Tumor development

Cells from tissues associated with primary and secondary sexual characteristics are under particular endocrine control. Sex hormones determinethe growth, differentiation, and proliferation of such cells. When a tumor develops in such tissues, it is sometimes hormone dependent and the use of anti hormones removes the impetus for the tumor s headlong growth. Many nonsteroidal compounds have estrogenic activity diethylstilbest-jrol (81) may be taken as an example. Certain more bulky an-... 

Lustig B, Behrens J (2003) The Wnt signaling pathway and its role in tumor development. J Cancer Res Clin Oncol 129 199-221... 

Booth V Keizer DW, Kamphuis MB et al (2002) The CXCR3 binding chemokine IP-IO/CXCLIO structure and receptor interactions. Biochemistry 41 10418-10425 Burns JM, Summers BC, Wang Y et al (2006) A novel chemokine receptor for SDF-1 and I-TAC involved in cell survival, cell adhesion, and tumor development. J Exp Med 203 2201-2213 Callebaut C, Krust B, Jacotot E et al (1993) T cell activation antigen, CD26, as a cofactor for entry of HIV in CD4+ cells. Science 262 2045-2050... 

Kang, S.Y. et al., Tart cherry anthocyanins inhibit tumor development in Apc(Min) mice and reduce prohferation of human colon cancer cells. Cancer Lett., 194, 13, 2003. 

Bums JM, Summers BC, Wang Y, et al. A novel chemokine receptor for SDF-1 and I-TAC involved in cell survival, cell adhesion, and tumor development. J Exp Med 2006 203 2201-2213. 

Balzarini J, Sobis H, Naesens L, Vandeputte M, De Clercq E. Inhibitory effects of 9-(2-phosphonylmethoxyethyl)adenine and 3 -azido-2, 3 -dideoxy-thymidinc on tumor development in mice inoculated intracerebrally with Moloney murine sarcoma virus. Int J Cancer 1990 45 486-489. 

The follicles are used to treat asthma and cough and to mitigate painful swollen breasts. A paste of the leave is applied to contusion. Essential oil distilled from the follicles induced apoptotic death in HepG2 human hepatoma cells in a concentration- and time-related manner, and inhibited tumor development of mice inoculated with Huh-7 human hepatoma cells (33). 

Two groups demonstrated that BRCA-1- and BRCA-2-deficient cells are acutely sensitive to PARPi [11,12]. Potent inhibitors like KU0058684 (5), KU0058948 (6), and AG14361 (26) were cytotoxic at nanomolar concentrations in HR-defective cells, and displayed excellent selectivity for BRCA-1- and BRCA-2-deficient cells over wild-type cells. After 24 h of exposure, 5 elicited G2 or M phase cell cycle arrest and a tetraploid DNA content. The applicability of this discovery was revealed when BRCA-2-deficient and BRCA-2-proficient cells were injected into mice and tumors were allowed to develop. Daily treatment with 5 or 26 had no effect on the BRCA-2 wild-type cells however, when BRCA-2-deficient cells were treated with PARPi, no tumors developed. 

Strel tsova, V. N. (1961). Liver tumors developing under the influence of cerium-144, Translated from Arkh. Patol. 23, No. 3, 9 also page 12 in Archives of Pathology, Report No. JPRS-9663 (National Technical Information Service, Springfield, Virginia). 

Finally, it is important that further research be carried out on the identification and mechanism of action of environmental cocarcinogens and tumor promoters which can enhance the carcinogenicity of PAH. Human exposure to at least trace amounts of PAH is unavoidable. The probability of eventual tumor development may be controlled primarily by repeated exposure to cocarcinogens or promoters. 

Chen MF, Chen LiT and Boyce HW, Jr. 1995. Cruciferous vegetables and glutathione their effects on colon mucosal glutathione level and colon tumor development in rats induced by DMH. Nutr Cancer 23(1) 77—83. 

Laboratory studies with mice and rats have conclusively demonstrated that the injection of cadmium metal or salts causes malignancies (sarcoma) at the site of injection and testicular tumors. However, the simultaneous administration of zinc is protective against sarcoma and interstitial cell tumor development (USEPA 1980). In rats, no dose-related increases in tumors were found at maximum oral daily doses of 4.4 mg Cd/kg BW (USPHS 1993). Among humans, the available epidemiological evidence is not sufficient to conclude that cadmium is definitely implicated as a carcinogen (USEPA 1980 Nomiyama 1982), although cadmium exposure is associated with lung cancer in humans (Shimada et al. 1998). 

Development of a colorectal neoplasm is a multistep process of genetic and phenotypic alterations of normal bowel epithelium structure and function leading to unregulated cell growth, proliferation, and tumor development. 

Gallium arsenide altered host resistance in B6C3F1 mice, resulting in increased resistance to infection by Streptococcus pneumoniae and Listeria monocytogenes [18], but increased susceptibility to Staphylococcus aureus [19] and to tumor development by B16F10 melanoma cells [18], However, inhalation exposure to As203 led to increased... 

Liver tumors developed in mice that were orally exposed to hexachloroethane for their whole lifetime. Tumors of this kind are common in mice. Hexachloroethane will not necessarily have the same effect on people. Male rats that were exposed to hexachloroethane for their lifetime developed kidney tumors. This type of tumor is not found in people, so it is unlikely that exposure to hexachloroethane would cause you to develop cancer of the kidney. The Department of Health and Human Services has determined that hexachloroethane may reasonably be anticipated to be a carcinogen (can cause cancer). The International Agency for Research on Cancer (IARC) has determined that hexachloroethane is not classifiable as to its carcinogenicity in people. EPA has determined that hexachloroethane is a possible human carcinogen. 

Metofluthrin (I) The committee determined that the new data were sufficient to support a mitogenic mode of action for the development of liver tumors in rats exposed to metofluthrin in the carcinogenicity study. The report summarized mode of action study data that characterized effects such as increased P450 enzyme levels, increased smooth endoplasmic reticulum, hepatocellular hypertrophy, hepatocellular proliferation, and inhibition of intracellular communication, which were described as steps leading to tumor development via a nongenotoxic mechanism (i.e., mitogenicity). Some of these studies used sodium phenobarbital as a positive control,... 

In general, the sensitivity of a carcinogenicity bioassay is increased when animals survive to the end of their natural life span, because weak carcinogens may induce late-occurring tumors. The potency of a carcinogen is often inversely related to the time to tumor development. By analogy, as the dose of a carcinogen is reduced, the time to tumor occurrence is increased (Littlefield et al., 1979 DePass et al., 1986). 

When reduced survival is related to factors other than excessive toxicity, the number of animals at risk for tumor development may be inadequate, and the validity of the study may be compromised even in the absence of a drug effect on survival. Obviously, the adjustments described above for excessive, drug-related toxicity are not relevant to this situation. 

There are three generally accepted criteria for a positive result in a carcinogenicity study. The first two are derived directly from the results of the statistical analysis (1) a statistically significant increase in the incidence of a common tumor and (2) a statistically significant reduction in the time-to-tumor development. The third criterion is the occurrence of very rare tumors, that is, those not normally seen in control animals, even if the incidence is not statistically significant. 

A threshold is operative, and must be exceeded for cell proliferation and tumor development to occur. 

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