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‐Treatment Specificity and Genetics‐

Cancer cells within the body differ greatly. These differences originate from the original form of the cell; for example, liver cancer describes the mal‐
transformation of hepatocytes, or liver cells, whilst certain forms of skin cancer are due to the aberrant transformation of a type of skin cells, called melanocytes.
Each different type of cell within the body has different receptors on their shell, which means that they interact differently with components of the surrounding
environment, most importantly in the case of cancer, immune cells and cancer treatments.

The genetics of cancer cells also contributes to their heterogeneity. Cancer cells become cancerous as a result of mutations in the expression of certain genes,
specifically, over‐expressed oncogenes (cancer genes) and under‐expressed tumour‐suppressor genes (anti‐cancer genes). In different parts of the body lie
different oncogenes and tumour suppressor genes. For example, in the breast tissue, mutations in the genes which encode for mismatch repair enzymes (enzymes
that repair DNA damage accumulated during replication), can lead to breast cancer. These genes are called BRCA‐1 and BRCA‐2. In the colon, mutations in the APC
gene can result in colon cancer.

It is for these reasons that bespoke cancer treatments and therapies are so vital in success. Mapping the genetics, and the susceptibility of cancer cells to different
treatments, allow for a tailored and targeted treatment; fine tuning in such a way provides a more informed treatment arsenal, whilst preventing unnecessary
destruction of healthy tissue that can occur as a result of more generalised treatments.

The Research Genetic Cancer Centre (RGCC) provides the most comprehensive analysis of blood and tumour biopsies. Testing the patient samples against a wide
variety of cancer treatments, both conventional and adjuvant‐complementary therapies. The results allow the patient to combine treatments from three classes:

Class I ‐ cytotoxic agents (agents that kill cells);
Class II ‐ immunostimulants and immunomodulants (agents that stimulate and support the immune system);
Class III ‐ inhibitors of growth factors, receptor inhibitors (EGFr, IGFr, VEGFr, PDGFr, FFGr) and signal transaction pathways

Presented with a list of components from each class, treatment can be chosen, combining one from each list; if cancer cells become resistant to any of the agents,
then treatment can be easily switched to another agent from the same class.