Canine and Feline Geriatric Oncology

Honoring the Human-Animal Bond

Alice Villalobos, Laurie Kaplan

• Publisher: Wiley-Blackwell
• Year: 2017
• ISBN:
  9781119290445
• Edition: 2
• Topic: Medicine
• Subtopic: Veterinary Medicine

Canine and Feline Geriatric Oncology: Honoring the Human-Animal Bond, Second Edition provides a complete clinical approach to the most common neoplasias in geriatric dogs and cats.

• Provides the tools needed to diagnose and treat aging pets with cancer and to help clients make the best decisions for themselves and their animals
• Addresses the "what-ifs" that often arise during interactions with clients of aging pets with cancer and helps to determine when a pet should enter the hospice phase
• Features many vignettes and real-life case studies to demonstrate the issues faced by clinicians and owners dealing with older dogs and cats with cancer and end-of-life issues
• Fully updated and expanded with new and revised information, including new knowledge on palliative and hospice care and self-care techniques for carers

Part One

Chapter 1
Molecular Biology of Cancer and Aging

The roots of the problems of cancer and aging involve the molecular changes of aging priming aging (cellular senescence). These changes prime aging cells to be more susceptible to the effects of environmental carcinogens. These changes are only partly understood and may or may not be reversible.

Lodovico Balducci, MD

What Is Cancer? How Does It Start?

Hippocrates coined the name for malignant cancer from the Greek word for crab (karkinos), because tumors resembled the claws of a crab. Cancer is an insidious, nefarious, complex, obstinate, and disruptive disease. Cancer is an intricate set of biological aberrations that originate in the nucleus of cells that transform and progress with diverse heterogeneity, which is not completely understood. Cancer results in the uncontrolled and reckless growth of destructive cells that overwhelm the body as they accumulate. Cancer's immortal cells replicate relentlessly. They can use existing vessels or recruit cells to form new blood vessels via angiogenesis for nourishment. Cancer cells slip into the lymphatic and vascular systems and invade vital structures via metastasis to ultimately kill its host with its fatal agenda.

This chapter will attempt to describe the intricacies of cancer's malignant processes. Terms are defined and readers will be subjected to only a small taste of the alphabet soup milieu that drives the intracellular and extracellular microenvironment. As you read, keep in mind that this is an attempt to illustrate the essentials of a complex disruptive process and forgive or congratulate me if the text has oversimplified or exemplified cancer!

Normal cellular division creates a constant flow of injured genes. These defective genes are regularly corrected by innate repair mechanisms present in normal cellular function. Certain genetic point mutations become multifarious if they are not repaired. Genetic damage occurs in cells that lack coordinating signals necessary for self-repair. If genetically damaged cells escape innate detection and destruction and are allowed to live and replicate, cancer gets a foothold and then proceeds with its mechanistic drivers to grow and metastasize and disrupt vital functions.

Each of the trillions of cells that compose a body contains over one hundred thousand genes, arranged in chromosomes. The DNA that composes normal genes is called a “proto-oncogene.” A proto-oncogene encodes all genetic information and regulates cell replication so that cells can replenish themselves normally in the bone marrow, intestine, skin, connective tissue, and organs when needed. Genes also regulate normal wound healing, hair growth, puberty, and gestation (Abeloff et al. 2004).

About one in every million cell divisions undergoes a point mutation resulting in defective, aberrant, or altered genes that clone and initiate tumorigenesis. These genetic mutations can be seen by the immune system as copy errors and they are normally corrected by immunosurveillance. If the mutations are involved in the mechanism that controls repair, replication, proliferation, tumor suppression, or telomere (the terminal portion of genes, encoding programmed cell death) control, the defective genes are converted into oncogenes and their descendant cells take on a renegade behavior.

Cancer evolves on a cellular and sub-cellular level through three basic stages: initiation, promotion, and progression. Initiation involves exposure to carcinogens such as sun, tobacco smoke, alcohol, herbicides (2,4-D weed killer), insecticides, asbestos, free radicals, viruses, infections and so forth. This initial exposure may result in permanent damage “hits” to DNA. Initially this damage may not be a direct cause of cancer; however, continued exposure causes more gene “hits” and increases the risk of tumorigenesis. Tumor initiation and promotion is also seen in chemically induced tumors in experimental animals.

Promotion events are poorly understood. The promoter (an abnormal DNA base sequence in genes) stimulates cell division and results in the accumulation of cells that cause the formation of tumors. Aging, poor diet, obesity, toxins, smoke, and chemicals injure the stability of genes and are also considered potential promoters.

Progression to malignancy occurs when the tight controls that normally govern cell cycle progression are suppressed or break down. This results in the uncontrolled growth of abnormal immortal cells (cells that do not respond to normal cell death signals). Progression also involves the ability of cancer cells to initiate the formation of new capillaries (angiogenesis) to nurture growth. The most malignant cancer cells invade surrounding tissue, work their way into vessels and lymphatics and metastasize to distant parts of the body.

These events involve proteins that function by giving and receiving signals on the surface of the cell and along complex and intricate intracellular pathways in the process of cell-to-cell communication. Understanding the complexity and specifics of cell signaling and the alphabet soup that names the proteins and receptors can be overwhelming to the busy practitioner. There are basic families and systems of signaling that share certain pathways that aid and abet neoplastic changes. These basic mechanis...