22 results
Decreased Hospitalizations and Costs From Infection in Sixteen Nursing Homes in the SHIELD OC Regional Decolonization Initiative
- Gabrielle M. Gussin, James A. McKinnell, Raveena D. Singh, Ken Kleinman, Amherst Loren Miller, Raheeb Saavedra, Lauren Heim, Marlene Estevez, Tabitha D. Catuna, Eunjung Lee, Thomas Tjoa, Rachel Slayton, Nimalie Stone, John Jernigan, Matthew Zahn, Lynn Janssen, Shruti K Gohil, Philip Alan Robinson, Steven Park, Robert Weinstein, Mary Hayden, Cassiana E. Bittencourt, Ellena M. Peterson, Susan Huang
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- Infection Control & Hospital Epidemiology / Volume 41 / Issue S1 / October 2020
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- 02 November 2020, pp. s7-s8
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- October 2020
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Distinguished Oral
Background: Shared Healthcare Intervention to Eliminate Life-threatening Dissemination of MDROs in Orange County, California (SHIELD OC) was a CDC-funded regional decolonization intervention from April 2017 through July 2019 involving 38 hospitals, nursing homes (NHs), and long-term acute-care hospitals (LTACHs) to reduce MDROs. Decolonization in NH and LTACHs consisted of universal antiseptic bathing with chlorhexidine (CHG) for routine bathing and showering plus nasal iodophor decolonization (Monday through Friday, twice daily every other week). Hospitals used universal CHG in ICUs and provided daily CHG and nasal iodophor to patients in contact precautions. We sought to evaluate whether decolonization reduced hospitalization and associated healthcare costs due to infections among residents of NHs participating in SHIELD compared to nonparticipating NHs. Methods: Medicaid insurer data covering NH residents in Orange County were used to calculate hospitalization rates due to a primary diagnosis of infection (counts per member quarter), hospital bed days/member-quarter, and expenditures/member quarter from the fourth quarter of 2015 to the second quarter of 2019. We used a time-series design and a segmented regression analysis to evaluate changes attributable to the SHIELD OC intervention among participating and nonparticipating NHs. Results: Across the SHIELD OC intervention period, intervention NHs experienced a 44% decrease in hospitalization rates, a 43% decrease in hospital bed days, and a 53% decrease in Medicaid expenditures when comparing the last quarter of the intervention to the baseline period (Fig. 1). These data translated to a significant downward slope, with a reduction of 4% per quarter in hospital admissions due to infection (P < .001), a reduction of 7% per quarter in hospitalization days due to infection (P < .001), and a reduction of 9% per quarter in Medicaid expenditures (P = .019) per NH resident. Conclusions: The universal CHG bathing and nasal decolonization intervention adopted by NHs in the SHIELD OC collaborative resulted in large, meaningful reductions in hospitalization events, hospitalization days, and healthcare expenditures among Medicaid-insured NH residents. The findings led CalOptima, the Medicaid provider in Orange County, California, to launch an NH incentive program that provides dedicated training and covers the cost of CHG and nasal iodophor for OC NHs that enroll.
Funding: None
Disclosures: Gabrielle M. Gussin, University of California, Irvine, Stryker (Sage Products): Conducting studies in which contributed antiseptic product is provided to participating hospitals and nursing homes. Clorox: Conducting studies in which contributed antiseptic product is provided to participating hospitals and nursing homes. Medline: Conducting studies in which contributed antiseptic product is provided to participating hospitals and nursing homes. Xttrium: Conducting studies in which contributed antiseptic product is provided to participating hospitals and nursing homes.
Contents
- Robert G. McKinnell, University of Minnesota, Ralph E. Parchment, Wayne State University, Alan O. Perantoni, National Cancer Institute, Bethesda, Maryland, G. Barry Pierce, University of Colorado Medical Center, Ivan Damjanov, University of Kansas
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1 - The pathology of cancer
- Robert G. McKinnell, University of Minnesota, Ralph E. Parchment, Wayne State University, Alan O. Perantoni, National Cancer Institute, Bethesda, Maryland, G. Barry Pierce, University of Colorado Medical Center, Ivan Damjanov, University of Kansas
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Summary
Introduction
Our first task is to provide you with a working knowledge of the pathologic terms and concepts used throughout the text. This chapter defines terminology, compares and contrasts malignant and benign tumors, considers characteristics and behavior of malignant cells, and discusses how invading malignancies kill an individual. Tumors, with time, undergo changes that lead to autonomy. This progression of events is also examined.
