Tangible Outcomes in Canine Oncology Research
Since 1995 the AKC Canine Health Foundation has awarded 188 oncology grants and funded nearly $10.7 million in canine cancer research. This would not be possible without your support.
The scientific results that you made possible have helped move veterinary medicine forward, advancing the health of all dogs. While these are just a few of the highlights CHF has been able to deliver through the dedication of our funded-researchers, these steps forward show real progress in the understanding and treatment of canine cancer.
Tumor Suppressor Genes
1999 – Scientists knew that there were genes that controlled a cell’s ability to replicate by suppressing cell division, and began to suspect that these genes may be altered in cancer. The hypothesis was that loss of function of these “tumor suppressor genes” lead to metastasis in our most insidious forms of cancer, including melanoma, osteosarcoma and hemangiosarcoma.
2014 – Through sponsorship of research into tumor suppressor genes, we now have documented genomic instability in canine tumor suppressor genes and irregularities in gene copy number. These landmark findings may lead us to better drugs to halt the spread of cancer and help us understand the role of genomics in the development of cancer.
Chromosomal Aberrations in Lymphoma
2002 – Abnormalities in chromosomes, those threadlike linear strands of DNA in the nucleus of cells that carry the genes, were known to contribute to cancer in humans. Documentation of chromosomal abnormalities were being used to diagnose, prognose, and clinically manage human cancer. Yet we knew nothing about whether canine cancer was defined by similar anomalies.
2013 – CHF-funded research brought molecular cytogenetic technology – the technology needed to document chromosomal anomalies – to the dog. Scientists identified tumor-associated abnormalities in the number of copies of genomic regions and whole chromosome abnormality. For the first time we have a documented treatment response using molecular cytogenetic techniques in the dog. This “cytogenic remission” ushers in personalized medicine (Pmed) in the dog – the ability to determine if a dog will respond to chemotherapy and how well they are responding.
Genetic Lesions in Osteosarcoma
2007 – The search began to identify genetic mutations and their functional consequence in osteosarcoma.
2013 – Genetic lesions upstream of a gene called CDKN2A/B were identified. The functional consequence is the altered regulation of cell’s ability to replicate. Importantly, canine CDKN2A/B is surrounded by genes that are highly similar to human genes, ushering in the potential to use the naturally occurring disease in the dog as a model for human osteosarcoma.
Mast Cell Tumors
2005 – Mast cells are a type of white blood cell that normally reside in the skin, lungs, nose, mouth, and gastrointestinal tract. Their primary functions include defense against parasites and allergens, but they also contribute significantly to formation of new blood vessels. When mast cells begin to replicate out of control they form a particularly aggressive cancer. These mast cell tumors were poorly understood in the dog because we lacked a basic understanding of mast cell biology in the dog. CHF funded the research to start understanding of mast cell biology and function.
2006 – Mast cell function was fully characterized and a mast cell tumor line (CL1) was created and shared with the scientific community. Targeted therapeutics were still unavailable. Work began to establish a test to measure mast cell “mitotic index,” which is a measurement of the cell’s ability to replicate and potentially an indication of a mast cell tumor’s ability to metastasize. Because of our lack of basic knowledge targeted therapeutics were still unavailable.
2014 – Modulation of mast cell-derived prostaglandins and leukotrienes were found to impair mast cell function and a commercially available non-steroidal anti-inflammatory drug (NSAID) called Tepoxilan was found to be most effective in halting mast cell tumor progression.
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