CANCER, medically termed as CA or cellular aberration is one of the major causes of sufferings and death around the globe. It is cause by a carcinogen and co-carcinogen (required for carcinogen to affect human cell), and this was initiated by wrong and faulty life­style. A combined of these two produces cancer cell called oncogene, which triggers cancerous characteristics by producing protein that accelerates multiplication of cells, increases its responsiveness and growth—thus cancer means any malignant growth in any part of the body which can metastasized if severe or malignant (Smeltzer & Bare, 2004; Bellan et al., 2003). Cancer is a perilous disease resulted from mutant DNA sequences—which redirect important pathways affecting the regulation of tissue homeostasis, cell survival, and cellular death (DeVisser et al., 2006).Cancer Begin picture

Metastasis, or the spread of cancer cells to other parts of the body—happens when these cells break into tissues and penetrate lymph and blood vessels. Malignant cell transformation or carcinogenesis undergoes three cellular processes—initiation, promotion, and progression (Smeltzer & Bare, 2004).

Carcinogens are cancer causing agents creating a process of DNA genetic mutation forming abnormal cells. The CA disease process disregards the cell’s growth regulating signal, prompting abnormal cell to develop a clone and propagate abnormally (Price & Wilson, 1992). Bacteria and viruses, genetics, radiation, physical/chemical agents, hormonal/dietary factors, immunity, behavior, and lifestyle are considered as carcinogenic (Smeltzer & Bare, 2004).

Carcinogenic Agents

Viruses and Bacteria. Oncogenic viruses—e.g., herpes virus—are related to cervical cancer; DNA virus that cause hepatitis B is associated to hepatocellular carcinoma (Balabagno et al., 2006). Hodgkin’s and non-Hodgkin’s lymphoma, Burkitt’s lymphoma, and nasopharyngeal cancers are related to Epstein-Barr virus. Viruses of cytomegalovirus and human papillomavirus are related to cancer of the cervix and dysplasia. Human immunodeficiency virus (HIV) is related to Kaposi’s sarcoma (Carbone & Gaidano, 2001), while the human T-cell lymphotropic virus may be behind some lymphocytic leukemias and lymphomas. The Helicobacter pylori bacterium has been related with a higher occurrence of gastric malignancy, probably secondary to injury and inflammation of gastric cells (Smeltzer & Bare, 2004).

Physical Agents and Radiation. Radiation therapy, ionizing radiation and X-ray causes cellular mutations. Exposure to radioactive materials at nuclear power plants or nuclear weapon manufacturing sites is related to an increased incidence of multiple myeloma, leukemias, and cancers of the bone, lung, thyroid, breast, and other tissues. Lung cancer has been associated to background radiation coming from the natural decay processes that manufacture radon (Smeltzer & Bare, 2004). Skin cancers have been associated to ultraviolet radiation from the sun (Price & Wilson, 1992; Balabagno et al., 2006).

Chemical Agents. Studies support the link between bronchogenic carcinoma and lung cancer to agents such as polycyclic hydrocarbons and nitrosamines found in cigarettes and tobacco (Balabagno et al., 2006; Price & Wilson, 1992). Smoking is strongly associated with cancers of the lung, head and neck, esophagus, pancreas, cervix, and bladder. Chewing tobacco is associated with cancers of the oral cavity (Smeltzer & Bare, 2004). Tobacco may also act synergistically with other substances, such as alcohol, asbestos, uranium, and viruses, to promote cancer development (Smeltzer & Bare, 2004). Smoking and alcohol synergistic effects increase risk of cancers of esophagus, mouth, pharynx and larynx, including the cirrhotic process (Balabagno et al., 2006). The long list of suspected chemical substances keeps on growing and covers: aromatic amines and aniline dyes; pesticides and formaldehydes; arsenic, soot, and tars; asbestos; benzene; betel nut and lime; cadmium; chromium compounds; nickel and zinc ores; wood dust; beryllium compounds; and polyvinyl chloride (Smeltzer & Bare, 2004). Polycyclic aromatic hydrocarbons of automobile exhaust and combustion are known to be carcinogenic. The liver’s angiosarcoma is associated with polyvinyl chloride from plastic products (Balabagno et al., 2006).

