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. Normal colon cells are shown at the top of the diagram as a line of six, cuboidal, beige-colored cells, each with a tan, circular nucleus. After the cells accumulate two APC mutations, they develop into an adenomatous polyp. The adenomatous polyp is shown as an upside-down U-shaped loop of nine yellow, cuboidal cells each with a darker yellow circular nucleus; the yellow cells protrude from the center of the six original healthy beige cells.
After acquiring one RAS mutation, the adenomatous polyp develops into a dysplastic polyp. The dysplastic polyp looks like a dense clump of irregularly-shaped, yellow cells of different sizes that fill the upside-down U-shaped cavity.
After acquiring two TP53 mutations, the dysplastic polyp develops into colon carcinoma, in which the clump of yellow cells has changed into a larger mass of orange-colored, irregularly shaped cells of different sizes. After the colon carcinoma acquires chromosomal aberrations, it develops into a metastatic carcinoma. The orange-colored cells have changed to form an aggregation of red, irregularly shaped cells of different sizes with darker red, circular nuclei.
A rupture has formed at the base of the clump, and four of the irregularly shaped red cells appear to be dislodged and falling away from the larger cell aggregation as the cancer spreads. Later, a second mutation might provide the cancer cell with yet another reproductive advantage, which in turn intensifies its competitive advantage even more. And, if key checkpoints are missed or repair genes are damaged, then the rate of damage accumulation increases still further.
This process continues with every new mutation that offers such benefits, and it is a driving force in the evolution of living things — not just cancer cells Figure 1, Figure 2.
During the early stages of cancer, tumors are typically benign and remain confined within the normal boundaries of a tissue. As tumors grow and become malignant , however, they gain the ability to break through these boundaries and invade adjoining tissues.
Sometimes these symptoms will lead your doctor to do necessary tests to find the metastases. Researchers are learning more about how metastases may differ from the original tumor at the molecular and genetic level. This is why treatment for metastasis is often different from the treatment used for the original tumor. Treatment may include chemotherapy or hormone therapy.
Surgery and radiation therapy may also be options for some types of cancer. Doctors might try one type of treatment and then switch to another when the first treatment no longer works. Or you might have a combination of treatments.
Treatment that affects your entire body. Doctors call this systemic therapy. It includes chemotherapy and other medications, such as targeted therapy, hormone therapy, and immunotherapy. Treatment for the area with cancer. Doctors call this local therapy. It includes surgery, radiation therapy, and some other treatments. When you choose a treatment, talk with doctors who have experience treating metastatic cancer. Doctors can have different opinions on the best treatment plan. Learn more about getting a second opinion.
In some situations, metastatic cancer can be cured, but most commonly, treatment does not cure the cancer. But doctors can treat it to slow its growth and reduce symptoms.
It is possible to live for many months or years with certain types of cancer, even after the development of metastatic disease. It is important to ask your doctor about the goals of treatment.
These goals may change during your care, depending on whether the cancer responds to the treatment. It is also important to know that pain, nausea, and other side effects can be managed with the help of your health care team. This is called palliative care and should be a part of any treatment plan.
Research shows that palliative care can improve the quality of your life and help you feel more satisfied with the treatment you receive. Learn more about palliative care , or supportive care. Clinical trials offer treatments that are not yet available to the public.
A clinical trial might be the main treatment for metastases, or just one of the options. Whether or not you choose to continue treatment to shrink the cancer or control its growth, you can always receive palliative care to control the symptoms of cancer and the side effects of treatment.
Information on coping with and planning for end-of-life care is available in the Advanced Cancer section of this site. Researchers are studying new ways to kill or stop the growth of primary and metastatic cancer cells. These ways include:. Menu Contact Dictionary Search. Understanding Cancer. What Is Cancer? Cancer Statistics. Cancer Disparities. Cancer Causes and Prevention. Risk Factors.
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