ChemInform Abstract: Synthesis of Novel Paclitaxel Prodrugs Designed for Bioreductive Activation in Hypoxic Tumor Tissue.

ChemInform ◽  
2010 ◽  
Vol 33 (13) ◽  
pp. no-no
Author(s):  
Eric W. P. Damen ◽  
Tapio J. Nevalainen ◽  
Toine J. M. van den Bergh ◽  
Franciscus M. H. de Groot ◽  
Hans W. Scheeren
2014 ◽  
Vol 27 (4) ◽  
pp. 425-430 ◽  
Author(s):  
Nilesh Mistry ◽  
Ashley M. Stokes ◽  
James Van Gambrell ◽  
Christopher Chad Quarles

2019 ◽  
Vol 7 (35) ◽  
pp. 5352-5362 ◽  
Author(s):  
Bin Zhang ◽  
Xiaochao Huang ◽  
Hengshan Wang ◽  
Shaohua Gou

Conjugated a hydrophobic HIF-1α inhibitor (YC-1) with a hydrophilic anticancer drug, irinotecan (Ir), into one molecular entity, provided a new insight into the design of smart nanodrug delivery systems to hypoxic tumor tissue.


ChemMedChem ◽  
2011 ◽  
Vol 7 (1) ◽  
pp. 57-61 ◽  
Author(s):  
Katrin Splith ◽  
Ralf Bergmann ◽  
Jens Pietzsch ◽  
Ines Neundorf

2015 ◽  
Vol 1086 ◽  
pp. 43-49
Author(s):  
S. Sreeja ◽  
Cherupally Krishnan Krishnan Nair

The present study aims to target a cytotoxic drug, Berberine to tumor tissues specifically by the use of iron oxide nanoparticles and a nitro triazole compound, Sanazole which gets accumulated in hypoxic tumor tissue. Under in vitro conditions the nanoparticles complexed with Berberine and Sanazole showed higher cytotoxicity to tumor cells than either of the drugs and complexes of single individual compounds. The tumor-bearing animals treated with these nanoparticle-drug complexes increased the regression in tumor volume and survival of the animals. The present work thus revealed the potential applications of Berberine and Sanazole in cancer therapy.


1988 ◽  
Vol 16 (1-3) ◽  
pp. 547-556 ◽  
Author(s):  
M. Watanabe ◽  
H. Okamoto ◽  
H. Ohyanaqi ◽  
Y. Saitoh ◽  
K. Yano ◽  
...  

Author(s):  
D. C. Swartzendruber ◽  
Norma L. Idoyaga-Vargas

The radionuclide gallium-67 (67Ga) localizes preferentially but not specifically in many human and experimental soft-tissue tumors. Because of this localization, 67Ga is used in clinical trials to detect humar. cancers by external scintiscanning methods. However, the fact that 67Ga does not localize specifically in tumors requires for its eventual clinical usefulness a fuller understanding of the mechanisms that control its deposition in both malignant and normal cells. We have previously reported that 67Ga localizes in lysosomal-like bodies, notably, although not exclusively, in macrophages of the spocytaneous AKR thymoma. Further studies on the uptake of 67Ga by macrophages are needed to determine whether there are factors related to malignancy that might alter the localization of 67Ga in these cells and thus provide clues to discovering the mechanism of 67Ga localization in tumor tissue.


1989 ◽  
Vol 28 (05) ◽  
pp. 193-200 ◽  
Author(s):  
E. Aulbert

Cellular uptake of 67Ga-labelled transferrin by the tumor tissue was studied in rats with tumors of different malignancy and different tumor mass using the slowly growing Morris hepatoma 5123C, the moderately growing Novikoff hepatoma and the very fast and aggressive Yoshida hepatoma AH130. The cellular accumulation of 67Ga-transferrin was found to correlate with the proliferation activity of the tumor. The 67Ga-transferrin concentration in the very fast growing Yoshida hepatoma was 4.8 times higher than the concentration in the slowly growing Morris hepatoma. The uptake of 67Ga-transferrin by the tumors resulted in a faster disappearance of circulating 67Ga-transferrin from the blood. The rate of disappearance correlated with the proliferation activity and the spread of the tumors. Using tumors of identical size the elimination of 67Ga-transferrin from the blood was much faster in the rats with Yoshida hepatoma than in those with the slowly growing Morris hepatoma. On the other hand, using tumors of different tumor size it could be demonstrated that the rate of disappearance of 67Ga-transferrin from the blood correlated directly with tumor mass. It is concluded that cellular incorporation of transferrin within the tumor cells results in a loss of circulating transferrin, which correlates with tumor mass and proliferation of tumor. This mechanism is supposed to be the cause for the hypotransferrinemia seen in patients with malignant tumors.


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