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https://fnote.me/notes/52gxYD have demonstrated that the non-ionizing RF EMF produces antiproliferative effects on HCC cells. Extra resources that drives AM RF EMF's anticancer activity in vitro is thought to involve down-regulation in cancer-related stem cells. This could be the reason for the long-term responses seen in some patients with advanced HCC. However, the mechanism behind AM EMF's effects on cancer patients is not yet clear.

Effects from AM RF EMFs on HCC tumour growth in vivo was studied in mice. The tumors were split into three groups. One group did not have exposure to RF EMF. Second group members were exposed to RF EMF at the same frequency to that used in humans. Third group members were exposed to the RF EMF in HCC-specific frequencies. The effects of HCCMF on tumours was evaluated against that of RCF. The results indicated that tumors treated by HCCMF had significant shrinkage. However, the tumours treated with RCF did not show any evidence of shrinkage in the tumour.

The reason for tumour-specific AM RF EMF might be based on the fact that cancer cells require Cav3*2 T-type voltage calcium channels to promote proliferation and down-regulation. AM RF EMF's antiproliferative effect in HCC cells is controlled by CACNA1H which is a protein which mediates tumour-specific Ca2+ influx. The results suggest that CACNA1H may have broader implications in the diagnosis and treatment of various cancers.

The tumors in the controls were never exposed to RF EMF, and were fed a normal mouse diet. The tumors of HCCMF HCCMF group were treated with Huh7 cells at the time they were between five and seven weeks old. The tumors were removed when they showed excessive burden.


The tumours in the three groups also displayed different growth curves. The HCCMF-treated tumors showed a significant decrease in size of the tumor after 8 weeks. However, the tumors that were treated using RCF didn't show signs of shrinkage. The difference was significant. The tumours treated with RCF showed necrosis, which is common when tumors are that are exposed to RCF. It is possible that the necrosis is caused by the lack of oxygen in larger tumors.

In summary, the results suggest the fact that AM EMF exhibits anticancer activity in vitro and in live. Several studies have shown the fact that AM RF EMF produces measurable tumour shrinkage within HCC patients. It is possible that AM RF EMF causes these effects due to CACNA1H which is a protein involved in tissue-specific Ca2+ influx. Furthermore, AM RF EMF may exert a sustained influence on the development of HCC tumours in vivo.