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Cancer-Critical Genes I: Proto-oncogenes01:33

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Engineering Oncogenic Heterozygous Gain-of-Function Mutations in Human Hematopoietic Stem and Progenitor Cells
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Energy parasites trigger oncogene mutation.

Jiří Pokorný1, Jan Pokorný1, Anna Jandová2

  • 1a Institute of Physics, Czech Academy of Sciences , Prague , Czech Republic ;

International Journal of Radiation Biology
|August 23, 2016
PubMed
Summary
This summary is machine-generated.

Parasitic virus energy consumption disrupts cellular electromagnetic fields, increasing random genome mutations and initiating cancer. This energy mechanism explains genome mutation and cancer development.

Keywords:
Cancer initiationLDH viruscell-mediated immunitycoherent electromagnetic statesgenome somatic mutationparasitic energy consumption

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Area of Science:

  • Oncology
  • Virology
  • Biophysics

Background:

  • Cell-mediated immunity (CMI) analysis of 12,000 cases revealed similarities between cancer antigens and lactate dehydrogenase-elevating (LDH) virus.
  • LDH virus RNA impacts cellular electromagnetic fields, affecting DNA stability.
  • Precancerous cervical lesions (CIN) showed mixed CMI responses, indicating a transitional state.

Purpose of the Study:

  • To investigate the role of parasitic virus energy consumption in cancer initialization.
  • To explore the relationship between cellular electromagnetic fields, genome stability, and cancer development.
  • To elucidate the energy mechanism underlying genome mutation and cancer initiation.

Main Methods:

  • Analysis of cell-mediated immunity (CMI) data from 12,000 healthy individuals, cancer patients, and patients with precancerous cervical lesions.
  • Comparison of immune responses to specific cancer antigens and a non-specific lactate dehydrogenase-elevating (LDH) virus antigen.
  • Assessment of the impact of LDH virus RNA on the ratio of coherent/random oscillations in cellular electromagnetic fields.

Main Results:

  • Both specific cancer antigens and the non-specific LDH virus antigen elicited similar CMI responses across various patient groups.
  • The non-specific LDH virus antigen showed efficacy in all examined cancers, unlike specific antigens.
  • LDH virus RNA was found to reduce the ratio of coherent/random oscillations, decreasing the influence of the cellular electromagnetic field on DNA bonding.

Conclusions:

  • Parasitic virus energy consumption, leading to reduced coherent cellular electromagnetic fields, increases the probability of random genome reactions and cancer initiation.
  • The energy mechanism involving cellular electromagnetic fields and biochemical reaction rates provides a novel explanation for genome mutation.
  • CMI responses to cancer and LDH virus antigens support an energy-based mechanism in cancer development.