An appreciation of embryology leads to a consideration of the origin of stem cells and the concepts of determination and differentiation. Both are important to understanding the origin of cancer cells, and such comprehension may lead to new modalities for treating cancers. Most textbooks of cancer biology begin with a discussion of cells. But we start with an examination of what cancer is to help you get a better grasp of the material that follows. Metastasis is difficult to understand without a prior foundation in the concepts of pathology. Similarly, carcinogenesis or chemotherapy is incomprehensible without knowledge of what a malignant cell is and how it behaves.
Much of our knowledge about tumors dates from antiquity. The streaks of hard gray tissue that extend from a tumor into the normal tissues reminded the Ancients of a crab, so they named the condition cancer (from the Greek word meaning crab). The term “tumor” denotes a mass, whether neoplastic, inflammatory, pathologic, or even physiologic. Today, tumor is used generically to describe any neoplasm, irrespective of its origin or biologic behavior.
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The Biological Basis of Cancer
- 2nd edition
- Robert G. McKinnell, Ralph E. Parchment, Alan O. Perantoni, G. Barry Pierce, Ivan Damjanov
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This is a revised and updated edition of a text used in undergraduate courses on cancer biology. It covers everything from the molecular basis of cancer to clinical aspects of the subject, and has a lengthy bibliography designed to assist newcomers with the cancer literature. An introduction acquaints students with the biological principles of cancer and the human dimensions of the disease by considering genuine cases of cancer in fictionalized letters. Other chapters discuss cancer pathology, metastasis, carcinogenesis, genetics, oncogenes and tumor suppressors, epidemiology, and the biological basis of cancer treatment. Also included are an appendix with descriptions of common forms of cancer, a glossary of cancer-related terms and colour plates to illustrate the pathology of many of the types of cancer discussed in the text. Upper-division undergraduates with a background in freshman biology and chemistry, as well as beginning graduate students will find this a valuable text.
Introduction: Letters illustrating clinical aspects of cancer
- Robert G. McKinnell, University of Minnesota, Ralph E. Parchment, Wayne State University, Alan O. Perantoni, National Cancer Institute, Bethesda, Maryland, G. Barry Pierce, University of Colorado Medical Center, Ivan Damjanov, University of Kansas
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Summary
Some may read this book because they or a loved one has cancer, students of science may read it because they are about to make career decisions, and students of cancer may read it because of a desire to be acquainted with aspects of cancer other than those with which they work. Although most students of cancer have never seen a malignancy in a human, they are nevertheless expert in one or more of the many fascinating and important aspects of the disease. They contribute to the understanding of DNA and its replication, control of gene expression, receptors and growth factors, developmental aspects, immunology, prevention, and treatment of cancer and a myriad of other important parts of the cancer problem. We are all impressed by the recent compounding of knowledge, but even more so by our lack of knowledge and understanding of how important facts generated in one aspect of investigation bear on another. Students, unaware of the clinical aspects of the disease, lack the information to make the correlations and see the important problems that result. In addition, they may be driven in their endeavors only by the intellectualism of their part of the problem. This book is designed to provide insight and understanding into the human aspects of cancer.
It is not our purpose here to present all-encompassing details of the clinical behavior of patients with cancer that are necessary for diagnosis, medical practice, and patient management.
7 - Epidemiology
- Robert G. McKinnell, University of Minnesota, Ralph E. Parchment, Wayne State University, Alan O. Perantoni, National Cancer Institute, Bethesda, Maryland, G. Barry Pierce, University of Colorado Medical Center, Ivan Damjanov, University of Kansas
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The study of occupational, dietary, habitudinal, and other environmental cancers can point the way to measures of cancer prevention.
