Cancer frequency, facts & stats
In Canada and the United States
- Approximately 1 in 2 will develop cancer in their lifetimes
- In Canada, cancer is the leading cause of death in men and women
- In the US, cancer is the 2nd most common cause of death – 2nd only to heart disease
Canadian Cancer Society (2017) estimates
- 206,200 new cases of cancer will occur in Canada this year alone.
- The number of new cases of cancer is expected to rise by about 40% in the next 15 years.
- Of new cancer cases, 51% will be lung, breast, colorectal and prostate
American Cancer Society (2017) estimates
- 1,688,780 new cases of cancer in the United States this year alone
Complementary & Alternative Medicine
- An estimated 50 to 80% of cancer patients use some form of complementary & alternative medicine (CAM) therapies in addition to conventional treatment (BIORC 2017).
- Of these patients, a smaller percentage obtain treatment from physicians who are trained in integrative care of cancer.
- Such physicians include: naturopathic doctors (NDs) board certified in naturopathic oncology (FABNO), MDs trained in integrative oncology, and traditional Chinese medicine practitioners with high level oncology training (BIORC 2017).
- The BIORC study showed a dramatic benefit with the incorporation of naturopathic medicine. 521 patients were enrolled in the prospective outcomes study treating breast, colon, lung, pancreatic, brain and skin cancers. For 8 patients with stage 4 colon cancer, those incorporating a naturopathic treatment protocol, BIORC reported an 80% survival rate after three years compared with 15% from a group at Seattle Cancer Care Alliance. With 12 patients with stage 4 lung cancer, BIORC reported 64% were alive after 3 years compared with 3% alive from a national data group (BIORC 2017).
- Natural treatments form an integral part of any cancer care program and an experienced naturopathic doctor with years of expertise in treating cancer is very important for any cancer patient. Dr. Ceaser has treated thousands of cancer patients in his 20 years of experience. Cancer deserves expert treatment with the most advanced natural therapies for the best outcomes. This is what is delivered through the care of naturopathic doctor Sean Ceaser, treating patients from all over the world.
What is Cancer?
Cancer goes by many names, including malignant tumours or neoplasms, and can affect any part of the human body. In general, the major characteristic of cancer is a group of cells that grow beyond their regular boundaries. Our bodies have amazing mechanisms in place to prevent such abnormal growth. However, the irregular division of cells is only one dimension of the formation and progression of cancer. Risk of cancer increases with sustained cell division in an environment rich in DNA-damaging agents, cellular changes normally used for wound-healing, growth factors, and inflammatory cells (Coussens and Werb 2002).
American Nobel Prize-winning virologist, Peyton Rous, was the first to identify cancer forming from “subthreshold neoplastic states” (Rous and Kidd 1941, Mackenzie and Rous 1941). That is to say, viral or chemical cancer-causing agents first cause cellular changes by modifying DNA irreversibly that are not necessarily apparent macroscopically. Nonetheless, these changes persist through future generations of cells until another stimulus directly or indirectly promotes visible cellular changes. Such changes include: the proliferation of cells, recruitment of inflammatory cells, more reactive oxygen species that damage DNA, as well as less DNA repair (Coussens and Werb 2002). As such, enhancing the body’s ability to detoxify metals and chemicals transmitted from the environment using chelation therapy can help prevent or reduce such changes to DNA and cell.
Tumours as Wounds
Furthermore, tumour cells irregularly dividing in the presence of cancer-causing agents and/or with DNA damage thrive in microenvironments with growth factors and inflammatory cells (Coussens and Werb 2002). Or, as Dvorak (1986) simply describes, tumours are wounds that fail to heal. In fact, tumour cells take advantage of our innate wound healing response to form the stroma (i.e. supportive tissue made up of connective tissue) necessary for self-sustaining maintenance and growth (Dvorak 1986). For example, tumours often secrete vascular endothelial growth factor – or VEGF (Dvorak et al. 1971, Senger et al. 1983, Senger et al. 1986). In the short-term, this growth factor increases the permeability of our vascular system (Senger et al. 1983) but in the long-term, this factor also reprograms vascular cells to form new blood vessels (Dvorak 2002, Dvorak 2003, Connolly et al. 1989, Ferrar and Keyt 1997, Keck et al. 1989, Leung et al. 1989, Benjamin, et al. 1999). When this process – called angiogenesis – occurs in tumours, it allows such overgrowth of cells to become self-sufficient with nutrients. Nonetheless, many therapies, such as hyperthermia and Poly-MVA, take advantage of the process of angiogenesis in order to cut off blood supply to tumors (anti-angiogenesis).
