Integrated Oncology Medicine
Integrative Oncology is becoming more and more prevalent in all facets of medical practice. Patients, families / caregivers demand for practitioners who have exposure to the basic tenants of integrative oncology grow daily. There are demands for medical care in the oncology patient far beyond the current standard of care. The purpose of this website is to allow all interested parties to access unbiased and evidence-based information on cancer management. There are a plethora of successful medical and palliative care strategies, incorporating integrative oncology with standard care, oral therapies, basics of diet, intravenous therapy updates and case management
Although some battles have been won since the declaration of the ‘war on cancer’ in 1971 in the United States, the war is ongoing. Despite enormous investments from industry and the public, oncology has an impressively poor success rate in the clinical development of effective drugs; less than a third of that in cardiovascular or infectious diseases. Drug development in oncology has typically focused on targets essential for the survival of all dividing cells, leading to narrow therapeutic windows. Non-essential targets offer more selectivity but not in all cases. The most important reason for the poor performance of cancer drugs is the remarkable heterogeneity and adaptability of cancer cells. The molecular characteristics of histologically identical cancers are often dissimilar and molecular heterogeneity frequently exists within a single tumour. The view that ‘there are many different types of cancers’ are increasingly shared by scientists and clinical oncologists. This has important implications, including the realisation that specific drugs must be developed and tested for molecularly defined tumours and effects in one might not necessarily be relevant to another cancer.
Conventional approaches to cancer management have focussed on eradicating the one underlying defect responsible for cancer progression. The focus has been on “fighting a war against cancer”, with no regard to the body’s intrinsic intelligence and protective defenses. A more holistic approach is needed – one that looks at the aetiology of this condition from a functional perspective. Central to this shift in paradigm is the understanding that cancer cells are different to healthy cells – they exhibit key differences in cellular physiology that allow them to flourish in unfavourable conditions, to proliferate in an uncontrolled manner, to establish their own blood and nutrient supply, to metastasise to distant sites and to avoid detection by the immune system.
There is considerable attention being paid to models of care delivery in cancer care. Much of cancer care is successfully delivered through a cancer specialist who refers to other specialist colleagues. There is a push to formalize cancer care planning by having a patient’s treatment planned by a multidisciplinary team. This approach may confer several benefits to patients, including :
- Improved confidence and reduced concerns that their treatment is based on the knowledge of just one individual
- Patient satisfaction and patient psychological wellbeing
- Continuity of good quality care that improves the quality of life and cost-effectiveness to the patient and third-party payers. Multidisciplinary teams comprise professionals from different disciplines, including general practice, who bring their expertise to bear simultaneously on individual cases.
Specifically targeting cellular differences characteristic of cancer cells is a key strategy we can employ to prevent and/or halt the progression of this disease.
Differences between cancer cells and healthy cells can essentially be grouped into two categories.
- Differences in intracellular (i.e. within the cell) physiology. These are:
- Alterations in cellular metabolism (i.e. how cells produce energy for survival);
- Differences in mitochondrial function
- Disruption to cell cycle control mechanisms.
- Differences in the extracellular environment (i.e. microenvironment) surrounding the cell. These are:
- Changes in production of pro-angiogenic factors, to stimulate localised angiogenesis.
- Altered environment to facilitate metastasis.
Cancer cells display an ‘addiction’ to glucose and a preference for energy production via anaerobic glycolysis, even if oxygen is available. This phenomenon is known as the Warburg effect and is mediated by cellular messengers such as:
- Hypoxia-inducible factors (HIFs). HIFs regulate the expression of genes that control cellular metabolism, angiogenesis, erythropoiesis, cell proliferation and apoptosis. It has been found that cellular HIF1 expression is raised in a variety of human tumours and that elevated HIF-1 activity in cancer correlates with poor patient outcomes.
- Phosphatidylinositol-3-kinase (PI3K). PI3K is involved in intracellular insulin signaling and also acts to halt cellular apoptosis. This pathway has been found to be overactive in many cancers, allowing for unregulated cellular proliferation. Activation of this pathway has also been noted to increase growth factor signalling and HIF activity. High insulin is a major inducer of PI3K activation.
New research indicates that starving cancer cells of glucose New research indicates that starving cancer cells of glucose can be highly beneficial and that dietary changes, nutrients and phytochemicals that inhibit HIF and PI3K activity, and/or promote AMPK activity, have been found to slow tumour growth and promote health.
Epigenetic research suggests that many cancers may not be initially caused by mutations in genes but rather by changes in how genes are transcribed. For example, methylation of oncogenes acts as a defensive mechanism against cancer, ensuring these are transcriptionally silenced and prevented from being read, and hypomethylation of oncogenes is implicated in tumorigenesis. However, hypermethylation has also been implicated in cancer; it is believed that the hypermethylation of CpG islands in the promoter regions of tumour suppressor genes results in reduced tumour suppressor activity and impaired DNA repair.
Research demonstrates that psychosocial stress and impairment in the stress response system (SRS) might be associated with cancer onset, progression and mortality. Stress hormones may affect tumour cell motility and invasion: noradrenaline, for instance, has been shown to induce breast and colon cancer migration, and glucocorticoids have been shown to inhibit cellular apoptosis in cervical and lung cancer cell lines. Management of stress and emotional support of patients undergoing cancer treatment is therefore vital.