Julian Huxley 1958Introduction
Epidemiology is the study of the distribution, prevalence, and etiology of disease and for this book the disease is, of course, cancer. Epidemiology is studied both by observation and with experiments. This chapter is confined to observational investigations. Risk factors identified in epidemiological studies have the potential, if put to use, to prevent or lower the incidence of certain cancers. These studies include an examination of the effects of occupational exposure to carcinogens as well as lifestyle activities that tend to make certain individuals prone to cancer (lifestyle is examined in greater detail in the following chapter). A practical example, already widely recognized, relates to lung cancer and smoking. Lung cancer does not randomly afflict individuals within a population. Rather, it appears disproportionately in people who smoke cigarettes. Lung cancer differences in different groups can be, and is, correlated with different exposure to cigarette smoking. When smoking increased, so too did the incidence and deaths due to lung cancer. In the United States, smoking-induced lung cancer remains the greatest cause of death by malignancy for men and women (Figures 7–1 to 7–3; Color Plates 5 through 10). Identifying tobacco as a risk factor for lung cancer has, inherent with that knowledge, the potential for prevention of much of the disease.
Preface
- Robert G. McKinnell, University of Minnesota, Ralph E. Parchment, Wayne State University, Alan O. Perantoni, National Cancer Institute, Bethesda, Maryland, G. Barry Pierce, University of Colorado Medical Center, Ivan Damjanov, University of Kansas
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This version of The Biological Basis of Cancer is referred to as a “second edition” which, of course, it is. The term “second edition” does little to inform the reader to what extent material has been updated or rewritten. Major changes were mandated throughout by the rapid pace of cancer research and the translation of new findings into improved clinical care. Be that as it may, some fundamental aspects of cancer do not change. The letters in the Introduction are such. The letters are provided to introduce the student to the impact of cancer on the lives of ordinary people and the resultant need for cancer research. That impact and need are the same today as they were several years ago and are perhaps best reflected in the remarkable cathartic writings of author John Gunther (Death Be Not Proud) on the untimely loss of his seventeen-year-old son in 1947 from a brain tumor to the recent trials and triumphs over cancer of international cycling star Lance Armstrong (It's Not About the Bike: My Journey Back to Life). Similarly, the distinction of benign versus malignant, as well as the concept of tumor grading and staging and certain other aspects of cancer discussed in the chapter on pathology remain the same. Other material has been carefully revised or rewritten – there is an entirely new Chapter 8 devoted to measures recommended by cancer organizations, and the authors of this book, to hopefully (and likely) reduce risk for cancer.
References
- Robert G. McKinnell, University of Minnesota, Ralph E. Parchment, Wayne State University, Alan O. Perantoni, National Cancer Institute, Bethesda, Maryland, G. Barry Pierce, University of Colorado Medical Center, Ivan Damjanov, University of Kansas
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4 - Genetics and heredity
- Robert G. McKinnell, University of Minnesota, Ralph E. Parchment, Wayne State University, Alan O. Perantoni, National Cancer Institute, Bethesda, Maryland, G. Barry Pierce, University of Colorado Medical Center, Ivan Damjanov, University of Kansas
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[A]ll cancers exist in both hereditary and nonhereditary forms … the heritable cancers are all uncommon.
A. G. Knudson 1985For decades there has been no doubt that cancer is genetic, in the sense that transformation of a normal cell to invasive and malignant growth is due to changes in the DNA. But most cancer is genetic only at the level of the transformed cell, not in the germline of the patients.
M-C. King, S. Rowell, and S. M. Love 1993Introduction
The heredity of cancer deals with familial aspects of neoplasia. “Familial aspects of neoplasia”means simply that more members of a family suffer from cancer than would be expected. Human pedigrees are examined to detect if a cancer is indeed familial, that is, is the cancer found in greater abundance than expected and thus perhaps inherited from previous generations? Understanding the heredity of cancer requires an investigation not only of the pedigree of families, that is, genealogy, but also of chromosomes, genes, and gene products. In this sense, this chapter concerns both the genetics and heredity of cancer. The term “genomics”refers to the structure and function of the entire genome of a species, including the complete DNA sequence, the regulation of its expression and how its genes and gene products function in a species. A related field is “oncogenomics”and that term pertains to the genomics of cancer. Oncogenomics is a rapidly evolving discipline resulting from new technology.