Genetic. Certain cancers, specifically those with underlying genetic abnormalities, include chronic myelogenous leukemia, Burkitt’s lymphoma, meningiomas, retinoblastomas, acute leukemias, breast and skin cancers, and Wilms’ tumor. Cancers related with familial inheritance include nephroblastomas, retinoblastomas, malignant neurofibromatosis, pheochromocytomas, as well as ovarian, breast, colorectal, endometrial, prostate, lung and stomach cancers (Smeltzer & Bare, 2004). The gene related cancer—xeroderma pigmentosa hereditary disease—has a very high risk of early onset skin cancer (Lowenfels & Maisonneuve, 1999). Ovarian cancer, leukemia, and lymphoma are associated to autosomal recessive disorders (Balabagno et al., 2006).

Dietary Factors. Dietary substances related with increased risk of cancer include fats, salt-cured, alcohol, burnt meat or smoked meats, foods containing nitrates and nitrites, and a high caloric diet (Smeltzer & Bare, 2004). Low fiber and high fat diet increases the risk of colorectal cancer (Balabagno et al., 2006). Obesity is linked with endometrial cancer and likely with postmenopausal breast cancers. Obesity may also heighten the risk for cancers of the kidney, colon, and gallbladder (Smeltzer & Bare, 2004).

Hormonal Agents. Diethylstilbestrol increases the possibility of adenomacarcinoma of the cervix and vagina. Estrogen supplement is related with the risk of uterine cancer and endometrial hyperplasia (Balabagno et al., 2006). Prolonged estrogen replacement therapy and oral contraceptives are linked with increased incidence of endometrial, hepatocellular, and breast cancers, although they seem to lessen the likelihood of ovarian and endometrial cancers. Breast, prostate, and uterus cancers are considered to depend on endogenous hormonal levels to grow (Smeltzer & Bare, 2004).

Lifestyle and Behavior. Cervical carcinoma is associated to sexually active polygamous women. Penal cancer is usual to uncircumcised men. STD is considered to be cancer causing diseases since they lower immunity and increase reproductive infections (Balabagno et al., 2006).

Immunity. Patients who are immuno-incompetent have been demonstrated to have a higher incidence of cancer. Organ transplant recipients—who obtain immunosuppressive therapy to avoid rejection of the transplanted organ—have a higher incidence of Kaposi’s sarcoma, lymphoma, squamous cell cancer of the skin, and anogenital and cervical cancers. Patients with immunodeficiency diseases, e.g., AIDS, have a higher incidence of lymphoma, Kaposi’s sarcoma, and rectal and head and neck cancers. Patients who were given alkylating chemotherapeutic agents to manage Hodgkin’s disease have a higher incidence of secondary malignancies. Autoimmune diseases like rheumatoid arthritis and Sjögren’s syndrome are linked with increased cancer development. Finally, age-related changes like declining organ function, increased incidence of chronic diseases, and diminished immuno-competence may add to a higher incidence of cancer in older people (Smeltzer & Bare, 2004).

Theories of Cancer Development

A multistage model, the “Multi-Hit” Theory suggests that a number of mutations should occur earlier than the development of cancer—i.e., DNA repair genes, apoptosis genes, tumor suppressor genes and oncogenes. The “Two-Hit” Theory—as conceived by Knudson—avers that a normal cell turns into cancerous one upon the injury of both alleles. One allele is already damaged in the cases of inheritable cancers, so these kindreds have the increased possibility to develop cancer considering that only a single additional mutation is required (Lowenfels & Maisonneuve, 1999).

The Somatic Mutation Theory avers that cancer is drawn from a single somatic cell that has collected multiple DNA mutations. Quiescence is the natural state of cell proliferation in metozoa, while cancer is a disease of cell propagation due to mutations in genes that control the cell cycle as well as proliferation. Carcinogenesis embodies a crisis in tissue organization and that propagation is the natural condition of every cell (Soto & Sonnenschein, 2004).

Baver in 1928, designed this theory that supports the concept that genetic abnormalities can be induced by progressive hereditary susceptibility and mutational carcinogenic agents (Balabagno et al., 2006).