Tumours can change their microenvironments by using abnormal metabolic pathways to make energy. Known as the Warburg effect, these cells typically rely more heavily on the process of glycolysis and lactic acid fermentation rather than the regular aerobic use of mitochondria (Warburg et al. 1924). More recently, Vander Heiden et al. (2009) have proposed that this inefficient switch to use of glycolysis allows cancer cells to incorporate nutrients into biomass in order to proliferate. Nonetheless, in tumours with little blood flow, we see a deficiency in oxygen whereas in tumours with high blood flow, we see such a deficiency oxygen once they have outgrown their vasculature (Vaupel et al. 1989). Ultimately, cancers cannot thrive in the presence of oxygen, and therefore potent anti-cancer treatments include IV Ozone.
Tumours and Anti-Growth Signals
As such, cancer cells are self-sufficient in that they do not need growth signals in order to grow – they can make their own! These cells also do not listen to the body’s regular anti-growth signals that stop growth. For example, the well-known retinoblastoma protein helps stop cell division when necessary; yet, several types of cancer have lost the function of this protein (Giacinti and Giordano 2006). In fact, we often see a virus binding onto the retinoblastoma protein and inactivating the protein in cervical cancer (Kim et al. 2005, Cobrinik et al. 1993) and AIDS-related Burkitt’s lymphoma (Cinti and Giordano 2000, Cinti et al. 2000, De Falco et al. 2003, Lazzi et al. 2002).
While normal cells replicate a set number times before they are programmed to die, malignant cells typically continue to infinitely replicate and evade signals for cell death (Elmore 2007). Ultimately, in inflamed microenvironments, this evasion of cell death and/or restriction points for proliferation leads to the cell growth that has lost control (Coussens and Werb 2002). The benefit of using alternative therapies, like IV ALA, is that they work more extensively stop these growth signals and induce apoptosis.
Tumours and Inflammation
A growing body of evidence supports that tumours with inflamed microenvironments often arise from sites of infection and chronic inflammation (Coussens and Werb 2002). For example, a liver infection with Hepatitis C increases the risk of liver carcinoma (Bartosch 2010, Sanyal et al. 2010, Trinchet et al. 2007). Likewise, schistosomiasis – a disease caused by parasitic worms – predisposes patients to bladder carcinoma (Mostafa et al. 1999, Zaghloul 2012) as well as colon carcinoma (Ming-Chai et al. 1981, Mohamed et al. 1990, Salim et al. 2010). Furthermore, chronic Helicobacter pylori infection increases the risk of stomach cancer (Ernst and Gold 2000, Zhang et al. 2014). Largely, the mechanism attributed to the proliferation of tumours from sites of inflammation is via inflammatory cells aggravating DNA damage (Coussens and Werb 2002).
One way in which inflammatory cells can magnify the extent of DNA damage in pre-cancer cells is through an increase release of macrophage migration inhibitory factor, or MIF, from macrophages and T lymphocytes (Coussens and Werb 2002). The signaling molecule MIF minimizes the function of a tumours suppressor protein called p53. As such, higher levels of MIF then allow for more proliferation of cell lines and evasion of cell death (Coussens and Werb 2002). Nonetheless, pre-cancer cells with high levels of MIF do not respond to DNA damage as well, which then increases the likelihood of these cells becoming cancerous. Thus, inflammation, through many newly researched mechanisms, allows for the proliferation, survival and migration of tumour cells (Coussens and Werb 2002). However, many alternative medicine therapies help reduce such inflammation seen in tumour microenvironments including a novel naturopathic therapy that addresses over 23 different cancer targets to stop cancer growth: IV curcumin
Metastasis of Tumours
Furthermore, inflammation also allows cancer cells to invade other distant sites in the body – a process called metastasis (Wu and Zhou 2009). One such mechanism of action is through an increase in inflammatory cells such as tumour-associated macrophages, or TAM. In fact, Condeelis and Pollard (2006) found that invasive forms of advanced carcinomas have high levels of TAM. While TAM normally have positive functions in the body by repairing and remodeling tissue (Wu and Zhou 2009), these macrophages change in the tumour microenvironment to also enhance the proliferation of cell through the release of growth factors and stimulating angiogenesis (formation of new blood vessels) (Pollard 2004). Furthermore, TAM lead to the breakdown of the matrix surround cells and remodel this matrix to support motility of tumour cells (Condeelis and Pollard 2006). Or, as Condeelis and Pollard (2006) describe, TAM become “obligate partners for tumor cell migration, invasion and metastasis.” Nonetheless, alternative and complementary therapies can reduce cancer metastasis. For example, IV vitamin C inhibits hyaluronidase, which is an enzyme that accompanies cancer and that prompts metastasis.
