How Cancer Starts

Cancer begins as a single cell that progresses through mutations to a malignancy. While there are over 100 distinct types of cancer, transformed malignant cells in all of the cancers can exhibit the following common properties:

• loss of anchorage dependence: whereas normal cells need to attach to surfaces in order to survive, cancerous cells can be found floating in suspension cultures
• loss of contact inhibition: whereas normal cells will arrest growth after they have filled up a defined area, malignant cells have no respect for this contact inhibition
• focus formation; in tissue cultures a single cell is transformed leading to a single cancerous colony
• genetic abnormalities such as deletions, translocations and chromosomal ploidy
• evasion of programmed cell death or apoptosis
• larger nuclear to cytoplasmic ratios
• sustained angiogeniesis through the secretion of growth factors
• Tissue invasion & metastasis of cancerous cells to other tissues
• Limitless replicative potential
• Insensitivity to anti-growth signals
• Self-sufficiency in growth signals

A Neoplasm is an abnormal mass, the growth of which is purposeless, autonomous and with a tendency to be an atypical and aggressive, new growth.  Oncology is the study of such neoplasms.

Carcinogenesis is the process by which cancer develops. By the time the cancer has been detected, it contains billions of cells, often including many normal cells like fibroblasts in the supporting connective tissue associated with the carcinoma. These normal connective cells of a tumor (neoplastic mass) are sometimes referred to as the stroma whereas the neoplastic cells of the tumor are called the parenchyma. However, There is evidence that cancers originate from a single abnormal cell. While most malignant tumors are monoclonal in origin, this does not mean that a singe mutation is by itself enough to cause cancer. In fact, evidence indicates the the genesis of a cancer typically requires several independent rare accidents that occur in the lineage of one cell. Cancers seem to arise by a process in which an initial population of slightly abnormal cells which are descendants of a single mutant ancestor, evolve from bad to worse through successive cycles of mutation. Such  evidence comes from epidemiological studies of the incidence of cancer as a function of age. If a single mutation were responsible, occurring with a fixed probability per year, the chance of developing cancer in any given year should be independent of age. In fact, for most types of cancer the incidence rises steeply with age as would be expected if cancer is caused by a slow accumulation of numerous random mutations in a single line of cells. Animal models also confirm that a single genetic alteration is insufficient to cause cancer but rather that multiple mutations are required in many genes (perhaps ten or more). For those cancers that have a discernible external cause, cancer also does not usually become apparent until long after exposure to the causal agent. The incidence of lung cancer, for example, does not begin to rise steeply until 1-2- after heavy smoking. The incidence of luekemias from radiation similarly do not show a marked rise until about 5 years after exposure.