Januvia Class Action News – 4/27/2012: If you were prescribed Januvia and have suffered negative side effects, please contact us today so that we can put you in touch with an attorney to advise you of your legal rights.
Januvia Class Action: To understand cancer, we must understand how the inner blueprint of normal cells tells them when they should multiply. We must know how that blueprint becomes deranged in the heart of the cancer cell. The roots of cancer lie in that blueprint. This copying of base sequences becomes important when a cell grows and divides. During the process, a mother cell prepares to endow each of its future daughters with exact replicas of the DNA helices that it carries. This mother-to-daughter transmission allows the genetic information initially present in the DNA of a fertilized egg to be transmitted faithfully through a succession of hundreds of rounds of cell division to all of the trillions of descendant cells that form the adult human body.
To understand the roots of cancer, let us leave our discussion of cells and genes and turn to a radically different way of studying and describing human beings and their maladies—the science of epidemiology. Epidemiologists study disease incidence in large groups of people. Cancer epidemiologists, in particular, study the frequencies of cancers in various human populations. Their work is almost always motivated by a central question: How do various kinds of behavior or environment influence the frequency of specific kinds of cancers? The very notion of cancer incidence as an interesting topic for scientific study is relatively new. Until the nineteenth century, cancer was relatively rare, an observation largely explained by the fact that cancer is a disease of older people. In many European countries at the beginning of the nineteenth century, expected life span was only about thirty-five years. Many people who might have contracted cancer late in life were struck down far earlier by infectious disease, malnutrition, or accident.
On the rare occasion when cancer did strike, most attributed it to a random accident or an act of God. But some evidence accumulating after the last decade of the eighteenth century suggested an alternative explanation—that the appearance of a cancer could be tied to specific experiences or lifestyles of the cancer patients. This new mind-set started with physicians who began to document particular kinds of tumors affecting very distinct subpopulations of humanity.
Cancer risk was also found to vary dramatically between countries. Liver cancer was eighteen times more frequent in certain parts of Africa than in Great Britain. Stomach cancer struck Japanese eleven times more frequently than Americans. Colon cancer was ten to twenty times more common in the United States than in certain regions of Africa. These dramatic differences were not due to differences in inherited susceptibility. When individuals migrated from one part of the world to another, their children soon assumed the cancer risks typical of their new locations.
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Januvia Class Action: The notion that cancer was not a random, spontaneous degeneration of the body’s tissues, but instead was actively induced, radically changed the thinking of many cancer researchers. If external agents triggered die disease, perhaps they could be identified and their mechanisms of action studied. Perhaps the entire process from the initial encounter with a cancer-causing agent to the appearance of a cancer could be uncovered. So, toward the end of the nineteenth century, scientists throughout the world tried to recreate cancer in laboratory animals—mice, rats, and rabbits. For years, all such attempts failed. Around 1950, several geneticists assembled the body of accumulated information on chemicals, X-rays, and mutations and came up with a grand unifying theory, which in truth was little more than speculation. It went like this. X-rays and certain chemicals can induce cancer. X-rays and cancer can also induce mutations in genes. Therefore, these cancer-causing agents act through their ability to cause mutations in the genes of exposed animals. Stated differently, carcinogens (cancer-causing agents) are really mutagens (mutation-causing agents), and the two processes are inextricably linked.
A human cell, normal or malignant, was suspected to carry many tens of thousands of genes in its DNA. Among these might be a small set of genes which, when mutated by chemical carcinogens, would trigger runaway cell growth. For the moment, the task of finding these few mutant genes inside a cancer cell was far beyond the reach of available technology. Interest in cancer viruses had revived in the 1960s, in part through the recruitment of a new generation of young researchers who were eager to exploit techniques of DNA analysis to dissect these cancer agents. Thinking about the origins of cancer underwent a revolutionary change. For the first time, it became plausible that the roots of the disease lay deep within normal cells. Each cell seemed to carry within its normal genome the seed of its own destruction in a gene that it used to carry out its normal, everyday business.
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Januvia Class Action: Plant foods present a double-edged sword, since they contain both cancer-causing and cancer-preventing compounds. Vegetables provide vitamins such as A, C, and E, which neutralize some important carcinogens, notably die oxidants and free radicals generated during normal cell metabolism. On the other hand, some plant components may actively contribute to cancer. Plants have evolved elaborate chemical defense systems to make themselves unpalatable to insect predators. Among these are compounds that are registered as potent mutagens in the Ames test. Ames himself has cited the case of a new strain of celery that was bred to require less synthetic insecticide during its cultivation; the increased insect resistance shown by this celery correlated with a tenfold increase in a potent mutagen that is found naturally in this vegetable.
Early detection of tumors will prove increasingly important. The discovery and removal of a tumor mass in its initial stages often results in a cure. But early detection presents two major difficulties. First, nests of cancer cells must be discovered while they are still very small. As we saw earlier, a tumor of one centimeter diameter constitutes less than 0.01 percent of the body’s mass. Few currently available biochemical assays are sensitive enough to detect such minute entities. Second, cancer cells, especially those in the early stages of tumor progression, are in almost all respects very much like normal cells. The task of finding distinctive markers that are specific to cancer cells is daunting. Almost all proteins that have been proclaimed “tumor-specific” have later been found to be produced also by normal tissues somewhere in the body.
Familial tumors also contribute to a substantial fraction of human cancer incidence. Some researchers estimate that as much as 10 percent of all human cancer derives from inherited genes. The ability to predict inborn susceptibility to cancer thus represents another highly useful dimension of early detection. The technology for detecting mutant genes in small tissue samples is improving rapidly. Soon, a mutant inherited gene predisposing an individual to one or another cancer will be readily detectable using only several chops of that person’s blood. Similar analyses will be available for prenatal diagnosis, to be used in families known to be afflicted with unusually high rates of certain cancers. These tests will identify those members of a family who are at high risk and those who are spared that risk. Family members who are found to be at risk will need to be monitored throughout their lives. In the case of especially life-threatening conditions, including familial polyposis and breast cancer, the patient may decide to have the target organ removed before a malignant tumor appears.
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