Copyright © 1985, 2011 by Migdalia Arnán, MD.

Library of Congress Control Number:       2011960988

ISBN:         Hardcover                               978-1-4653-0667-8

                   Softcover                                 978-1-4653-0666-1

                   Ebook                                      978-1-4653-0668-5

All rights reserved. Except as permitted under the Copyright Act of 1976, no part of this publication may be reproduced or distributed in any form or by any means, or stored in a database or retrieval system, without the prior permission of the author.

It is not intended to serve or as replacement for professional medical advice. Recommendations mentioned in this book are not to be taken without the advise of medical doctors, naturopatic physician, registered dietitian or other specialist.

This book was printed in the United States of America.

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Contents

INTRODUCTION

CHAPTER I Characteristics of Cancer Cells

CHAPTER II Cancer as an Immune Disease

CHAPTER III Cancer and Oncogenic Viruses

CHAPTER IV Photosynthesis, Chlorophyll, Chloroplasts, Bacteria Associated with Cancer

CHAPTER V Oxygen, Hemoglobin Transport, Bacteria in Cancer Tissues, Macrophages, and Alphafetoprotein

CHAPTER VI Cancer and Nutrition

CHAPTER VII Free Radicals, Oxygen, and Ozone

CHAPTER VIII Protein Molecules Tridimensional Confirmation

CHAPTER IX The Immunologic Basis of Diseases

CHAPTER X Cancer and Fungus

CONCLUSIONS

CANCER REFERENCES

DEDICATION

This book, Cancer Biology, A Study of Cancer Pathogenesis, is dedicated to the Almighty God, The Creator of the Universe, The Light of the World.

Also,

To the memory of my parents, Luis Arnan Suria and Mercedes Guerra Peres, who impregnated in my mind the importance of knowledge and the need to find answers to the why, who, what and how of situations.

To my sisters, Elive Arnan and Yvette Miller.

To the memory of my husband, David Archibald Morrissey Sanderson who supported me in my work.

To my daughter, Laura Gaebler, and to my grandchildren, David Alexander and Daniel Jackson Gaebler, to my granddaughter Jessica Olive Larson, and to my greatgrandchildren, Quintin, Cooper and Kieran Larson.

I am thankful to the many scientists, who in the quest for the truth, and with their important discoveries, have set basic foundations for those to follow. Without their work, this book would not be possible.

This book is not only intended for medical doctors of all specialties, but also it will be helpful to researchers, biologists, nurses, and to the general public interested in learning and desiring to take an active part in their health.

INTRODUCTION

Cancer has the unique ability to replicate endlessly as long as it has the proper environment. It can grow and infiltrate the adjacent normal tissue, crowding it with overlapping tumor cells. As cancer does not recognize cell boundaries, it stretches its cell-dividing tentacles to suffocate its victims.

Cancer grows at the expense of the patient’s healthy tissues. It is an infectious parasitic tumor growth that occurs in genetically predisposed individuals with a decreased immunity, when exposed to specific tumor sensitizers and promoters.

Why are cancer cells so unique, so different from normal cells that make them ageless? Why are cancer cells able to grow uncontrollably? Why are cancer cells unable to recognize cells boundaries? Why are cancer cells so pleomorphic?

Why do cancer cells replicate so effectively? Why do cancer cells have an anaerobic metabolism? What are the fundamental molecular changes that transform a normal cell into a malignant cell?

What is the significance of the green granules (GG) found in living cancer cells when exposed to light? Is there any similarity between the metabolism of a cancer cell and a plant cell? Is the cancer cell a proof of the survival of the fittest? What role does the macrophage play in cancer pathogenesis (initiation) and in cancer metastases?

What role does the immune system play in cancer pathogenesis? What is the effect of ozone gas (O2-O3) on cancer and on the membrane of the red blood cells (RBCs)?

Can cancer be prevented? Can it be cured?

These and other cancer-related subjects will be addressed in this book.