Immune Evasion & Hijacking of Tumours
Cancer is tricky to treat also because its ability to evade the immune system. To evade the immune surveillance system, tumours may “edit” immune system – called immuno-editing. Initially, tumour cells are attacked and killed off by the immune cells until only a cell line remains that is not detected by the immune system – known as the elimination phase (Dunn et al. 2002, Dunn et al. 2004). In this way, these surviving cell lines stay dormant in patients during the equilibrium phase for years (Dunn et al. 2004). Lastly, this new genetic variant of cancer cells re-emerge in the escape phase with a multitude of genetic mutations that allow the tumour to remain undetected by the immune system (Dunn et al. 2002, Dunn et al. 2004). Nonetheless, cancer has many more means for evading the immune system.
Another mechanism in which cancer takes advantage of the immune system is through immune cells called cytotoxic T cells (CD8+) and helper T cells (CD4+) (Vinay et al. 2015). In truth, these immune cells are responsible for restricting the proliferation of cancer cells by producing signaling molecules called interferon (IFN)-γ and cytotoxins (Zamarron and Chen 2011). Yet, other molecules secreted during chronic inflammation will negate the functions of these molecules (Balkwill and Mantovani 2002, Rakoff-Nahoum 2007, Zamarron and Chen 2011). Thus, malfunctioning T-cells will promote the proliferation of cancer under inflammatory conditions. Interestingly, therapies like mistletoe therapy help re-regulate T-cell function to act against cancer.
Bartosch, B. (2010) Hepatitis B and C viruses and hepatocellular carcinoma. Viruses. 2(8):1504–9.
Benjamin, L. E., Golijanin, D., Itin, A., et al. (1999) Selective ablation of immature blood vessels in established human tumors follows vascular endothelial growth factor withdrawal. J Clin Invest. 103:159–65.
Canadian Cancer Society, Statistics Canada, and Public Health Agency of Canada. (2017) Canadian
Cancer Statistics: Incidence; Mortality; Survival and prevalence. Data retrieved from: http://www.cancer.ca/en/cancer-information/cancer-101/canadian-cancer-st….
Cinti, C. and Giordano, A. (2000) The retinoblastoma gene family: its role in cancer onset and progression. Emerg Ther Targets. 4:765–83.
Cinti, C., Leoncini, L., Nwongo, A., et al. (2000) Genetic alterations of the retinoblastoma-related
gene RB2/p130 identify different pathogenetic mechanisms in and among Burkitt’s lymphoma subtypes. Am J Pathol. 156:751–60.
Cobrinik, D., White, P., Peeper, D.S., et al. (1993) Cell cycle-specific association of E2F with the p130 E1A-binding protein. Genes dev. 7:2393–404.
Condeelis, J. and Pollard, J. W. (2006) Macrophages: obligate partners for tumor cell migration, invasion and metastasis. Cell. 124:263–6.
Connolly, D. T., Heuvelman, D. M., Nelson, R., et al. (1989) Tumor vascular permeability factor stimulates endothelial cell growth and angiogenesis. J Clin Invest. 84:1470–8.
Coussens, L. M. and Werb, Z. (2002) Inflammation and cancer. Nature. 420(6917):860–7.
De Falco, G., Bellan, C., Lazzi, S., et al. (2003) Interaction between HIV-1 Tat and pRb2/p130: a possible mechanism in the pathogenesis of AIDS-related neoplasms. Oncogene. 22:6214–9.
Dunn, G. P., Bruce, A. T., Ikeda, H., et al. (2002) Cancer immunoediting: from immunosurveillance to tumor escape. Nat Immunol. 3(11):991–8.
Dunn, G. P., Old, L. J., Schreiber, R. D. (2004) The Three Es of Cancer Immunoediting. Annu Rev Immunol. 22(1):329–60.
Dvorak, H. F. (1986) Tumors: wounds that do not heal. Similarities between tumor stroma generation and wound healing. N Engl J Med. 315(26):1650–9.
Dvorak, H. F. (2002) Vascular permeability factor/vascular endothelial growth factor: a critical cytokine in tumor angiogenesis and a potential target for diagnosis and therapy. J Clin Oncol. 20:4368–80.
Dvorak, H. F. (2003) Rous-Whipple Award Lecture. How tumors make bad blood vessels and stroma. Am J Pathol. 162:1747–57.
Dvorak, H. F., Orenstein, N. S., Carvalho, A. C., et al. (1979) Induction of a fibringel investment: an early event in line 10 hepatocarcinoma growth mediated by tumor-secreted products. J Immunol. 122:166–74.
Elmore, S. (2007). Apoptosis: a review of programmed cell death. Toxicol Pathol. 35(4):495–516.
Ernst, P. B. and Gold, B. D. (2000) The disease spectrum of Helicobacter pylori: the immunopathogenesis of gastroduodenal ulcer and gastric cancer. Annu Rev Microbiol. 54:615–40.
