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What is cancer, anyway?
It is an abnormal growth of cells in the body that do not obey the rules. To be considered "cancer," the cells must
* look different from normal cells * divide rapidly enough to upset the body's status quo * have the potential both to invade adjoining cells and tissue and to spread to other parts of the body
Cancer is not one disease but more than one hundred different diseases. Each has its own personality, from slow-growing, sleepy "lapdogs" of cancers to those that move quickly and aggressively, but that may also be better targets for some of our current anticancer therapies.
THE WRONG KIND OF CELLS
A normal body cell viewed under a microscope looks rather round, oblong, or cubelike and has certain predictable parts. Cells that have similar functions in the body look alike because a particular kind of cell does a specific job best. Thus, normal breast duct cells look like each other, but very different from normal red blood cells.
Sometimes, in all the trillions upon trillions of cells in the body, a glitch occurs in the quality control, producing a cell that looks different, or atypical (abnormal), under the microscope. The shape may be irregular, the components (such as the cell membrane and the nucleus) broken or disrupted, and there may be extra or missing parts.
Some of these cells are only slightly atypical, while others are wildly different from normal cells. A group of cells that is slightly abnormal is still considered benign (not cancer); the very deviant ones are called malignant (cancer) cells.
Even among malignant cells, there is wide variation in just how abnormal the cells are. Many cancer cells somewhat resemble the normal cells from the same organ or tissue; at the other extreme are cells that look utterly bizarre. How abnormal these cancer cells appear under a microscope provides clues to how they are likely to behave.
Cancer cells are not "super" cells. In fact, they are poor-quality cells: weaker, less resilient, and less functional than normal cells. They are not invincible and they can be killed.
TOO MANY CELLS
The life cycle of every normal cell in the body follows a particular timetable. Each breast duct cell, for instance, divides about as often and lasts about as long as every other breast duct cell, but has a totally different pattern from that of a red blood cell. When a normal cell reproduces, on schedule, it divides into two daughter cells just like itself. The daughter cells mature to do whatever they are supposed to do, wherever they are supposed to do it, and then reproduce in turn. Because normal cells also wear out and die on schedule, the adult body maintains a "zero population growth" cell balance.
If, for any reason, the status quo is upset and there are too many cells, the resulting overgrowth is called neoplasia, or new growth. These cells can clump together as a tumor, one kind of neoplasm. Tumors and neoplasms can be benign or malignant.
Benign neoplasms include those in which older (but normal) cells pile up because they are living longer than they should and/or the body is not disposing of dead cells quickly enough. As long as the buildup in cells is not caused by the cells reproducing more often than they should, this is called nonproliferative change. If some cells begin dividing more often than normal, but the cells themselves are normal, the result is proliferative change without atypia; this condition is also called hyperplasia, meaning "too much" growth. A freckle, a wart, an ovarian cyst, and most benign breast tumors are examples of one of these two kinds of benign neoplasms.
If those cells that are dividing too quickly include some that are abnormal-but not too abnormal-the condition is still benign and is called proliferative change with atypia or dysplasia (for "bad" or abnormal growth). This kind of change may reverse itself during the normal turnover of cells, may stay the way it is, or may grow worse. A change like this is not in any way cancer, but it is a warning that a quality control problem exists that can be temporary and minor, or more serious. It can somewhat increase the chance that a cancer will develop in that organ later.
If the cells look quite atypical, but are confined to one limited site such as the duct of the breast or the top layer of the cervix, the changes are called carcinoma in situ or noninvasive carcinoma, among other names. The labels-"carcinoma" means cancer-are a holdover from earlier years when doctors considered this the very earliest stage of cancer. While some doctors still believe this, others believe that the cells have not shown that they are abnormal enough to behave like cancer cells (that is, invade neighboring tissues); they may never become that atypical. In any case, while the area needs to be removed or destroyed, carcinoma in situ is not in itself life-threatening. However, carcinoma in situ does significantly increase the risk of an invasive cancer developing in that organ later.
An invasive (or infiltrating) cancer means that the cells that are dividing too often are sufficiently abnormal to behave in ways that can threaten the body. The doctor can see under the microscope that the cells have invaded adjoining tissues. A cell that can do this has the potential to spread elsewhere in the body.