CHAPTER I

Characteristics of Cancer Cells

Immortality of Cancer Cells. Given the proper nutrition and environment, cancer cells outlive any normal cell. For example, cells from the Rous sarcoma and from the HeLa carcinoma are malignant cells lines kept alive and used in laboratory experiments years after their original host’s death.

HeLa cells were isolated by Gey in 1951 from a cell line of an adenocarcinoma of the uterine cervix of a thirty-seven-year-old woman, Henrietta Lacks. Descendents of the original HeLa cell line are still thriving in the laboratory, in tissue cultures throughout the world years after the demise of its original source. Similarly, Ehrlich’s ascitic tumor cells originated in 1938 from a solid mouse’s tumor and have been kept multiplying in vitro by mouse to mouse transfer. A two-year-old mouse is quite old, but Ehrlich’s solid tumor mouse cells are still growing while non-transformed normal cells in culture have a limited number of divisions. This indicates that somatic cells have a specific intrinsic number of divisions compared with the cancer cells.

While spontaneous cancer cells are immortal, this is not the case in carcinogen-transformed cells, whose life span is finite. Thus, immortality is a property of cancer cells, but not of normal or artificially transformed cells.

Cancer Cells Do Not Recognize Cell Boundaries. Normal tissue cells in culture stop growing when in contact with another cell—contact inhibition. Thus, in tissue culture, normal cells form a single cellular layer covering the culture plate surface. Cancer cells, on the contrary, do not recognize cell boundaries piling on top of each other, forming uneven mounds of unruly cellular growth.

Cancer Cells as Unruly Parasites. Cancer cells are programmed for unrestrained growth and to successfully compete for nourishment at the expense of the adjacent healthy tissue. Normal cells, on the contrary, are programmed to work in harmony with each other for the benefit of the whole body. Cancer cells are like the young cowbird, dropped in another bird’s nest by the mother, who eats voraciously and often pushes the other young birds out of the nest.

Abnormal Morphology. Cancer cells have a genetic predisposition to heterogeneity, which means they have a variety of forms. Not only is there a variation in size of the cancer cells, but there is also a multi-potential morphologic appearance with a tendency to vary from the original tissue character.

Examination of tissue from various areas of the cancer may show a diversity of cells, cellular patterns, and behavior from the original tumor site. Cancer cells vary from two to ten or more times the size of normal cells. Some of the cancer cells can be multinucleated, even forming giant tumor cells. The chromatin pattern is pleomorphic, hyperchromatic, and bizarre; and usually, there are numerous cells in mitosis (cell divisions). Changes are also noted by electron microscopy. A primitive cellular morphology suggests rapid tumor growth and a more guarded prognosis (poor outcome).

Abnormal Chromosomes in Cancer. Chromosome changes, such as the Philadelphia chromosome (Ph) found in chronic granulocytic leukemia, are usually one and a half to two times larger than normal chromosomes. This and other chromosomal anomalies are used as markers in tumors, in congenital and other diseases. Association of acute leukemia in mongolism is a known fact. However, the incidence of leukemia could be higher if mongols lived longer.

Chromosome anomalies can affect the sex chromosomes as well as the autosomes. Many diseases are now associated with specific chromosome alterations. Chromosome breakage is associated with oncogenic virus infection. It has been stated that if the oncogenic (cancer producing) gene is incorporated into a host genome, (genetic blue print) there will be a continue replication of the oncogenic gene, and tumor growth independent of the initial infection. There is a relationship between chromosome counts and both invation and degree of differentiation in transitional cell carcinoma of the bladder.

Certain human leukemias and lymphomas show specific and consistent chromosome translocations: Chromosome eight is involved with chromosome two, fourteen, or twenty-two. Other anomalies in the translocation between chromosome eight and fourteen. While in myeloid leukemia the long arm of chromosome nine translocates to chromosome twenty-two, but in acute promyyelocytic leukemia, the long arm of chromosome seventeen translocates to chromosome 15.

Karyotype alterations in malignancies of the gastrointestinal tract have been found. The changes affect not only the number of the chromosomes, but the morphology as well.