10 - Oncology: The difficult task of eradicating caricatures of normal tissue renewal in the human patient
- Robert G. McKinnell, University of Minnesota, Ralph E. Parchment, Wayne State University, Alan O. Perantoni, National Cancer Institute, Bethesda, Maryland, G. Barry Pierce, University of Colorado Medical Center, Ivan Damjanov, University of Kansas
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In the previous chapter, the biology of malignancies and their caricature of normal tissue renewal suggested important principles that guide the development and use of treatment strategies. The current chapter presents how the treatment principles have been reduced to practice and how treatment principles relate to biological principles governing malignant growth. The chapter is organized around the four conventional treatment modalities available today: surgery, radiotherapy, cytotoxic chemotherapy and targeted therapy. (The term “conventional” refers to therapy accepted as the best available standard treatment.) Because of their different strategies, each modality is associated with specific risks and side effects, and this chapter builds a scientific understanding of the modalities' approved uses, successes, limitations, and toxicities. As explained in the preceding chapter, the goal of using the modalities is cytoreduction – hopefully the complete eradication of all cancer cells from the body. If not possible, then the goal becomes reducing the number of cancer cells in the body to the point that the time required for malignant stem cells to replace them is longer than the patient's life, giving rise to a cure. If sufficient cytoreduction is not achievable, then relapse ensues at some point in the future that depends on the amount of surviving malignant tissue and its rate of repopulation. The younger the patient at time of diagnosis, the more effective the treatment must be at eradicating malignant cells.
Glossary
- Robert G. McKinnell, University of Minnesota, Ralph E. Parchment, Wayne State University, Alan O. Perantoni, National Cancer Institute, Bethesda, Maryland, G. Barry Pierce, University of Colorado Medical Center, Ivan Damjanov, University of Kansas
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Appendix: Description of selected tumors
- Robert G. McKinnell, University of Minnesota, Ralph E. Parchment, Wayne State University, Alan O. Perantoni, National Cancer Institute, Bethesda, Maryland, G. Barry Pierce, University of Colorado Medical Center, Ivan Damjanov, University of Kansas
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Adenocarcinoma of the breast
Adenocarcinoma of the breast usually presents as a small painless mass (Figures A–a,b). The disease rarely occurs in the second and third decades but then increases in incidence through and past the menopause. Because of the seriousness and great range in age incidence of the disease, any mass in the breast must be viewed as cancer until proven otherwise (see letter in Introduction).
The stem cell population of the breast that will give rise to the milk-producing acini are located in the small ductules and persist in the fibrotic stroma of the senile breast. These stem cells are the target in carcinogenesis (Figures A–2 a,b,c). The majority of adenocarcinomas of the breast arise in these same small ductules. They may present in several ways: the vast majority develop as small solitary painless nodules, but some within the ductules may present with a bloody discharge from the nipple as the nodule develops. As the adenocarcinomas grow, they infiltrate surrounding tissues and eventually become fixed to the deep tissues and to the skin. This may cause dimpling of the skin or, if it invades the nipple, retraction of the nipple (Figure A–1a). With further growth and development it may spread first to the lymph nodes in the axilla, and shortly thereafter to the lungs, pleura, and to the bones of the spine and pelvis.
3 - Carcinogenesis
- Robert G. McKinnell, University of Minnesota, Ralph E. Parchment, Wayne State University, Alan O. Perantoni, National Cancer Institute, Bethesda, Maryland, G. Barry Pierce, University of Colorado Medical Center, Ivan Damjanov, University of Kansas
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For the first time in the history of the world, every human being is now subjected to contact with dangerous chemicals, from the moment of conception until death.
Rachel Carson, Silent Spring, 1962Introduction
Our environment has been described as a “sea of carcinogens” awash with a variety of chemicals and, to a lesser extent, with oncogenic viruses and high-energy radiations, all of which may contribute significantly to cancer incidence in humans. Although much of our attention has been focused on the proliferation of synthetic chemicals and their waste byproducts, an examination of these substances has revealed that, in fact, most chemicals are not carcinogenic. Testing by the U.S. National Toxicology Program (NTP), an agency within the Department of Health and Human Services charged with the responsibility of defining human carcinogens in the United States (Huff et al. 1988), and the International Agency for Research in Cancer (IARC), a part of the World Health Organization (WHO) with a similar but broader mission (Tomatis 1988), has shown that only one-fourth to one-third of those substances even suspected of being carcinogenic on the basis of their chemistries actually are cancer-causing agents. In fact, of the more than 80,000 chemicals listed for commercial use with the NTP, thus far only 228 have been categorized as being “known” or “reasonably anticipated” as human carcinogens according to the tenth Report on Carcinogens (released December, 2002).
