My book Neoplasms: principles of development and diversity was published last week. The full table of contents is available.
In the next few blogs, I will provide some short excerpts from the book. In Chapter 1,I review the properties of neoplasms.
Cancer cells do not create new biological properties. They use the same properties that normal cells use, only they tie them all together in a package that nobody wants to receive. Let us examine the normal tissues that have properties of cancer cells.
You can think of the body as a collection of two types of cells: those that grow persistently and those that grow intermittently or never. The most numerous persistently growing cells line the outside and the inside surfaces of the body: squamous cells of the skin’s epidermis and enterocytes of the gastrointestinal tract (the gut). The growing cells of skin and gut exactly balance a second population of cells that are actively dying. The reason that the skin epidermis and the gut mucosa maintain a constant thickness is that the dead skin cells are sloughed into the air (as dust specks) and the dead enterocytes are sloughed into the fecal stream. Otherwise, both the epidermis and the gut would double in size every few weeks, a rate of normal growth that easily exceeds the growth rate of neoplasms.
Epithelial tissues (the tissues that line surfaces and populate most solid organs and glands) contain a subpopulation of growing (dividing) cells. Each division of a dividing cell yields two cells: one cell that performs the normal functions of the tissue, and another cell that is capable of dividing. The cell that performs the normal functions of the organ is referred to as a differentiated cell, because it has completed the developmental process and has attained a distinct morphologic appearance. Most differentiated epithelial cells are incapable of dividing and will eventually die. The precise balance of cell growth and cell death yields a zero net growth in normal adult tissues.
Some organs, like the liver, are composed of epithelial cells that cease to divide or divide only rarely. The liver of an elderly man may contain many of the same, hard-working hepatocytes (liver cells) it had when the man was a youth. In the event of a liver injury, the other-wise quiescent hepatocytes quickly divide, enlarging individual acini (i.e., microscopic liver glands), quickly restoring the liver. In the rat, the full weight of the liver is restored a week after surgically removing two thirds of the liver. The remarkable regrowth of the liver after partial hepatectomy appears in the myth of Prometheus, whose liver is eaten by eagles each night and restored the next day.
Some nonepithelial tissues lose the ability to divide at about the time that the human body has reached its adult size. Many of the diseases of aging are actually just the consequences of wear and tear in populations of cells that cannot renew themselves. Osteoarthritis is a joint disease that results from damage, over time, to articular cartilage. Cartilage cells (chondrocytes), in contrast to liver cells, have only limited ability to divide. When cartilage is damaged, it usually stays damaged, and this may cause a chronic inflammatory disease involving the damaged joint cartilage and the underlying bone (osteoarthritis). The dementia that accompanies aging is due, in part, to the limited ability of senescent neurons to renew themselves through division. You can think of the degenerative diseases of aging as the medical opposite of neoplasia. Aging results from accumulated damage in cells that cannot divide. Neoplasia is the result of accumulated damage in cells that must divide. (to be continued)
Chapter 1 Table of Contents:
1 What Properties Are Shared by All Cancers? 3
1.1 Background 3
1.2 Are There Any Properties of Neoplasms that Are Not Found in Normal Cells? 4
1.3 Persistent Growth in Normal Cells 4
1.4 Invasion by Normal Cells 5
1.5 Metastasis by Normal Cells 5
1.6 Is There a Common Temporal Sequence Leading to the Development of Cancer? 7
1.7 Why Is It Important to Treat Cancers Early? 7
1.8 Cancer Morphology 8
1.9 General Rules for Naming Neoplasms 8
1.10 What Is a Cytologic Diagnosis? 9
1.11 Morphology of Malignant Cells 10
1.12 Cancerous Atypia and Reactive Atypia 12
1.13 How Can You Distinguish Reactive Atypia from Cancerous Atypia? 13
1.14 Dysplastic Cells and How They Differ from Cancer Cells 14
1.15 Nuclear Atypia in Cancer Cells 15
1.16 Why Are the Nuclei of Malignant Cells Different from Nuclei of Normal Cells? 15
1.17 Tumor Monoclonality 15
1.18 Monoclonal Proliferative Lesions 16
1.19 Clonal Expansion in Paroxysmal Nocturnal Hemoglobinuria 17
1.20 Clonal Expansions of Normal Cells that May Not Lead to Cancer 18
1.21 Polyclonal Expansions that May Lead to Monoclonal Cancer 18
1.22 Tumor Growth Regulation and Tumor Autonomy 18
1.23 Limits on Tumor Autonomy 19
The full table of contents is available. In the next few days, I will continue to discuss content from Neoplasms in my blogs.
Key words: tumors, tumour, neoplasms, neoplasia, carcinogenesis, tumor development, cancer research, neoplastic development, precancer preneoplasia, preneoplastic