increased remission rates
  • Reduced morbidity
  • Direct destruction of the tumor cells
  • Improved palliation and stability of this effect
  • Improved quality of life
  • Increased effectiveness of other forms of treatment without increased toxicity
  • Improvement in tumor oxygenation, to increase the efficiency of radiation therapy
  • Destruction of heat sensitive and radiation-resistant cells
  • Improvement in the response rate to cytostatica (doxorubicin, mitomycin C, mitoxantrone, bleomycin, cisplatin, nitric acid, uric acid, and cyclosphosphamide)
  • Specific activation of the immune system
  • Expansion of the treatable range of tumors in terms of size and status
  • Increased uptake of cytostatica in cells
  • Synergistic interaction with cytostatica
  • Destruction of chemotherapy-resistant cells
  • Activator for gene therapies
  • Reduction in tumor size to enable resection and/or make it safer
  • Reduced disfiguration due to surgical tumor resection
  • Improvement in functional results after surgery
  • Increased effectiveness when repeating radiation therapy
  • Improved results when combined with radiation therapy and chemotherapy (thermoradiochemotherapy

Summarized by Dr. Sennewald, Medizinticchnik, gmbh

Molecular effectors of hyperthermia

  • Cell membrane, cytoskeleton
  • Changes in fluidity/stability of cell membrane
  • Changes in cell shape
  • Impaired transmembranal transport
  • Changes in membrane potential
  • Modulation of transmembranal efflux pumps (MDR)
  • Apoptosis induction
  • Intracellular proteins
  • Impairment of protein synthesis
  • Protein denaturation
  • Aggregation of proteins at the nuclear matrix
  • Induction of HSP synthesis(Heat Shock Proteins)
  • Nucleic acids
  • Impairment of RNA/DNA synthesis
  • Inhibition of repair enzymes
  • Altered DNA conformation
  • Other alterations of cell function
  • Intracellular metabolism of other substrates
  • Gene expression, signal transduction

Critical Reviews in Oncology/Hematology 43 (2002) 33–56

Interactions between heat and drugs

  • Acceleration of primary mode of action (alkylating reaction, protein damage, oxygen-radicals; DNA-strand breaks)
  • Increased intracellular drug concentration (drug uptake, membrane damage, protein damage, pH changes)

Critical Reviews in Oncology/Hematology 43 (2002) 33–56

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