2 - Invasion and metastasis
- Robert G. McKinnell, University of Minnesota, Ralph E. Parchment, Wayne State University, Alan O. Perantoni, National Cancer Institute, Bethesda, Maryland, G. Barry Pierce, University of Colorado Medical Center, Ivan Damjanov, University of Kansas
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The significance of metastases is that they “form an ineluctable hindrance to successful therapy.”
Alton Ochsner and M. DeBakey 1942The detection of metastases constitutes decisive evidence for categorizing a proliferating primary lesion, previously of uncertain potential, as neoplastic and “malignant,” and the phenomenon is a topic of unparalleled importance in cancer medicine and biology.
D. Tarin 1992Introduction
Ochsner and DeBakey's use of the terms “ineluctable hindrance” in describing the effects of metastasis on cancer therapy, written well over a half century ago, is essentially valid today. Metastasis is feared by both patient and physician and that fear is not without merit. Metastases remain the principal cause of death by cancer. But, changes in the understanding of invasion and metastasis may soon necessitate reconsideration of this dismal prospect for cancer patients. The phenomena of cancer invasion and metastasis, with its many steps forming a “cascade,” have remained unchanged. However, the molecular events of metastasis, in particular metastasis suppressor genes and their expression, are now recognized and their understanding is evolving. Implicit with that understanding is the possibility, indeed the likelihood, of chemotherapeutic agents that specifically target metastasis suppressor genes. Understanding invasion and metastasis is critically important to the understanding of the pathogenesis of cancer.
It has been said that cancer is infrequently a localized disease. This is because of the propensity of malignant neoplasms to disseminate early in the disease and to grow as secondary tumors in the body of the host.
6 - Cancer in nonhuman organisms
- Robert G. McKinnell, University of Minnesota, Ralph E. Parchment, Wayne State University, Alan O. Perantoni, National Cancer Institute, Bethesda, Maryland, G. Barry Pierce, University of Colorado Medical Center, Ivan Damjanov, University of Kansas
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The archived specimens (in the Registry of Tumors in Lower Animals) provide historical data to establish epidemiological associations, geographic ranges and prevalence trends. It provides reference material for study by students and research scholars and provides residual material for retroactive genetics studies as new tools in molecular genetics are developed. Further, whole tumor displays in the Registry impart a convincing reality of the disabling effect of this disease on endangered species to visiting reporters, government representatives, scientists and lay public. If one picture is equal to a thousand words, an actual specimen is worth at least a hundred pictures.
J. C. Harshbarger 2002Workers who deal with cancer problems only in man and his closest relatives among the homeothermic vertebrates may look disdainfully at those who invest some of their energies in studies of neoplasms in creatures such as fish, frogs, snakes, and the numerous species of spineless, often slimy animals that were, in the days of the ancients, lumped together as “vermin.” After all, Alexander Pope, a poet of some wisdom, admonished: “The proper study of man is man.”
So it may be. But Aristotle, long before modern ecologists, recognized that man is an organism within a greater organism, the earth ecosystem. The ecosystem is not dependent on man, though man is dependent on the ecosystem. Ought not the study of man be extended to include the other animals that coexist with and support him on this motherly planet? They share with man many diseases, including cancers, and it is pertinent to ask: In what ways do neoplasms of animals at various phyletic levels differ from or resemble those of man in relation to etiology, natural history, immune factors, biochemistry, morphology, molecular biology, and the rest?
Index
- Robert G. McKinnell, University of Minnesota, Ralph E. Parchment, Wayne State University, Alan O. Perantoni, National Cancer Institute, Bethesda, Maryland, G. Barry Pierce, University of Colorado Medical Center, Ivan Damjanov, University of Kansas
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5 - Cancer-associated genes
- Robert G. McKinnell, University of Minnesota, Ralph E. Parchment, Wayne State University, Alan O. Perantoni, National Cancer Institute, Bethesda, Maryland, G. Barry Pierce, University of Colorado Medical Center, Ivan Damjanov, University of Kansas
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Introduction
Over the past twenty years, more than a hundred genes have been identified that can convert nontumorigenic tissue-cultured test cells from rodent cell lines to a transformed phenotype, that is, foci of piled-up and crisscrossed cells that grow in soft agar and form tumors when explanted into immunocompromised rodents. These dominant transforming genes, or oncogenes, encode proteins involved in signal transduction or cell cycle regulation and affect a variety of normal cellular functions, including apoptosis, proliferation, cell differentiation, and adhesion. When overexpressed or structurally altered by point mutation, deletion, or fusion, most oncogenic proteins selectively induce the proliferation of cells that express them. More recently, studies of families predisposed to specific types of cancers have yielded a growing number of recessive tumor suppressor genes. Loss of suppressor function by deletion or point mutation of both gene copies allows cells to proliferate unregulated or with reduced restraints. The discovery of both oncogenes and suppressor genes has proven pivotal in our understanding of the mechanisms of carcinogenesis by allowing scientists to focus on the genetic targets of carcinogens and thus finally link the details of carcinogen activation, adduct formation and repair, and neoplastic conversion and metastasis with definable molecular events. Furthermore, targeting of these genes with drugs that modulate their function has already led to effective therapies for human cancers.