Ferrara, N. and Keyt, B. (1997) Vascular endothelial growth factor: basic biology and clinical implications. EXS. 79:209–32.
Giacinti, C. and Giordano, A. (2006) RB and cell cycle progression. Oncogene. 25:5220–7.
Keck, P. J., Hauser, S. D., Krivi, G., et al. (1989) Vascular permeability factor, an endothelial cell mitogen related to PDGF. Science. 246:1309–12.
Kim, Y. T. and Zhao, M. (2005) Aberrant cell cycle regulation in cervical carcinoma. Yonsei Med J. 31:597–613.
Lazzi, S., Bellan, C., De Falco, G., et al. (2002) Expression of RB2/p130 tumor-suppressor gene in AIDS-related non-Hodgkin’s lymphomas: implications for disease pathogenesis. Hum Pathol. 33:723–31.
Leung, D. W., Cachianes, G., Kuang, W. J., et al. (1989) Vascular endothelial growth factor is a secreted angiogenic mitogen. Science. 246:1306–9.
Balkwill, F. and Mantovani, A. (2001) Inflammation and cancer: back to Virchow? Lancet. 357(9255):539–45.
Ming-Chai, C., Chi-Yuan, C., Fu-Pan, W., et al. (1981) Colorectal cancer and schitosomiasis. Lancet. 317(8227): 971–3.
Mohamed, A. R., al Karawi, M. and Yasawy, M. I. (1990) Schistosomal colonic disease. Gut. 31:439–42
Mostafa, M. H., Sheweita, S. A., and O’Connor, P. J. (1999) Relationship between Schistosomiasis and Bladder Cancer. Clin Microbiol Rev. 12(1):97–111.
Pollard, J. W. (2004) Tumour-educated macrophages promote tumour progression and metastasis. Nat Rev Cancer. 4:71–8.
Rakoff-Nahoum, S. (2006) Why cancer and inflammation? Yale J Biol Med. 79(3-4):123–30.
Salim, O. E. H., Hamid, H. K. S., Mekki, S. O. et al. (2010) Colorectal carcinoma associated with schistosomiasis: a possible causal relationship. World J Surg Oncol. 8:68.
Sanyal, A. J., Yoon, S. K., and Lencioni, R. (2010) The etiology of hepatocellular carcinoma and consequences for treatment. Oncologist. 15(4):14–22.
Senger, D. R., Galli, S. J., Dvorak, A. M., et al. (1983) Tumor cells secrete a vascular permeability factor that promotes accumulation of ascites fluid. Science. 219:983–5.
Senger, D. R., Perruzzi, C. A., Feder, J., et al. (1986) A highly conserved vascular permeability factor secreted by a variety of human and rodent tumor cell lines. Cancer Res. 46:5629–32.
Siegel, R. L., Miller, K. D., and Jemal, A. (2017) Cancer Statistics, 2017. CA: Cancer J Clin. 67:7–30.
Trinchet, J. C., Ganne-Carrié, N., Nahon, P., et al. (2007) Hepatocellular carcinoma in patients with hepatitis C virus-related chronic liver disease. World J Gastroenterol. 13(17):2455–60.
Vander Heiden, M. G., Cantley, L. C., and Thompson, C. B. (2009) Understanding the Warburg effect: the metabolic requirements of cell proliferation. Science. 324(5930):1029–33.
Vaupel, P., Kallinowski, F., and Okunieff, P. (1989) Blood flow, oxygen and nutrient supply, and metabolic microenvironment of human tumors: a review. Cancer Res. 49(23):6449–65.
Vinay, D. S., Ryan, E. P., Pawelec, G., et al. (2015) Immune evasion in cancer: Mechanistic basis and therapeutic strategies. Semin Cancer Biol. 35:S185–98. Warburg, O., Posener, K., and Negelein E. (1924) “Ueber den Stoffwechsel der Tumoren”
Biochemische Zeitschrift. 152:319–44. (German). Reprinted in English in the book On metabolism of tumors by O. Warburg (1930) Publisher: Constable, London.
Wu, Y. and Zhou, B. P. (2009) Inflammation: a driving force speeds cancer metastasis. Cell Cycle. 8(20):3267–73.
Zaghloul, M. S. (2012) Bladder cancer and schistosomiasis. J Egypt Natl Canc Inst. 24(4):151–9.
Zamarron, B. F. and Chen, W. (2011) Dual roles of immune cells and their factors in cancer development and progression. Int J Biol Sci. 7(5):651–8.
Zhang, W., Lu, H., and Graham, D. Y. (2014) An Update on Helicobacter pylori as the Cause of Gastric Cancer. Gastrointest Tumors. 1(3):155–65.