HOW CANCER CELLS BEHAVE
At best, the cancer cell is a parasite, taking up space, devouring nourishment, and crowding out the normal cells. Because it is abnormal, the cancer cell lacks the capacity to function as a full team member. Depending on how abnormal it is, the cancer cell may continue to do some of the things that normal cells are supposed to do, but it usually contributes little or nothing to the body community. It works less efficiently than a normal cell and thus needs larger amounts of cell nutrients to keep going. The cancer cell exists primarily to eat and reproduce.
What is more dangerous is that the cancer cell pays little heed to the body's territorial rules. Normal cells with intact cell parts keep to themselves and stay at a distance from other kinds of cells. Even when benign cells overgrow and jostle or push against neighboring tissue, which is what is happening when benign tumors cause discomfort, they still respect the boundaries of other cells.
Not so the cancer cell when it gets pushed into adjoining body tissue. Lacking a normal "wall" and needing to survive in this new terrain, it penetrates and takes over the cells there for its own use. This is invasive cancer.
These maverick cancer cells can break away, hitch a ride through the circulatory system, and wander elsewhere (metastasize) in the body. Extremely abnormal cells are able to plant themselves and grow elsewhere in the body, away from the organ where they originated. This spread is called metastatic cancer.
HOW CANCER COMES ABOUT
We do not know yet what causes cancer, but we are learning more about how it happens. For cancer to develop, there must be an abnormal cell, a mechanism through which it can divide rapidly and establish a colony, and a body immune system that does not destroy it.
Inside the nucleus, or command chamber, of each body cell are twenty-three pairs of chromosomes along the double helix ("twisted ladder") molecule of DNA. DNA contains the general information for any living cell. The pairs of chromosomes contain millions of genes; each gene carries the code for a specific characteristic, rather like a bar code that identifies a piece of merchandise for a scanner at a supermarket. This genetic code, which is passed from each cell to its offspring, tells the daughter cell which parts of the DNA message it should read and follow: what kind of cell it is, what it is supposed to do, when to divide, and how to repair itself.
When the cell divides, the DNA "ladder," along with its chromosomes, splits down the middle through the rungs. Each half of the ladder is made whole again using material brought to it by the cell's supply source (RNA), whereby it becomes the DNA for one of the two daughter cells.
A mistake in one of the millions of genetic messages in a cell produces a change, or mutation. The change may be for the better and make the cell function more effectively, or it may be so catastrophic that the cell dies immediately. It may also be a flawed message that can get passed down from generation to generation of daughter cells without noticeable effect. But a cell with a flawed genetic message-the atypical cell-is more vulnerable than the normal cell to additional mutations and may eventually become a cancer cell. The more atypical the individual cell is, and the more atypical cells there are, the greater the chance for a cancer to develop.
Most cancer researchers now believe that cancer occurs not because of a single major event that turns a normal cell cancerous, but as a result of multiple hits to the genes. Thus, damage accumulates until it reaches a kind of critical mass, at which point the cancer "switch" turns on. The result of a combination of hits may be far greater than the sum of the individual effects. So, whether or not cancer occurs seems to depend not only on how many hits there are, but also on what kinds they are, how often they come, how strong they are, and how much chance the body has to recover between them.
Some hits are called initiators because they can cause direct damage to the genes. Substances that produce these hits are called carcinogens or mutagens because they can produce cancer or cell mutations. Tobacco is a known initiator for lung cancer, for example, as is the hormone DES for one kind of vaginal cancer. Other hits, like alcohol, are promoters-they encourage atypical cells to grow. Then there are miscellaneous hits such as a family history of a certain cancer, for instance.
The likelihood of developing most cancers increases with age. The longer a person lives and the more genetic messages that get passed on, the more opportunities there are for a message to get scrambled.
The total number of cells in the body is normally controlled by a balance of growth genes that urge a cell to divide and suppressor genes that tell it to wait. Current thinking about genes and cancer focuses on three types of genes, all related to how often cells divide.
The first type is the proto-oncogene. "Onco" means tumor, but proto-oncogenes are the ordinary healthy genes that control how often a cell divides. Cells in the body normally reproduce very rapidly while a person is growing (from a fertilized egg to a baby in nine months is impressive!), is repairing a broken bone, or is pregnant or breastfeeding. Except at these times, cells divide on a strict schedule: They replace only those that die and thus maintain the body's status quo.
