How can cell division cause cancer
An accumulation of a combination of such genetic errors leads to a neoplastic phenotype. Examples are discussed of human cancers in which increased cell division, which drives the accumulation of genetic errors and can lead to neoplastic transformation, is caused by hormones, drugs, infectious agents, chemicals, physical or mechanical trauma, and other chronic irritation.
Abstract Carcinogenesis research is increasingly focused on chemicals that are not genotoxic and yet, at high doses, can induce cancer, apparently by increasing cell proliferation.
The challenge for medical researchers is to identify which of these mutations are responsible for particular kinds of cancer. This process is akin to searching for the proverbial needle in a haystack, because many of the mutations present in these cells have little to nothing to do with cancer growth.
Different kinds of cancers have different mutational signatures. However, scientific comparison of multiple tumor types has revealed that certain genes are mutated in cancer cells more often than others. For instance, growth-promoting genes, such as the gene for the signaling protein Ras, are among those most commonly mutated in cancer cells, becoming super-active and producing cells that are too strongly stimulated by growth receptors.
Some chemotherapy drugs work to counteract these mutations by blocking the action of growth-signaling proteins. The breast cancer drug Herceptin , for example, blocks overactive receptor tyrosine kinases RTKs , and the drug Gleevec blocks a mutant signaling kinase associated with chronic myelogenous leukemia.
Other cancer-related mutations inactivate the genes that suppress cell proliferation or those that signal the need for apoptosis. These genes, known as tumor suppressor genes , normally function like brakes on proliferation, and both copies within a cell must be mutated in order for uncontrolled division to occur.
For example, many cancer cells carry two mutant copies of the gene that codes for p53 , a multifunctional protein that normally senses DNA damage and acts as a transcription factor for checkpoint control genes. Gene mutations accumulate over time as a result of independent events. Consequently, the path to cancer involves multiple steps. In fact, many scientists view the progression of cancer as a microevolutionary process.
Figure 1: Microevolution of a cancer cell A series of mutations in a cell causes it to proliferate more than its immediate neighbors. As the cluster of dividing cells grows over time, further mutations turn atypical hyperplasia into a cancer carcinoma.
The spreading of cancer cells to other tissues and organs metastasis occurs when the adhesion of these cancerous cells breaks down, and they are able to travel easily to new locations. The population at the far left side has normal cells; these are shown arranged in a single layer to form a closed, hollow, ring. In the second population, hyperplasia, a group of cells on the left side of the ring begins to divide and increase in number, forming a second and third layer of cells within the ring.
In atypical hyperplasia, the three layers of cells on the left side of the ring have expanded to form a small mass of purple and blue, rapidly proliferating cells. The cells are no longer organized in rows, and some are even piled up on top of one another.
In carcinoma in situ , the small mass of cells has expanded further to form a dense population of blue and purple, mutant cancer cells that occupies most of the space within the ring of normal healthy cells. In the final cell population, microinvasive, a rupture in the left side of the ring of healthy cells has appeared, and several purple, mutant cancer cells are shown spilling out from the dense mass of cancer cells inside.
The diagram shows five different groups of cells, which are labeled: normal, hyperplasia, atypical hyperplasia, carcinoma in situ , and microinvasive. Figure 2 colon is shown in five stages. Genes make sure that cells grow and make copies reproduce in an orderly and controlled way. And are needed to keep the body healthy.
Sometimes a change happens in the genes when a cell divides. This is a mutation. It means that a gene has been damaged or lost or copied too many times. Mutations can happen by chance when a cell is dividing. Some mutations mean that the cell no longer understands its instructions. It can start to grow out of control.
There have to be about 6 different mutations before a normal cell turns into a cancer cell. What is cancer and how does it start? Cancer Research UK ! Content not working due to cookie settings. Neuroendocrine tumors form from cells that release hormones into the blood in response to a signal from the nervous system. These tumors, which may make higher-than-normal amounts of hormones, can cause many different symptoms. Neuroendocrine tumors may be benign or malignant.
Our definition of neuroendocrine tumors has more information. Carcinoid tumors are a type of neuroendocrine tumor. They are slow-growing tumors that are usually found in the gastrointestinal system most often in the rectum and small intestine. Carcinoid tumors may spread to the liver or other sites in the body, and they may secrete substances such as serotonin or prostaglandins, causing carcinoid syndrome.
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