Infiltrating poorly differentiated carcinoma

Infiltrating mucus-producing carcinoma of colon

Anaerobic Metabolism of Cancer Cells. Otto Warburg won a Nobel Prize in 1936 because of his discovery of the anaerobic or fermentative metabolism of cancer cells. Normal healthy cells have an aerobic or oxidative metabolism, while cancer cells have an anaerobic or fermentative metabolism. What triggers the metabolic change that transforms a normal cell into a cancer cell?

Because of the ineffective fermentative metabolism of the cancer cells, the cancer cell energy is channeled toward cellular replication instead of having a harmonious and cooperative relationship with other cells and tissues.

It is the anaerobic metabolism of cancer cells that make them susceptible to radiotherapy. During radiation, energy is transferred to electrons which ionize the matter they reach. This ionization also affects the DNA and the RNA by weakening them. Changes are possible due to the recombination of the damaged molecule with the available free O2 (oxygen) in the environment. The cellular changes produced by the radiation under oxygenated conditions can be fatal to the cell, or it can inhibit cell proliferation. Without the presence of oxygen, the radiotherapeutic effect is impossible. The limiting effect of radiation is dependent upon the degree of vascularization of the tumor. Cancers that have poor vascularization are more radioresistant because there is less oxygen available.

Healthy cells rely on mitochondria for their normal oxidative metabolism. Mitochondria are microscopic spheres or rods found in a cell’s cytoplasm. Their number varies from a few to hundreds, depending on the cell’s activity. For example, a rat’s hepatocyte (liver cell) is a very active cell and may contain one thousand mitochondria.

Altmann first observed and described the mitochondria toward the end of the nineteenth century. A few years later, Benda named them mitochondria, but it was Otto Warburg who associated the mitochondria with respiratory enzymes and therefore with cell respiration.

Examined by electron microscopy, the mitochondria are round or cylindrical bodies enclosed by two membranes. The inner membrane has projections or folds called cristae. These are at the inner membrane level, where formation of adenosine triphosphate (ATP) occurs with oxidation of reduced enzymes and where oxidative phosphorylation occurs. The cristae are more numerous in areas of greatest activity. Mitochondria membranes have a greater amount of lipids than the endoplasmic reticulum membranes.

Cancer cells decrease the number and size of mitochondria. These frequently contain calcium deposits and are ineffective.

Mitochondria in Cancer Cells. There is a marked reduction in the number of mitochondria in tumors with high fermentative or glycolytic rate. Tumor cells grown in a glucose-containing medium may produce large amounts of lactic acid in comparison with the normal control cells. Some tumor cells in vitro use predominantly fatty acids and amino acids, specifically glutamine, as a source of fuel.

Warburg theorized in 1930 that cancer cells have an anaerobic or fermentative metabolism resulting in increased glycolysis. Since the respiratory or oxidative capacity of the cell depends on its mitochondria and its function is inhibited or not present in cancer cells, it is of the utmost importance to study not only the physiology of the normal mitochondrion, but that of the cancer cell as well.

There is a 50 percent or more reduction in the number of mitochondria in rapidly growing tumors. Why? In a rapidly growing tumor, where fast production of nutrients is necessary, why revert to a less-efficient anaerobic metabolism? Is this occurring because nourishment of the cancer cells is already available from the surrounding environment, ready-made for the fast-dividing cancer cells?

Pendersen has reported on the low number of mitochondria in most rapidly growing tumors and on the lower yield of mitochondria from such tumors in comparison with the content in the slow-growing tumors.

Pendersen and others interpreted that the poor respiratory capacity may be due, at least in part, to the low mitochondrial content rather than to an inhibition of the electron transport chain per se. But not all tumors have abnormal content or deficiency in the electron transport chain as reported by Wallach in 1975. Ruggiere and Falani in 1968 and others have found an increase of cholesterol in tumor mitochondria and that the inner mitochondrial membrane has a higher concentration of cholesterol than the outer membrane.

Hepatoma’s (cancer of the liver) mitochondria contain more calcium than a normal hepatocyte (normal liver cell). Calcium inhibits the ATP/ADP