The second type of gene is the anti-oncogene (tumor suppressor or growth suppressor gene), the normal gene that keeps the brakes on the proto-oncogenes so that cells divide on just the right timetable. For instance, anti-oncogenes seem to "switch off" or suppress the "rapid growth" genes that program cells to divide so frequently during the first nine months of life. Healthy anti-oncogenes also detect abnormal cells and do not give them "permission" to divide. The problem arises when one or more anti-oncogenes mutate so that they can no longer keep the brakes on-and cells begin dividing too often. With this speedup, cell quality control suffers.
A proto-oncogene may mutate to become the third type of gene: the oncogene (or carcinogenic oncogene), an abnormal gene that gives its cell the message to make more growth factors so it matures faster and divides sooner. When the cell divides, it passes this genetic message to the two daughter cells. These cells, both flawed and dividing too often, are at high risk for becoming more abnormal through more mutations. Meanwhile, the mutated anti-oncogene no longer withholds permission for the flawed cell to divide and no longer keeps the rate in check. The result is often cancer.
But how and why do proto-oncogenes "switch on" to become carcinogenic oncogenes? What causes anti-oncogenes to mutate? Are there ways to prevent or even reverse these mutations? These are key puzzles in basic cancer research.
For example, researchers have focused on a particular gene, p53, one of the genes that normally acts as an anti-oncogene, or tumor suppressor. If the DNA in p53 is damaged (perhaps by tobacco smoke or some other carcinogen), it mutates and may no longer be able to hold the proto-oncogenes in check, beginning a quality control breakdown.
Scientists looking for a common mechanism in the development of various cancers have found that p53 appears to be damaged in about 90 percent of all human cancers. The mutation may occur decades before cancer appears and is only one of several genetic changes that move the cell along the path toward cancer-but it appears to be a necessary step. If this step could be prevented or reversed, ...
Scientists researching p53 are looking for the "fingerprints" of factors that may have led to the original mutation. During the last several years, publicity has linked mutated copies of several genes (BRCA1, BRCA2, and others) to family clusters of breast cancer and ovarian cancer. These genes, mostly anti-oncogenes or tumor suppressor genes, may mutate at any time during a woman's life, but the greatest concern is that a mutated copy of one of these genes may be passed down in some families. The baby who receives one of these mutated genes has already, before birth, taken a major step toward cancer.
Only 5 to 10 percent of all breast cancers seem to fall into this category, with the disease striking many people from several overlapping generations in a family, all at an early age. This is not usually the problem if a woman has a family history of one or two people diagnosed with the same cancer after age fifty-five or so. A woman who receives the gene may also never develop cancer, because this is only one mutation in a series required for the disease. (For more information, see "Who Gets Breast Cancer?" in Chapter 11.)
A big factor in whether a person develops cancer is the body's immune system. Our bodies defend us against atypical cells all the time. The cell itself may repair some small mutations. Some abnormal cells may lose the ability to reproduce. Normal cell turnover disposes of abnormal cells as well as normal ones.
Throughout our lives, the body's immune system recognizes atypical cells (including cancer cells) as "enemy" and destroys them. Unfortunately, some cancer cells seem able to slip through the body's surveillance: They pass for normal cells or disguise themselves. Others may divide so rapidly or are so aggressive that they overwhelm even the strongest body defenses.
Or, the immune system may be exhausted or operating at partial power. People with AIDS or people on certain medications that suppress the body's immune system (to keep it from rejecting a transplanted organ, for instance) are especially vulnerable to cancer. When the immune system is stressed severely and continuously by anything, such as poor diet, personal losses, or relationship difficulties, it may become less effective, less able to search out rogue cancer cells and destroy them.
SEARCHING FOR CANCER CAUSES
With our current level of knowledge we cannot say, "Such-and-so caused this cancer." If we were to try to indicate the causes of an individual cancer on a pie-shaped chart, we would have to draw a piece for the person's inherited vulnerability, a piece for age, a piece for possible initiators (many of which we do not know yet), a piece for a weakened immune system, and so on. Each person's chart would be different and, knowing what we do now, we could only guess at how big each section of the pie would be.
But more information about possible causes of cancer comes in all the time, much of it from researchers working at the molecule and gene level. Statisticians and epidemiologists (scientists who study patterns of disease in large populations of people) continue searching for common factors among women diagnosed with a particular women's cancer. The challenge for all these researchers lies in clarifying which factors actually contribute to the disease, which are effects of the disease, and which are innocent bystanders.
Excerpted from Women's Cancers by Kerry A. McGinn Pamela J. Haylock Copyright © 2003 by Kerry A. McGinn and Pamela J. Haylock. Excerpted by permission.
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