scholarly journals The Effectiveness and Tolerance of TS-1 a Monotherapy for Relapsed Thymic Cancer Patient Who could not Tolerate Platinum Compounds

2014 ◽  
Vol 04 (01) ◽  
Author(s):  
Naohiro Taira Tsutomu Kawabata
Author(s):  
S. K. Aggarwal ◽  
P. McAllister ◽  
R. W. Wagner ◽  
B. Rosenberg

Uranyl acetate has been used as an electron stain for en bloc staining as well as for staining ultrathin sections in conjunction with various lead stains (Fig. 1). Present studies reveal that various platinum compounds also show promise as electron stains. Certain platinum compounds have been shown to be effective anti-tumor agents. Of particular interest are the compounds with either uracil or thymine as one of the ligands (cis-Pt(II)-uracil; cis-Pt(II)-thymine). These compounds are amorphous, highly soluble in water and often exhibit an intense blue coloration. These compounds show enough electron density to be used as stains for electron microscopy. Most of the studies are based on various cell lines (human AV, cells, human lymphoma cells, KB cells, Sarcoma-180 ascites cells, chick fibroblasts and HeLa cells) while studies on tissue blocks are in progress.


2019 ◽  
Vol 476 (24) ◽  
pp. 3705-3719 ◽  
Author(s):  
Avani Vyas ◽  
Umamaheswar Duvvuri ◽  
Kirill Kiselyov

Platinum-containing drugs such as cisplatin and carboplatin are routinely used for the treatment of many solid tumors including squamous cell carcinoma of the head and neck (SCCHN). However, SCCHN resistance to platinum compounds is well documented. The resistance to platinum has been linked to the activity of divalent transporter ATP7B, which pumps platinum from the cytoplasm into lysosomes, decreasing its concentration in the cytoplasm. Several cancer models show increased expression of ATP7B; however, the reason for such an increase is not known. Here we show a strong positive correlation between mRNA levels of TMEM16A and ATP7B in human SCCHN tumors. TMEM16A overexpression and depletion in SCCHN cell lines caused parallel changes in the ATP7B mRNA levels. The ATP7B increase in TMEM16A-overexpressing cells was reversed by suppression of NADPH oxidase 2 (NOX2), by the antioxidant N-Acetyl-Cysteine (NAC) and by copper chelation using cuprizone and bathocuproine sulphonate (BCS). Pretreatment with either chelator significantly increased cisplatin's sensitivity, particularly in the context of TMEM16A overexpression. We propose that increased oxidative stress in TMEM16A-overexpressing cells liberates the chelated copper in the cytoplasm, leading to the transcriptional activation of ATP7B expression. This, in turn, decreases the efficacy of platinum compounds by promoting their vesicular sequestration. We think that such a new explanation of the mechanism of SCCHN tumors’ platinum resistance identifies novel approach to treating these tumors.


2004 ◽  
Vol 171 (4S) ◽  
pp. 413-413
Author(s):  
Deborah M. Spaine ◽  
Renata Fraietta ◽  
Agnaldo P. Cedenho ◽  
Miguel Srougi

1964 ◽  
Vol 11 (02) ◽  
pp. 404-422 ◽  
Author(s):  
Annemarie Amris ◽  
C. J Amris

Summary14 patients (5 diabetics with arteriosclerotic complications, 4 patients with thrombo-embolic disease, 4 with cirrhosis, coagulation defects and increased fibrinolytic activity, and 1 cancer patient) and 3 control patients were subjected to turnover studies with 13iodine labelled human fibrinogen.Half-life times in the control patients were found to be 4 days, the fractional turnover rates 19–23 per cent, of intravascular fibrinogen per day, and the absolute turnover 0.02 to 0.06 gm per day per kg. body weight. The other patient’s half-life times and turnover rates varied considerably from 0.9–5.5 days, 13–160 per cent, per day of intravascular fibrinogen and 0.02–0.4 gm per day per kg. body weight respectively.As fibrinogen unlike other proteins subjected to turnover studies, is converted to fibrin, it is not possible to measure the true intra-extravascular distribution ratio of fibrinogen. But intravascular fibrinogen could be approximated to constitute 68–99 per cent, of the total fibrinogen. There is justification in believing that fibrinogen is degradated through a continuous coagulation in equilibrium with fibrinolysis, and that the organism contains a greater mass of fibrin, the “fibrin pool”. Considerations of the turnover mechanism can however only be hypothetical.


2007 ◽  
Vol 20 (2) ◽  
pp. 213 ◽  
Author(s):  
Ji Yon Jo ◽  
Jeong Hoon Suh ◽  
Hwa Yong Shin ◽  
Yong Min Choi ◽  
Moon Sun Bang ◽  
...  

2018 ◽  
Author(s):  
Goknur Yorulmaz ◽  
Aysen Akalin ◽  
Toygar Kalkan ◽  
Ilknur Ak Sivrikoz ◽  
Eren Gunduz ◽  
...  

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