What Is Cancer?
The fundamental unit of all living things is the cell. To maintain the health of the organism, all cells naturally expand and divide (multiply) to replace worn-out ones. When a cell multiplies swiftly and uncontrolled, it becomes cancer. This mechanism causes tumors to expand in the majority of malignancies. A tumor is an abnormal tissue development brought on by unchecked cell proliferation.
Malignant or benign tumors both exist. Unwanted growths are not cancer. Benign tumor cells do not spread to other bodily regions. Most benign tumors do not pose a threat to life.
Tumors with malignancy are cancer. Near the tumor, other tissues and organs may become infected with cancerous cells. Through the circulation or lymphatic system, they can potentially move to different parts of the body. We refer to this spreading as metastasis. Cancer may affect anybody, although it most frequently affects persons over the age of 55. Every third person develops cancer at some time in their lives.Even if we are more knowledgeable about some cancers than others, we frequently don’t understand why or how a healthy cell transforms into a cancer cell. We are aware that changes take place over a lengthy period of time in a succession of phases. The latency period is the interval between the initial cell change and the cancer’s detection.
All cells of an embryo are descended from the same fertilized egg and have the same genes. As the embryo develops, cells develop different morphologies and functions as a result of selective activation of certain groups of genes.
Cell differentiation: selective activation of genes that synthesize proteins not found in other cell types. Cells become specialized in structure and function. Embryonic development involves an orderly program of cellular changes that contribute to the embryo’s size and shape the form and function of cells, tissues, and organs. Example: only lymphocytes make antibodies.
Normal Cell Growth & Division
In a normal cell, division is controlled; it divides only when appropriate for its type and circumstances, and it does not lose its specialized differentiated identity. The generation of new cells replaces old or damaged cells.
About 12 cells make up the epidermis, the skin’s outermost layer. The basal layer’s (bottom row) cells divide only quickly enough to replace shed cells. A basal cell creates two cells when it divides. One continues to exist in the basal layer and is still able to divide. The other leaves the basal layer and is no longer able to divide. Thus, the bottom layer maintains the same number of dividing cells.
The Transition to Tumor Formation
Skin cancer develops when the regular ratio of cell division to cell death is upset.
Basal cells frequently maintain the ability to divide after each division, which results in a higher number of dividing cells than would otherwise be necessary to replace the cells being shed. As a result, a swelling mass of tissue known as a “tumor” or “neoplasm” is produced. The tissue eventually loses its typical structure as more and more dividing cells assemble.
Because of abnormalities in the genes that control these processes, tumors (also known as neoplasms) are collections of cells that are no longer subject to the normal regulation of growth and division.
Skin moles and lipomas are examples of benign tumors. These aberrant growths are no longer subject to regular control, but they still retain surface recognition proteins that hold them together and prevent them from spreading or invading. They also develop slowly and resemble normal cells.
Warts are benign tumors of the epidermis caused by any one of 60 types of human
papillomavirus (some of which cause cervical cancer). Warts do not have “roots“; but when they grow down, they displace the dermis.
They are most common in children and young adults. They spread by direct contact, and frequently resolve over several months, but some may take years.
Rx: salicylic acid: First pare the wart with a blade, pumice stone, or emory board. Soak it in warm water to increase uptake of salicylic acid, apply the acid, & let it dry, and cover. Normal skin may be protected with petroleum jelly. Repeat daily.
Hyperplasia & Dysplasia
Hyperplasia: Cell number is increased, but structure & arrangement are normal. It can be a normal, reversible response, e.g., a callus.
Dysplasia (precancerous) involves both excess proliferation AND loss of normal tissue arrangement & cell structure. Dysplasias can revert back to normal, but they may become malignant. Therefore, dysplasia should be carefully monitored or treated.
Stages in Progression to Breast Cancer
In the benign nevus, BRAF mutation and activation of the mitogenactivated protein kinase (MAPK) pathway occur. Atypia in dysplastic nevi reflect lesions within the cyclin-dependent kinase inhibitor 2A (CDKN2A) and phosphatase and tensin homologue (PTEN) pathways. Progression is associated with loss of differentiation. The verticalgrowth phase and metastatic melanoma are notable for striking changes in the control of cell adhesion.
A cancer’s microscopic appearance reveals its expected behavior and treatment response. Poorly differentiated tumors tend to develop more quickly, spread to other organs more often, and be less susceptible to therapy than tumours whose cells have a more typical look. They also have vast numbers of dividing cells. The majority of malignancies are given a numerical “grade” by doctors based on these variations in microscopic appearance. A cancer with a low numerical grade (grade I or II) has fewer aberrant cells than one with a greater number (grade III, IV).
Types of Cancer
Carcinomas, the most common types of cancer, arise from the cells that cover external and internal body surfaces. Lung, breast, and colon are the most frequent cancers of this type in the United States.
Sarcomas are cancers arising from cells found in the supporting tissues of the body such as bone, cartilage, fat, connective tissue, and muscle.
Lymphomas are cancers that arise in the lymph nodes and tissues of the body’s immune system.
Leukemias are cancers of the immature blood cells that grow in the bone marrow and tend to accumulate in large numbers in the bloodstream.
Proto-oncogenes: normal genes that code for proteins involved in cell division. These “growth factors” or hormones bind to receptors on the cell surface & activate enzymes inside the cell, which in turn activate protein transcription factors in the nucleus. The activated transcription factors turn on genes required for cell growth and proliferation.
Tumor Suppressor Genes (Anti oncogenes)
Anti-oncogenes (tumor suppressor genes): encode for protein signals that halt division or promote differentiation. If a pair of tumor suppressor genes are lost from a cell or inactivated by mutation, their functional absence can cause cancer. Individuals with familial retinoblastoma are born with one defective copy of the tumor suppressor gene “Rb”. This will not cause cancer as long as the other copy of the gene is functional, but if the 2nd copy mutates, the suppressor is knocked out.
Human Papilloma Virus
Papilloma viruses were recognized years ago as the cause of warts on the hands and feet or condyloma accuminata on the pubic area (penis and urethra in males or vulva and vagina in females).
For years, warts were considered just an ugly nuisance, rather than a forerunner of cancer. Warts on fingers and toes usually are not dangerous, but virus types that target the face can make skin cancer more likely.
Industrial Pollutants & Cancer
“The fact that many environmental chemicals can cause cancer has fostered the idea that industrial pollution is a frequent cause of cancer. However, the frequency of most human cancers (adjusted for age) has remained relatively constant over the past half century, in spite of increasing industrial pollution. Hence, in spite of evidence that industrial chemicals can cause cancer in people who work with them or in people who live nearby, industrial pollution does not appear to be a major cause of most cancers in the population at large.” – Source: NIH
Diet and Cancer
Diet may also play a role in determining cancer risk, but unlike tobacco and sunlight, the exact dietary components that influence cancer risk are unclear.
Limiting fat & calorie intake may decrease risk of some cancers (e.g. breast and colon cancer).
Consumption of fruits & vegetables correlates with a reduction in cancer risk. The responsible components remain unknown, but many recommend at least 5 servings/day.
Other sources of protein have not been linked to heterocyclic amines (HCAs), a class of carcinogenic compounds produced during the cooking of muscle meats (beef, pig, poultry, and fish) (e.g. eggs, tofu). When amino acids and creatine, a substance present in muscles, combine at high heating temperatures, HCAs are produced. The highest levels of HCAs are produced by frying, broiling, and grilling since these methods involve cooking the meat at extremely high temperatures. They have been linked to a higher risk of pancreatic, colorectal, and stomach cancer.