Neoplastic conversion

It has seemed pretty clear for several decades, from both studies in humans and in experimental settings, that carcinogenesis is a multistage process. At the broadest level, the process can be thought of as one in which a normal cell is first converted to a permanently deranged cell, which is called a neoplastic cell, and a second sequence in which the neoplastic cell develops into a tnmor, a neoplasm, that the pathologist can observe neoplastic conversion and neoplastic development. 

The influence of host factors, including cellular genetics and factors such as the host s hormonal and immune systems, that may either restrict or enhance neoplastic conversion or development. 

Williams GM, GebhardtR, SirmaH, Sten-back F. 1993. Non-linearity of neoplastic conversion induced in rat liver by low exposures to diethylnitrosamine. Carcinogenesis 14 2149—56... 

Cote RJ, Cardon-Cardo C, Reuter VE, Rosen PP. Immuno-pathology of adrenal and renal cortical tumors Coordinated change in antigen expression is associated with neoplastic conversion in the adrenal cortex. Am J Pathol. 1990 136 1077-1084. 

The nature of the permanently altered effector that is critical to neoplastic conversion increasingly appears to involve activation of cellular oncogenes (14,18.19), see below. Specific mutations in oncogenes have been identified (1 ), as well as other changes. These occur in oncogenes isolated from neoplasms arising in both experimental animals and humans (20,21). 

Cocarcinogenesis Enhancer acting before or together with carcinogen or when carcinogen effects still persist Enhancer facilities neoplastic conversion nongenotoxic and noncarcinogenic... 

The SHE cell transformation assay at pH 6.7 is conducted to determine the ability of a test article to induce morphological transformation in cultured SHE cells. The SHE cell transformation assay is one of the most widely used cell transformation assays. The endpoints of this assay are related to the conversion of normal cells into preneoplastic or neoplastic cells. The assay provides a valuable tool in the process of assessment and evaluation of the carcinogenic potential of a test article.2 28... 

Transformation the conversion of normal cells into neoplastic cells. 

Figure 5.2 Therapeutic interventions for decreasing colorectal mucosal bile acid exposure as a CRC chemoprevention strategy. 1) Lifestyle modifications including reduction in dietary animal fat and increased fibre intake may, at least partly, be explained by reduction in luminal primary (cholic acid [CA] and chenodeoxycholic acid [CDCA]) and secondary (deoxycholic acid [DCA] and lithocholic acid [LCA]) bile acids. 2) Reduction of secondary bile acids, which are believed to have pro-carcinogenic activity could be obtained by decreased bacterial conversion from primary bile acids. 3) Alternatively, bile acids could be sequestered by chemical binding agents, e.g. aluminium hydroxide (Al(OH)3) or probiotic bacteria. 4) Exogenous ursodeoxycholic acid (UDCA) can reduce the luminal proportion of secondary bile acids and also has direct anti-neoplastic activity on colonocytes in vitro.

Transformation (neoplastic) The conversion of normal cells into tumor cells (see below). Frequently this is the result of a genetic change and the same term is used to describe the genetic modification of bacteria for biotechnological purposes. 

The exact cause of many cases of neoplastic disease is unknown. However, a great deal has been learned about possible environmental, viral, genetic, and other elements, or carcinogens, that may cause or increase a person s susceptibility to various types of cancer. Conversely, certain positive lifestyles, including adequate exercise, a high-fiber diet, and the avoidance of tobacco products, may be crucial in preventing certain forms of cancer. Of course, routine checkups and early detection play a vital role in reducing cancer mortality. 

Chemotherapeutic agents, useful in me treatment of neoplastic diseases, exert their therapeutic effects by modifying me synthesis or functions of nucleic acids (see Chapter 51 and Chapter 58). For example, 6-mercaptopurine inhibits purine-ring biosynthesis, cytarabine inhibits DNA polymerase, alkylating agents crosslink DNA, and hydroxyurea inhibits the conversion of ribonucleotides into deoxyribonucleotides. However, other pharmacologic agents such as chlorpromazine, a... 

The drug 6-mercaptopurine [mer kap toe PYOOR een] (6-MP) is the thiol analog of hypoxanthine. It and thioguanine (6-TG) were the first purine analogs to prove beneficial for treating neoplastic disease. Azathioprine, an immunosuppressant, exerts its effects after conversion to 6-MP. 

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