Epidermoid carcinoma

Seco-3,4-taraxerone and seco-3,4-friedelin 2 abrogated the survival of human hepatocellular carcinoma (Hep-G2) and human epidermoid carcinoma (A-431) cell lines cultured in vitro with IC50 values of 11.7 and 38.2 mM, and inhibited the enzymatic activity of topoisomerase at dose of 7 pM (35). 

Exposure to arsenic has been associated with different types of human cancers such as respiratory cancers and epidermoid carcinomas of the skin, as well as precancerous dermal keratosis. The epidemiological evidence of human carcinogenicity is supported by carcinogenesis in experimental animals (Deknudt et al. 1986). 

Conversion of 4-aminopyrazolo [3,4-d] pyrimidine (VIII) to its ribonucleotide by mouse tumours and host tissues has been observed [118,119]. Although no evidence of the anabolism of A -methyladenine (111) [120] to the ribonucleotide was obtained in mice with Ehrlich ascites carcinoma [121, 122], it is anabolized by bacteria [123. 124] and the enzyme responsible was partially purified from Salmonella typhimurium [125]. Human epidermoid carcinoma No. 2 cells resistant to 2-fluoroadenine (H.Ep.-2/FA) have lost adenine phosphoribosyl-... 

Nasal tumors were induced in rats by inhalation exposure to HMPA for 6-24 months at levels of 50, 100, 400, and 4000 ppb, 6 hours/ day, 5 days week, but not in rats exposed to 10 ppb for 24 months. Most nasal mmors were epidermoid carcinomas and developed from the respiratory epithelium or subepithelial nasal glands, both of which revealed squamous metaplasia or dysplasia in the anterior nasal cavity. 

A statistically significant dose-related increased incidence of epidermoid carcinomas of the lung and thorax was seen in rats that received lung implants of IP for life. 

Some of the effects of acute arsenic intoxication are nausea, vomiting, diarrhea, and irritation inflammation and ulceration of the mucous membranes and skin and kidney damage. Among the effects of chronic arsenic poisoning are increased pigmentation and keratinization of the skin, dermatitis, and epidermoid carcinoma. Other effects seen after ingestion, but which are not common from industrial exposure, are muscular paralysis, visual dismrbances, and liver and kidney damage. ... 

Akiyama T, Yoshida T, Tsujita T, Shimizu M, Mizukami T, Okabe M, Akinaga S (1997) G1 phase accumulation induced by UCN-01 is associated with dephosphorylation of Rb and CDK2 proteins as well as induction of CDK inhibitor p21/CiplAVAFl/Sdil in p53-mutated human epidermoid carcinoma A431 cells. Cancer Res 57 1495-1501... 

Fujii R, Mutoh M, Sumizawa T, Chen Z, Yoshimura A, Akiyama S. Adenosine triphosphate-depen-dent transport of leukotriene C4 by membrane vesicles prepared from cisplatin-resistant human epidermoid carcinoma tumor cells. J Natl Cancer Inst 1994 86 1781-1784. 

Eschwege F, Sancho-Garnier H, Gerard JP, et al. Ten-year results of randomized trial comparing radiotherapy and concomitant bleomycin to radiotherapy alone in epidermoid carcinomas of the oropharynx experience of the European Organization for Research and Treatment of Cancer. NCI Monogr 1988 6 275-278. 

Finally, the triterpenoid cucurbitacin B, isolated from L. intrapetiolaris, showed activity in the KB (human oral epidermoid carcinoma) assay with EC50 value of 0.008 pg/ml. The clerodane diterpenes intrapetacin A and intrapetacin B displayed moderate activity vs KB as well [4],... 

Rat. Four groups of 120 male and 120 female Sprague-Dawley rats were exposed to 0 (control), 50,400 and 4000 ppb [0, 0.37,2.9 and 29 mg/m- ] hexamethylphosphoramide vapour for 6 h per day on five days per week for periods ranging from nine months to two years. In an additional study, four groups of 100 male and 100 female rats were similarly exposed to 0, 10, 50 and 100 ppb [0, 73, 370 and 730 pg/m ] atmospheres. Nasal tumours were first found after approximately seven months of exposure at 400 and 4000 ppb, after nine months at 100 ppb and after 12 months at 50 ppb. No exposure-related tumours were found at 10 ppb. Tumour incidences at 24 months were 50 ppb, 15% (12 months of exposure) and 25% (24 months of exposure) 100 ppb, 19% (six months of exposure) and 56% (13 months of exposure) 400 ppb, 82% (10 months of exposure) 4000 ppb, 83% (nine months of exposure). Most tumours developed in the squamous or respiratory epithelium and nasal glands, all of which showed squamous metaplasia or dysplasia in the anterior nasal cavity. Exposure concentrations correlated with tumour incidence and latency, but not with tumour type. The total of 473 nasal tumours included 72% epidermoid carcinomas, 15% adenoid squamous carcinomas and 8% papillomas. Most tumours (59%) developed in the anterior nasal cavity and then progressed to the posterior nasal cavity (41%) (Lee Trochimowicz, 1982a). 

Didemnolines A (31) and C (32) from the marine ascidian Didemnum sp. are cytotoxic to human epidermoid carcinoma KB cells (IC5o values of 6.1 and 0.28 pg/ml, respectively) and antimicrobial toward Staphylococcus aureus, Bacillus subtilis, and Escherichia coli [44,45]. 

Keramamide E (74) exhibits cytotoxicity against L1210 murine leukemia cells and KB human epidermoid carcinoma cells with IC50 values of 1.60 and 1.55 pg/ml, respectively [66]. 

Adhami YM, Afaq F, Ahmad N. 2001. Involvement of the retinoblastoma (pRb)-E2F/ DP pathway during antiproliferative effects of resveratrol in human epidermoid carcinoma (A431) cells. Biochem Biophys Res Commun 288 579-585. 

Ahmad N, Adhami VM, Afaq F, Feyes DK, Mukhtar H. 2001. Resveratrol causes WAF-l/p21-mediated G(l)-phase arrest of cell cycle and induction of apoptosis in human epidermoid carcinoma A431 cells. Clin Cancer Res 7 1466-1473. 

Kim AL, Zhu Y, Zhu H, Han L, Kopelovich L, Bickers DR, Ather M. 2006. Resveratrol inhibits proliferation of human epidermoid carcinoma A431 cells by modulating MEK1 and AP-1 signalling pathways. Exp Dermatol 15 538-546. 

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