The product of transmembrane and coiled-coil domains 1 (TMCO1) gene is a member of several eukaryotic proteins with unknown function. In a preliminary Bioinformatics and Stanford Microarray Database data-mining and some of our preliminary data, transmembrane and coiled-coil domains 1 (TMCO1) immunohistochemistry (IHC) was identified to be up-regulated in non-invasive bladder cancer. To further studies on the functions and regulatory mechanisms the role of TMCO1 gene. In the present study, we examined the TMCO1 expression levels in human bladder cell lines, RT4, TSGH8301, J82. We observed TMCO1 high expression in RT4 and low expression in TSGH8301. We investigate overexpression and knock down of TMCO1in RT4 and TSGH8301. Further we study the expression change of TOMCO1 how to change cell function and morphology. In this study, we can get transfection of shRNA interference targeting TMCO1 in RT4 cell enhanced cell proliferation.

Issued also as thesis, Univ. de Lyon. / "Bibliographie": p. [207]-219.

Thesis (Ph. D.)--Ohio State University, 2003. / Title from first page of PDF file. Document formatted into pages; contains xx, 400 p.; also includes graphics (some col.). Includes abstract and vita. Advisor: John A. Bauer, College of Pharmacy. Includes bibliographical references (p. 397-400).

Thesis (Ph. D.)--West Virginia University, 2003. / Title from document title page. Document formatted into pages; contains vi, 110 p. : ill. Includes abstract. Includes bibliographical references.

Diss. (sammanfattning) Stockholm : Karol. inst. / Härtill 6 uppsatser.

Thesis (doctoral)--University of Lund, 1997. / Added t.p. with thesis statement inserted.

Thesis (Ph. D.)--University of Wisconsin--Madison, 1963. / Typescript. Vita. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references.

Thesis (doctoral)--University of Lund, 1997. / Added t.p. with thesis statement inserted.

Thesis (doctoral)--Freie Universität Berlin, 1979.

No / The quinone based bioreductive drug apaziquone (EO9) failed to demonstrate efficacy in previous phase II studies following intravenous administration. We determined the dose of apaziquone that can be safely administered intravesically and explored its activity for superficial bladder transitional cell carcinoma. Six patients with multifocal, Ta/T1 and G1/G2 transitional cell carcinoma of the bladder received escalating doses of apaziquone formulated as EOquin¿ (0.5 mg/40 ml up to 16 mg/40 ml) weekly for 6 weeks. A further 6 patients received weekly apaziquone at the highest nontoxic dose established. Pharmacokinetic parameters were determined in urine and blood, and the pharmacodynamic markers NQO1 (reduced nicotinamide adenine dinucleotide phosphate:quinone oxidoreductase-1) and glucose transporter 1 were also characterized. Efficacy was determined against a marker lesion. Local toxicity (grades 2 and 3 dysuria, and hematuria) was observed at doses of 8 mg/40 ml and above but 4 mg/40 ml was well tolerated with no systemic or local side effects. Apaziquone in urine increased linearly with the dose but no apaziquone was detected in plasma. In 8 of 12 patients complete macroscopic and histological disappearance of the marker lesion occurred. A correlation between response and NQO1 and/or glucose transporter 1 expression could not be established. Intravesical administration of 4 mg/40 ml apaziquone was well tolerated and had ablative activity against superficial bladder cancer marker lesions.