Tests for cancer

Aziz, K. J. Perspectives on tumor marker tests for cancer diagnosis and monitoring. J. Biomed Lab. Sci. 6, 1-9 (1994). 

McCann, J., In Vitro Testing for Cancer-Causing Chemicals, Hosp. Prac., 73-85, September (1983). 

The U.S. FDA recently approved the first gene test for cancer, MammaPrint (the 70-gene signature) of Agendia (Amsterdam, the Netherlands) (18), for node-negative women under 61 years of age with primary breast cancer tumors. 

It is unclear if PBDEs can cause cancer in people, although liver tumors developed in rats and mice that ate decabromodiphenyl ether throughout their lives. Decabromodiphenyl ether is one type of PBDEs other kinds of PBDEs have not yet been tested for cancer. Based on the evidence... 

It has not been tested for cancer, reproductive, and other long-term effects. It can initiate tumors via in vivo formation of N-nitroso compounds from butyl nitrite following exposure. 

In closing, it is difficult to predict the role of POCT in self-testing as part of a weUness program. For example, the level of self-testing for cholesterol has not reached the predictions that were made several years ago—and the reasons for this are not entirely clear. If testing for some analytes remains restricted as is the case in some countries today, then it is possible that individuals will seek the tests from a POCT source. Examples include tests for cancers such as prostate, bladder, and colon that have attained a high level of media coverage in recent years. 

CURRENT STATUS OF HAZARD TESTING FOR CANCER FOR REGULATORY RISK ASSESSMENT 379... 

Manenti et al. (M2) reported that plasma MMP-9, TIMP-1, and TIMP-2 levels were higher in the plasma of ovarian cancer patients than in the plasma of women with nonmalignant disease or healthy women plasma MMP-2 levels were not increased in cancer patients. Of these parameters, only TIMP-1 was associated with a poor survival and mortality risk. They reported that levels of activated MMP-9 (identified by gelatin substrate zymography) were increased in the plasma of patients with either ovarian cancer or nonmalignant ovarian disease as compared to healthy subjects, thus negating the discriminative value of the test for cancer. 

Prof. Ames (1928) is a living legend in toxicology one of the most basic method to test for cancer causing potential was named after him. 

It now seems reasonably certain that the continuous release of these hydrolytic enzymes from neopicistic cells is responsible for their invasive capability, for the selective routing by increased diffusion of nutrients towards the tumor cells, and perhaps even for sustaining the whole momentum of autonomous neoplastic proliferation (48,54). The effect of these hydrolytic enzymes on the matrix is to release a whole spectrum of glycosaminoglycan and glycoprotein breakdown products into the blood stream, the so-called "acute-phase reactants, the estimation of which forms the basis for the majority of serochemical tests for cancer. 

Fifty-five percent of the chemicals on the Toxic Release Inventory list have full testing data. Of the 3000 high-volume chemicals (where their production is around 1 million Ib/year) on this list, 43% have no testing data or basic toxicity, and only 7% have a full set of basic test data. For 38,000 chemicals (66% listed by the EPA), fewer than 1000 have been tested for acute effects, and only about 500 have been tested for cancer-causing, reproductive, or mutagenic effects. It was estimated that it would cost only US 427 million to collect the basic data. So it is not the cost of data collection that is the bottleneck but the industries collective lack of will that is the cause. 

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