The War on Pet Cancer: Past Approaches
THE WAR ON PET CANCER
Published in the November 2019 issue of Natural Awakenings
We are not winning the war on pet cancer.
In 1971 President Nixon signed the National Cancer Act, which created the National Cancer Institute (NCI). In addition to granting broad discretionary powers to the Director of the NCI, the act also provided additional funding for NCI to establish 15 new cancer research centers, local control programs, and an international cancer research data bank. The mood of the country was optimistic, with many hoping that in a decade we would defeat the rising tide of cancer deaths. Almost 50 years later, cancer is surpassing cardiovascular disease as the leading cause of death for middle-aged people, with few successful reductions in the mortality rates for most types of cancers.
Our companion animals suffer from similar disease patterns, and “One-Medicine” initiatives are bridging the research and treatments for humans and non-human animals. November is National Pet Cancer Awareness Month; we should pause to think about the six million dogs and six million cats that are diagnosed with cancer every year. Cancer is now the leading cause of death in almost half of American dogs and about a third of cats. This was once regarded as a disease of old animals, but we are diagnosing cancer in younger and younger patients. This series of three articles will look at our current understanding of cancer and how we treat it, why the proclivity for cancer is part of our evolutionary heritage, and how treating cancer as a metabolic disease elucidates pathways for prevention and treatment.
The nightmare of cancer usually begins with the diagnosis. Options for treatment typically include surgery, chemotherapy, radiation therapy and, rarely for companion animals, newer “smart” drugs. In veterinary medicine typical oncology protocols are not as devastating as those used for people. Still, pet guardians are often scared by the potential and known side effects of treatment, yet they want to provide the best quality of life for their beloved companions. The cost of treatment can run into the tens of thousands of dollars, and few pets are covered by veterinary health insurance. Newer smart drugs that target mutated genes or their protein product cost even more, and currently these drugs have very limited success for people.
Our current understanding of cancer began with observations. Historically we saw that environmental substances such as snuff, coal tar and radium caused characteristic cancers, although the mechanism was unknown. X-rays and radiation also led to cancers in medical professionals exposed to many x-rays and in the survivors of atomic bombs in WWII. Certain cancers could be inherited, and lifestyle clearly caused other forms of cancer. To complicate matters, bacteria and viruses were also implicated as causal agents. We call substances that can cause cancer carcinogens. The National Cancer Institute was tasked with understanding this complex causality and sorting through the variables.
Eventually, research pointed to mutations in the nuclear genes involved in cell reproduction as the cause for most cancers. Specifically, it is thought that several changes have to happen in order for cancer to arise, grow and spread:
- Genes that cause growth must be activated
- Genes that suppress growth must be de-activated
- Genes that lead to cell immortality must be switched on
- Genes that cause cell suicide (apoptosis) must be switched off
- Genes that lead to blood vessel formation and growth must be turned on
- Normal DNA repair mechanisms must be inactivated
Benign tumors typically display the first four changes, while metastatic tumors also acquire the last two. But why do these changes arise?
Our current belief is that carcinogens cause random mutations to certain nuclear genes. Patients are viewed as having tumors with unique genetic fingerprints, with individualized genetic mutations that characterize their cancer. Much current research is focused on developing drugs that specifically target each critical mutation. The most successful of these smart drugs are the ones that are anti-hormone therapies used in breast and prostate cancer in people. Drugs that target genes producing growth-promoting signals have numerous side effects, and their benefits tend to be short in duration.
This picture is similar for drugs that induce cell suicide genes and drugs that inhibit blood vessel-forming genes. These drugs take decades to develop, and at tremendous cost. They require analyzing and understanding the genetic fingerprint of each individual’s cancer. Most importantly, these therapies do not target the underlying cause of cancer, and thus will have limited success.
There is another way to look at cancer. The possibility of cancer is part of the evolution of multi-cellular life. Cancer is a mitochondrial disease and a disease of energy production. Understanding this evolution can lead to pathways for specific nutritional modalities to become a part of cancer management and prevention. Exploring the evolutionary underpinnings of cancer will be the subject of the second article in this series.YBP_DoylestownVeterinaryHospital_1119 (1)