4 ‘Adult Heal 432 Ht Neng : of Cancer 1 et dae fundamental and common process involved in aj mT ion. withi Il, deregulation 4 neop! jignancy. Due to mutation within a cell, gulati OE ae thas abnormal multiplication of cells tesujy a cy deregulation of genes or chromosomes. ‘ ‘The factors discussed below and shown in figure 8.3 istic the normal a functioning and involve in the pathogenesis of malignancy: — 1) Viruses: These agents cause many cancers and are easily transmitteg fn ‘one animal species to another either by direct or indirect contact, Son examples of viral cancers are: Lymphoma “tr leukaemia caused by Human T-cell Lettie, Lymphoma Virus (HT LV-1). ii) Chronic viral hepatitis caused by various strains of hepatitis i Vins ultimately, leading to liver cancer. 2) Gene and Chromosomal Abnormalities 3) Hereditary Factors 1) Virus Ne |<] 5) Other Factors Cell Serna ol i) Toxic stimli Carcinogen) + ii) Physical agents (Disturbed ‘Abnormal Cells Life Style) [> Fattreof immune iii) Chemical agents (eg, ystem/Defense | ———> zene) Abnormal ES ) [Proliferation of Cells| Malignancy/Cancer Figure 8.3: Etiological Factors Involved in Cancer 2) Gene and Chromosomal Abnormalities: Normal functioning of cel regulated by three sets of genes. Abnormality in any of these genes Teads malignancy or cancer. The responsible genes are: \cXGroup of Genes. | Normal Malfunction/Abnormal Seer op Roymel Fanetng) Function F tT a SUSAN: Proto- ( Regulate normal cell|Uncontrolled cell growth due 20 Pf" Oncogenes —_| growth point mutation, translocation.“ ,o amplification, | pei BNA Repair|Conect errors in DNA|Gene inactivation may eee Genes replication uncontrolled cell proifesion— >) Tumour Inhibit cell proliferation |Gene inactivation result ‘ ‘ iferation. Ke “Io ioe abnormal cell proliferati i ott- wit Management of Patient with Oncological Conditions 433 itary Factors: Individuals with family hi ir Hered ec tiskeat developing that partogan no ct any Hind of cancer pave @ gests fk wen ping t = Particular type of cancer. The chances cancer le genetic differences in vari iologi as ene es in various physiological and |). Differences in cell metabolism, inactivati iminati 9 e m, ion, and elimination of cancer | causing agents to which the tissues or cells are exposed. Differences in the cell’s ability to repair DNA damaged by injurious agents, ii) Variations in the levels of circulating hormone influencing the cell growth rate. ii) Variations in the immune system’s efficiency of eliminating the abnormal cells. 4) Failure-of Immune System or Defense Mechanism: Different environmental factors [Weak immunity or failure of . ns F defense mechanism leads to fuce mutation seeing ee ntti 01 4, 5) Other Factors: Various Immune system fails to recognise and destroy or environmental factors, eliminate mutant-gene encoded proteins chemical agents, and 4 Vise carcinogens either induce or normal cell proliferation disturb the normal cell Figure 8.4: Failure of Defense Mechanism mechanism, leading to uncontrolled cellular growth. For example, i) Environmental Factors: a) Tobacco, smokes, diets, environmental pollutants, etc. b) Heavy smaking causes lung, oral cavity and oesophagus cancers. ©) Excessive intake of alcohol causes liver cancer. ii Hormones: The relationship between malignancy and hormone is not clearly known; however, it is believed that hormones induce cell division of a malignant phenotype. For example(‘it is observed that cancers of ovary, breast, and endometrium in females and of the prostate and testis in males are influenced by hormones: iil) Obesity: In endometrial, breast “and prostate cancers, obesity is considered as a risk factor. Various metabolic and immunologic mechanisms are responsible in the development of cancer due to obesity. iv) Tonising Radiations: Gene mutation is induced by different types of radiations} (The carcinofenic effects of these radiations can be clearly seen in ‘atomic attack survivors, patients exposed for diagnosis.) physicians, scientists, and industrial workers. most common cancers caused by ionising radiations are leukaemia and malignant epitheliomas of skin. Gender and age of the individual, as Well as the rate and duration of radiation exposure decide the type of cancer developed. \434 ' Ada He r arcino moters: Cancer-causing chemi, vy) os ed Te ede Yalow environmental and The Sad 7 function as chemical carcinogenesis. Chemical carcinogen fi direct-acting agents (ie., are not activated in the body ce carcinogenic) or indirect-reacting agents OF Procarcnogey activated after metabolic spaversitia in the body). & Promoters themselves dornot cause cancer but induce carcings. other chemicals. For example, exposure of various carcing, hig wt (ike cigarette smoke) is associated with the risk for cancer develo as cigarette smoke contains procarcinogens and promoter, qi affecting the upper respiratory system. ay Given below are some examples of carcinogenic agents: a) Polycyclic and Heterocyclic Aromatic Hydrocarbons: 14, combustion (cigarette smoke), animal fat in broiled ang sma meats, benzopyrene, vinyl chloride, etc. b) Aromatic Amines and Azo Dyes: B-Naphthylamine and aniline c) Naturally Occurring Carcinogens: Aflatoxin B1, Briscofulvin, betel nuts./ar2ca- sV \s 4) Nitrosamines and Amides: These agents are formed in GIT fxg nitro-stable amines and nitrates, (which are used to. presne processed meats and other foods.’) vi) Miscellaneous Agents: Various metals (e.g. asbestos, chromium, nickel), insecticides, fungicides, and chemicals (e.g., polythlorinasé biphenyls) when volatilised and inhaled, induce cancer. 