Even genetics researchers Hanselmann and Welter, who wrote the highly cited paper Origin of Cancer: An Information, Energy, and Matter Disease , 7 have been gathering evidence for and against alternative cancer etiology theories. In addition to the 1 SMT, these other theories are 2 microenvironment, 3 mitochondrion , and 4 aneuploidy categories, characterized by Hanselmann and Welter as each having 'supporting' and 'contradicting' evidence for the validity of the category itself.
The Warburg Effect is detectable in all tumors , whereas the research shows that the microenvironment can cause cancer , or most cancer cells show mutations and most tumors show aneuploidy. Some research argues against a reductionist model, while still upholding the majority view that cancer begins with the SMT, progresses to the microenvironment and then to the mitochondrion. An alternate holistic model suggests that the underlying mechanisms of deregulated cellular metabolism are associated with, but not necessarily caused by, mitochondrial dysfunction, and that mitochondrial dysfunction can promote cancer progression to an apoptosis-resistant or invasive phenotype through a variety of mechanisms.
This research allows him to conclude that respiratory insufficiency is the origin of cancer, and that the other initiation theories, including the SMT, arise either directly or indirectly from insufficient respiration. He believes that without a unifying agreement of how cancer arises, it becomes difficult to formulate a successful plan for effective treatment and prevention. Mechanisms of Mitochondrial Disruption Provide Therapeutic Opportunities Many vital cellular parameters are controlled by mitochondria.
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These include regulation of energy production, modulation of oxidation—reduction redox status, generation of reactive oxygen species ROS , contribution to cytosolic biosynthetic precursors such as acetyl-CoA and pyrimidines, and initiation of apoptosis through the activation of the mitochondrial permeability transition pore and Cytochrome C.
Changes in these parameters can shift the cell from a dormant state of differentiation to a proliferation state. There are many thorough investigations and positions on the role of mitochondrial dysfunction in cancer 1,10,11,16,17 and following is a summary.
Genetic Mutations. Cancer cells have been shown to display genetic and epigenetic mutations that activate irregular programs that are important in development, stress response, wound healing and nutritional status.
Mitochondria regulate the transcription factor Hypoxia-Inducible Factor 1 HIF-1 , which induces glycolysis under hypoxic conditions allowing cancer to thrive. HIF-1 is increasingly studied because it allows for survival and proliferation of cancerous cells due to its angiogenic properties thus inhibition of HIF-1 potentially could prevent the spread of cancer. Cancer cells require altered metabolism to efficiently incorporate nutrients into biomass and support abnormal proliferation. In addition, the survival of tumor cells outside of normal tissue context requires adaptation of metabolism to different microenvironments.
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Warburg theorized that to treat cancer is not to target mutated genes but enzymes that cancer cells depend upon more than normal cells for tumor cell growth, survival and proliferation. They are present in virtually all cancers.
Reactions involving electron transfers are known as oxidation-reduction reactions or redox reactions for which OXPHOS is the metabolic pathway. A redox reaction occurs as a result of two smaller reactions; one molecule loses one or more electrons, and simultaneously gains an oxygen atom, to become oxidized and another molecule gains an electron and loses an oxygen atom to become reduced. Cancer cells have an amazing tendency to reprogram their metabolic capability by inhibiting OXPHOS to elevate glycolytic metabolism. Reactive Oxygen Species and Antioxidants.
The increase of ROS in cancer cells is linked to many irregularities in cellular functions such as cell proliferation, migration, differentiation and apoptosis. High production of mitochondrial ROS in hypoxic cells has been shown to link cancer to ischemic disorders.
Mitochondria come together to kill cancer cells
When mitochondrial ROS production is too high, it is toxic to the cell and can induce apoptosis or necrosis as well as contribute to new abnormal tissue. The tumor suppressor p53 can arrest growth and initiate apoptosis.
In other contexts, p53 activation can also induce cellular deterioration. Excessive shortening of chromosomal telomeres activates p53, which results in mitochondrial dysfunction, increased ROS levels, and deterioration. Page 1, 2.
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Nearly a century of scientific research has revealed that mitochondrial dysfunction is one of the most common and consistent phenotypes of cancer cells.
Could Mitochondria Numbers Be the Key to Solving Cancer Drug Resistance?
A number of notable differences in the mitochondria of normal and cancer cells have been described. These include differences in mitochondrial metabolic activity, molecular composition of mitochondria and mtDNA sequence, as well as in alteration of nuclear genes encoding mitochondrial proteins. This book, Mitochondria and Cancer , edited by Keshav K. Singh and Leslie C.
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