8 - Lifestyle: Is there anything more important?
- Robert G. McKinnell, University of Minnesota, Ralph E. Parchment, Wayne State University, Alan O. Perantoni, National Cancer Institute, Bethesda, Maryland, G. Barry Pierce, University of Colorado Medical Center, Ivan Damjanov, University of Kansas
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Louis Pasteur (1822–1895), when considering a disease, was more interested in how can it be prevented, not, how can it be cured.
A. Ochsner 1954The most desirable way of eliminating the impact of cancer in humans is by prevention.
L. Wattenberg 1985The ultimate goal in the control of any disease is prevention, and so it is with cancer.
Y. Hayashi et al. 1986Evidence suggests that one third of the more than 500,000 cancer deaths that occur in the United States each year can be attributed to diet and physical habits, with another third due to cigarette smoking.
T. Byers et al. 2002Introduction
It has been estimated that two-thirds of all cancers can be prevented by lifestyle modification (see Byers epigraph above). In contrast to the abundance of cancer that is clearly preventable, it may come as a surprise to learn that there is an anticipated massive 50 percent increase worldwide in cancer incidence by 2020 (Stewart and Kleihues 2003). The title to this chapter is thus entirely appropriate and readers of this book, with the possible exception of those who are already afflicted with cancer, should take heed. Of course, those who already suffer with cancer have family and friends and hence, it is not inappropriate for them to read this for the benefit of those they love. Ochsner (1954) believed that education must play a role in risk reduction.
Plate section
- Robert G. McKinnell, University of Minnesota, Ralph E. Parchment, Wayne State University, Alan O. Perantoni, National Cancer Institute, Bethesda, Maryland, G. Barry Pierce, University of Colorado Medical Center, Ivan Damjanov, University of Kansas
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9 - The stem cell basis of cancer treatment: concepts and clinical outcomes
- Robert G. McKinnell, University of Minnesota, Ralph E. Parchment, Wayne State University, Alan O. Perantoni, National Cancer Institute, Bethesda, Maryland, G. Barry Pierce, University of Colorado Medical Center, Ivan Damjanov, University of Kansas
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Introduction
Notwithstanding physical removal of malignant tumors by surgery and regional control of malignant tumors by radiation, the concept of cancer as a disease of abnormal stem cell biology leads to three philosophies for treating the disseminated, metastatic disease that most patients will face. Only one of these philosophies has become clinically useful, whereas the others are developing or remain at the conceptual level.
Therapies remaining at the conceptual level
One treatment to attack this caricature of normal renewing biological tissue is conversion, or perhaps reversion, of the malignant phenotype to a benign state. As studies of the fate of micro-injected cancer cells in the embryo have revealed (detailed in Section 1.15, Chapter 1), it is possible for malignant cells to lose their malignant potential without losing their proliferative potential, such that they contribute to normal formation of chimeric organs in the developing embryo. The development of chimeras containing some functional tissue derived from the implanted malignant cells indicates that the cancer cells reacquire the capacity to properly respond to biological controls on tissue renewal even into adulthood after the embryonic environment disappears. The concept is that once converted back to normalcy by these embryonic control mechanisms, wherein the malignant phenotype is removed or suppressed, cancer-derived normal cells in the adult chimera can no longer cause disease. Therapeutic strategies harnessing this biological control might not be toxic in the adult patient, because they would target malignant, embryonic-like stem cells, converting them into normally functioning adult stem cells.
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