8.4.9. Classification of Cancer On the basis of the tissues involved, malignancy can be categorised into th following three groups: 1) Carcinomas: These malignancies arise from the surface, glandular, parenchymal epithelium. For example, transitional cell carcinoma of tt bladder (involving transitional epithelium), adenocarcinoma of the panes (nvolving glandular epithelium of pancreas), squamous cell carcinoma of oesophagus (involving squamous epithelium of the oesophagus), etc. 2) Sarcoma: This involves malignant tumour arising from primary tissues ob than the glandular or parenchymal epithelium, For example, i) Chondrosarcoma (cartilage malignancy), ii) Fibrosarcoma (fibroblast malignancy), iii) Liposarcoma (fat cell malignancy), iv) Myosarcoma (muséte cell malignancy), ¥)_ Osteosarcoma (bone-forming cell malignancy), and vi) Angiosarcoma (blood vessel malignancy), . 8 3) Leukaemia: It is the malignancy of blood-forming tissues, and de" from the precursors of WBCs. In this malignancy, any solid tumov fi formed. In leukaemia, cells multiply abnormally, diffuse within_— using Management of Patient with Oncological Conditions 435 marrow to multiply further and replace the normal blood-forming cells. Thus, the neoplastic cells ‘spill over’ into the circulation and a large number of abnormal cells circulate in the peripheral blood, qable 8.3 enlists the types of tumour classified based on the origin tissue: Table 8.3: Tumour Classificat tion Based on Specific Tissue of Origin [Tissue of Origin Malignant Tissue ial Carcinomas 1) Glands or ducts ‘Adenocarcinomas 2) Respiratory tract Small- and large-cell carcinomas 3) Kidney Renal cell carcinomas 9 Skin Squamous cell, epidermoid, and basal cell carcinoma, melanoma ‘Connective Tissue Sarcomas 1) Fibrous Fibrosarcoma 2) Cartilage Chondrosarcoma 3) Bone Osteogenic sarcoma (Ewing's tumour) 4) Blood vessels, Kaposi’s sarcoma 5) Synovia Synoviosarcoma Mesothelium Mesothelioma Lymphomas (Lymph | Hodgkin's disease Tissues) Non-Hodgkin’s disease Multiple myeloma Nerve 1) Glial Glioma = 2)_Adrenal medulla nerves_| Pheochromocytoma Blood (White Blood Cells) | Leukaemia 2 3) 8.4.10. Pathophysiology of Cancer At the cellular level, cancer prog mutation and selection for cells wit and metastasis. }) First Step (Mutation and Tumour Initiation): In this step, ression is a multi-step process including ith increased proliferation, survival, invasion, a genetic change causes a mutation in a single cell, causing it to multiply abnormally and become a tumour cell. Second Step (Cell Proliferation and Tumour Progression): i) In this step, the cells of the tumour population undergo further mutations resulting in continuous tumour development. ii) Mutated cells proliferate and divide more rapidly than normal cells. As a result, the resultant cell having an’ additional mutation will become dominant in the tumour population. Third Step (Clonal Selection and Malignancy): i) Clonal selection is a process in which tumour cell proliferation leads to the formation of a new clone of tumour cells having higher growth rate or other characteristics (like, survival, invasion, or metastasis). ii) In this stage, tumours continue to proliferate faster and become more malignant due to continuous clonal selection throughout tumour growth, iii) For example, the first step of tumour formation in colon cancer is increased proliferation of colon epithelial cells. Clonal selection occurs Shee 0Adult Health Nursing i ithin a proliferative cell population produces ie Se hen clonal selection continues furs, the size a proliferation potential of the benign neoplasm aaa eat ng in malignay carcinoma. The cancer cells then subsequently gro A ad across te ‘connective tissues of the colon wall. Finally, the cee | el Pent te colon’s wall and invade the bladder and small aan tg bloog and lymphatic vesselsgallowing them to metastasise body, Acquired = (environmental) Normal Cell [A‘dammaging agents: |—> ; chemicals } ‘Successful DNA repair 2) Radiation 3) Viruses DNA Damage Failure of Inherited mutations in: DNA repair 1) Genes affecting DNA repair Motations inthe a] 9) Genes affecting cell ‘genome of somatic cells garth or agua ‘Activation of Alterations of Inactivation of ywth-promoting || genes that regulate cancer. ee tpoptons suppressor genes | Expression of altered gene products and loss of regulatory gene products ‘Clonal expansion Additional mutations (progression) Heterogeneity Malignant neoplasm Figure 8.5: Progression of Cancer at Cellular Level 4) Fourth Step (Metastasis): i) Metastasis is a complex process in which cancer cells break down from the primary tumour and spread through the bloodstream or lymphatic system to other parts of the body. ii) The cells continue to proliferate at new sit tumours made up of cells that indicate the ti iii) The ability of tumours, like pancreatic cancer id iris, ciliary body. * choroid of eye) cancers, eer and uveal (iris, ciliary body tO metastasise is a major factor in their A 8.4.11, Staging of Cancer Staging is the process of assessing the level and location of cancer in the patient's body, It is the method through which the healthcare Provider identifies the st@8° of cancer. ites, eventually forming ne¥ issue of origin.