Muon disrupts AKT hydrogen bond network in cancer

Abstract

A cancer microenvironment generates strong hydrogen bond network system by the positive feedback loops supporting cancer complexity and robustness. Such network functions through the AKT locus generating high entropic energy supporting cancer metastatic robustness. Charged lepton particle muon follows the rule of Bragg effect during a collision with hydrogen network in cancer cells. Muon beam dismantles hydrogen bond network in cancer by the muon‐catalyzed fusion, leading to apoptosis of cancer cells. Muon induces cumulative energy appearance on the hydrogen bond network in a cancer cell with its fast decay to an electron and two neutrinos. Thus, muon beam, muonic atom, muon neutrino shower, and electrons simultaneously cause fast neutralization of the AKT hydrogen bond network by the conversion of hydrogen into deuterium or helium, inactivating the hydrogen bond networks and inducing failure of cancer complexity and robustness with the disappearance of a malignant phenotype.

Lysosome activates AKT inducing cancer and metastasis

“…Lysosome size depends on its activity, it is in the range from 0.1 to 1.2 μm and the size for example of an epithelial cell is about 10 μm. Excessive hyperactivation of lysosome by the fungi A. fumigatus causes prolonged oxidative burst, which activates aspergolam (aspergillus late activated molecule), the fungal protein inducing the formation of the constitutively active (permanently active) AKT locus, generating cancer complexity, robustness, metastasis, and cancer relapse in leukemia, lymphoma, or plasmocytoma . Such phosphorylated and activated AKT then controls lysosome function by the positive feedback loops, inducing an increase of lysosome size, number, acidification, cathepsin release, thus, inducing cancer metastasis or cancer relapse (Figure ).…”

“…During daily activity, humans inhale A. fumigatus conidia several hundred that can disseminate from lung and infect all organs, [49][50][51][52] which participates in the AKT lysosomal activation process. [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15] A. fumigatus as a very strong stimulant for the lysosomes and it is very important for the pathogenesis of cancer, inducing cancer by the activation of the AKT, transforming the AKT into constitutively active signaling element causing cancer. [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15] A. fumigatus is a strong inducer of inflammation and keeps inflammation prolonged especially in vitamin D deficiency 53 causing the lysosomal AKT activation inducing cancer development and metastasis or cancer relapse.…”

“…Such network is generated by the positive feedback loops of the cancer hypoxic microenvironment through the AKT locus activated by the oxidative burst of the intracellular organelle lysosome. [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15] Phosphorylated and activated AKT controls lysosome size, number, acidification, and autophagy process. 16 Activated AKT then regulates lysosomes, phagolysosome, phagosome, and autophagosome in their interconnected signaling.…”

“…Phosphorylated AKT induces cancer cell proliferation through the Rb/AKT/NO pathway, 3 the PI3K/AKT/mTOR/RAN pathway, 14 angiogenesis, and cancer cell migration through the VEGF/AKT/NOS/ICAM1 pathway, 15 generating a robust and complex system for cancer metastatic process or leukemia, lymphoma relapse through the AKT locus. [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15] Phosphorylated and activated AKT induces lysosome degradation of PTEN causing tumor metastasis. 17 Metastatic cells are sensitive to lysosomal inhibition, 18 which is controlled by the AKT.…”

“…17 Metastatic cells are sensitive to lysosomal inhibition, 18 which is controlled by the AKT. [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15] Excessive stimulation of lysosome causes release of cathepsin and proteolytic enzyme-inducing metastasis or leukemia relapse. 19,20 Such excessive process occurs in the Aspergillus fumigatus induced lysosomal AKT activation, by the lysosome burst causing generation of the constitutively active AKT gene inducing cancer.…”