The Tissue Organization Field Theory suggests that carcinogens first act by disturbing the normal interactions that happen among cells in the parenchyma and stroma of an organ and, similar to what SMT avers, that proliferation is the normal state of every cell (Soto & Sonnenschein, 2004).

John Beard’s Trophoblastic theory of cancer suggests that cancer arises from germ cells that stray or get arrested in their journey. Trophoblasts and cancer cells are akin in their biological features. Under the influence of carcinogenic stimuli, these cells convert into malignant trophoblastic cells. These malignant trophoblastic cells assume features of the resident cell types in different organs, but the resulting cancers, no matter their site of origin or how distinct they appear morphologically, are of trophoblastic origin. Beard ascribed the destructive, invasive, and metastatic features of cancer to function normally displayed by trophoblastic cells, e.g., invasion of blood vessels, growth into the uterine wall, and spread beyond the uterus (Old, 2001).

Immune Surveillance is the method by which an organism develops an immune response against the antigens shown by a tumor (Balabagno et al., 2006). The Theory of Immune Surveillance explains why tumor cells escape immune-surveillance mechanisms. It says that neoplastic microenvironments favor polarized chronic pro-tumorigenic inflammatory states instead of those that represent acute anti-tumor immune responses. Based on classical theories of immune-surveillance and more recent awareness of the tumor-promoting properties of innate immune cells, researchers are currently investigating the effectiveness of novel anticancer strategies that are based on immunotherapeutics that can either bolster anti-tumor adaptive immunity or neutralize cancer-promoting properties of innate immune cells (De Visser et al., 2006).

Pathophysiology of Carcinogenesis

People believed that whatever medical terms or meanings have used to refer  cancer, still cancer is a killer. Cancer is fate of hopelessness, a fate of sufferings and a fate of dying and death. It is a traitor, a disease that has been diagnosed on unexpected times when you have nothing to do but to wait for your time.

In the world of healthcare where cancer is ubiquitous to death, the debilitating effects of psychological symptoms—such as the subtle, lack of fortitude, an easy sense of defeat, or the pessimistic notion that nothing else can be done—are actually more deadly than the disease itself. It is the anxiety … it is the stress brought about by the disease that defeats the human spirit more than the actual source, more than cancer.


  • Balabagno, A.V., Tuazon, J.A. & Cruz, J.G. (2006). Pathophysiology. Los Banos: UP Open University, 88–103, 113–213. Bellan, C., De Falco, G. & Leoncini, L. (2003).
  • Pathologic Aspects of AIDS Malignancies. Oncogene, 22, 6639–6645. Carbone, A. & Gaidano, G. (2001).
  • Acquired Immunodeficiency Syndrome–Related Cancer: A Study Model for the Mechanisms Contributing to the Genesis of Cancer. European Journal of Cancer, 37(10), 1184–1187. De Visser, K.E., Eichten, A. & Coussens, L.M. (2006).
  • Parodoxical Roles of the Immune System During Cancer Development. Nature Reviews Cancer, 6, 24-35. Lowenfels, A.B. & Maisonneuve, P. (1999).
  • Pancreatic Cancer: Development of a Unifying Etiologic Concept. Annals of the New York Academy of Sciences, 191–200. Old, L.J. (2001).
  • Cancer/Testis (CT) Antigens – A New Link Between Gametogenesis and Cancer. Cancer Immunity, 1, 1. Price, S.A. & Wilson, L.M. (1992).
  • Pathophysiology: Clinical Concepts of Disease Process, 4th ed. St. Louis: Mosby, 96–99. Smeltzer, S.C. & Bare, B.G. (2004). Brunner & Suddarth’s Textbook of Medical-Surgical Nursing, 10th Ed. PA: Lippincott Williams & Wilkins, 316–322. Soto, A.M. & Sonnenschein, C. (2004).
  • The Somatic Mutation Theory of Cancer: Growing Problems with the Paradigm? BioEssays, 26(10), 1097–1107. 

Originally posted 2012-08-25 07:22:44. Republished by Blog Post Promoter