Abstract

In this review, we propose a holistic approach to understanding cancer as a metabolic disease. Our search for relevant studies in medical databases concludes that cancer cells do not evolve directly from normal healthy cells. We hypothesize that aberrant DNA damage accumulates over time—avoiding the natural DNA controls that otherwise repair or replace the rapidly replicating cells. DNA damage starts to accumulate in non-replicating cells, leading to senescence and aging. DNA damage is linked with genetic and epigenetic factors, but the development of cancer is favored by telomerase activity. Evidence indicates that telomere length is affected by chronic inflammations, alterations of mitochondrial DNA, and various environmental factors. Emotional stress also influences telomere length. Chronic inflammation can cause oxidative DNA damage. Oxidative stress, in turn, can trigger mitochondrial changes, which ultimately alter nuclear gene expression. This vicious cycle has led several scientists to view cancer as a metabolic disease. We have proposed complex personalized treatments that seek to correct multiple changes simultaneously using a psychological approach to reduce chronic stress, immune checkpoint therapy with reduced doses of chemo and radiotherapy, minimal surgical intervention, if any, and mitochondrial metabolic reprogramming protocols supplemented by intermittent fasting and personalized dietary plans without interfering with the other therapies.

Highlights

  • Cancer is a tumorigenesis process that forms a mass of cells that we call a tumor

  • Mutations result from errors during DNA replication, mitosis, and meiosis, or other types of DNA damage; in order for a normal cell to evolve into cancer, it must undergo one or more types of DNA damage [12,13,14,15]

  • Sci. 2020, 21, 6521 of known cancer types develop because cell replication is affected directly by the telomere length, which is maintained by the telomerase enzyme abnormal activity

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Summary

Introduction

Cancer is a tumorigenesis process that forms a mass of cells that we call a tumor. During tumorigenesis, the cells that compose the tumor can be benign or malignant. When the cells in the tumor are abnormal and can grow uncontrollably, the tumor is malignant. Sometimes a benign tumor can transform into a malign one if the normal old cells begin to develop abnormalities, such as DNA mutations, and grow rapidly [1,2]. Benign tumors neither metastasize nor invade local tissues. Over time, they grow and displace or compress tissues, which may cause nerve damage, reduce blood flow, or stimulate necrosis and organ damage. The tumor cells can transform into cancer cells and continue growing, invading tissues, and metastasizing throughout the body. The American Cancer Society has estimated that 1,762,450 new cancer cases were diagnosed, and 606,880 cancer deaths occurred in the United States in 2019 [8]. In 2020, 1,806,590 new cancer cases were diagnosed, and 606,520 cancer deaths are projected to occur in the United States [9]

Cancer Mechanism
DNA Cell Mutations and Telomere Length
Cancer Complex Mechanism Schematics
Cancer and the Mitochondria Metabolic Dysfunction
Cancer Cell Behavior
Autophagy as a Potential Treatment
Main Autophagic Mechanisms
Autophagy and Cancer Treatment
Novel Cancer Immune Checkpoint Therapy
Mitochondrial Metabolic Reprogramming in Cancer Therapies
Cancer and Growth Factors Therapies
Nutrition as an Adjuvant in Cancer Therapy
Findings
10. Discussions and Conclusions for a Complex Multilevel Personalized Treatment
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