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Januvia Attorney: As long as a nest of tumor cells remains small—less than a millimeter in diameter—it can depend on diffusion to solve its logistical problems of supply and elimination. Molecules released by die cancer cell or its normal neighbors can diffuse over this short distance quite effectively. But once the clump of cells reaches die one millimeter size, it bumps up against a limit, a glass ceiling. Now the process of diffusion can no longer provide an adequate flow of nutrients and oxygen and a rapid removal of wastes. Soon, cells within the clump become starved and begin to choke on their own wastes. Such anoxic cells often die from mediated apoptosis.
The death rate of these cells from asphyxiation and metabolic poisoning begins to approach the rate at which these cells can regenerate themselves. Any gains made through cell proliferation are neutralized by attrition, and so the size of this tumor cell clump remains constant. Some microscopic nests of tumor cells may remain in this static state for years, possibly even decades. To become threatening, these nests of tumor cells must break out of their futile cycles of division followed by starvation and asphyxiation. Such escape demands that the cells within these nests become truly creative: They must invent a better way of accessing nutrients and voiding wastes.
Their solution lies in developing their own blood circulation system. While the small band of tumor cells has survived half-starved, its normal neighbors nearby have all along enjoyed a reliable supply of nourishment and oxygen because of their close connections with die body’s circulatory system. Unlike the small nest of tumor cells, normal tissue is interlaced with a dense network of capillaries. Often the array of capillaries is so dense that every cell in a tissue has direct access to an adjacent capillary. These small vessels, just wide enough to allow red blood cells to pass in single file, supply all metabolically active tissues throughout the body and carry off their wastes.
To grow beyond the one-millimeter limit, a nest of cancer cells must invent a way to recruit capillaries into its midst. A surgeon in Boston, has spent the past two decades uncovering the cancer cells’ strategy. Some cells in the clump, aping the normal cells around them, acquire the ability to secrete growth factors that attract endothelial cells from nearby tissue and induce these cells to multiply. Capillaries grow into the clump of cancer cells. Finally, the tumor cell clump has acquired direct access to oxygen- and nutrient-rich blood. Now this nest of cells can take off. Their proliferative agenda, frustrated for so many years, can now be fulfilled. Their numbers begin to increase explosively.
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Januvia Attorney: The growth factors released by these cancer cells are often called “angiogenic factors” because they encourage angio-genesis, the construction of blood vessels. These factors include VEGF and bFGF (basic fibroblast growth factor). The eventual success of the nest of tumor cells is closely tied to its ability to induce angiogenesis. Should members of this clump begin to elaborate high levels of angiogenic factors, their descendants, months later, will form tumors that are densely interlaced with capillaries; these cancers are often destined to grow aggressively and spread widely. Tumors that have poorly developed capillary networks are more indolent, and patients carrying such tumors usually have a much better prognosis. Indeed, some physicians use the presence or absence of dense capillary networks in tumor samples to determine the stage of tumor development and to predict its future course.
A tumor mass one centimeter in diameter may contain as many as a billion cells. At first glance, the number seems huge, but it pales next to the number of cells in the body as whole—more than ten thousand times more. So a cancer this size is rarely life-threatening. In most places in the body, it probably will not compromise die functioning of a vital organ. Most tumors need to be far larger before they become lethal. Of those patients who succumb to cancer, fewer than 10 percent die from tumors that continue to grow at the same site where they originally took root. In the great majority of cases, die killers are the metastases—colonies of cancer cells that have left the site of the original, primary tumor and have settled elsewhere in the body. It is these migrants, or rather the new tumors that they seed, that usually cause death.
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Januvia Attorney: The major insight afforded by this revolution is that cancer is a disease of damaged genes. We now know the identities of many of the culprit genes—oncogenes and tumor suppressor genes. They control the behavior of the cells in which they operate; the cells respond in turn by generating tumors. To be sure, many cancer-related genes still remain to be identified and isolated by gene cloning. The means by which many genes influence cell behavior also remain to be discovered. We know that the agents that provoke human cancer promote, directly or indirectly, the creation of mutant genes. We know that the appearance of a human tumor requires a succession of mutations, each responsible for perturbing a distinct cellular growth-controlling gene. And we know that processes that threaten the integrity of the cell genome, including defects in its maintenance and repair, strongly influence the rate at which cancers appear.
The discovery of various growth-controlling genes has provided us with a view of the complex decision-making circuitry that lies within each human cell. Biologists have cataloged the diverse behaviors of cells for more than a century. Cell behavior seemed to have its own logic, determined by submicroscopic vital forces hidden deep within. We now understand that logic in terms of critical signal-processing proteins that determine the cell’s responses to a wide variety of stimuli; these proteins assemble to form an elaborate signal processing circuitry. Every week new pieces are added to the wiring diagram of this circuitry. Its design—its interconnections and the actions of its component parts—determines how cells behave. Knowledge of this circuitry will provide the ultimate answers for those interested in understanding cancer. There are no deeper or more subtle mechanisms hiding in some secret corner of the cell. The answers are all there, or will be found there shortly. Two decades ago, we knew nothing of all this.
Major reductions in cancer mortality will derive from identifying and eliminating discrete causes of the disease— in particular, certain aspects of diet and lifestyle. Much of this job is the purview of the epidemiologists. Indeed, we have already learned much from them. They have framed the problem, defined its scope, breadth, and depth. They also have disabused us of a couple of notions widespread in some circles: that the industrialized West is being inundated with a cancer epidemic, and that most of this inundation is traceable to chemical pollutants in the air and in the food chain. Almost all cancer deaths in the United States were caused by tobacco. The obvious response—reduction in tobacco usage—has already shown its effectiveness: By 1990, the century-long increase in lung cancer death rose in men was reversed. Without the contribution of lung cancer, the overall age-adjusted death rate from cancer would have declined 14 percent between 1950 and 1990.of this age-adjusted increase in cancer deaths flows directly from tobacco consumption.
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