DNA-PLOIDY AND PROLIFERATIVE ACTIVITY IN UTERINE-TUMORS - AN IN-VIVO STUDY USING BROMODEOXYURIDINE AND FLOW-CYTOMETRY

1994 ◽  
Author(s):  
G FRANCHINI ◽  
A TUSEI ◽  
L BABILONTI ◽  
N DONADELLO ◽  
M FRANCHI ◽  
...  
1998 ◽  
Vol 16 (4) ◽  
pp. 223-231 ◽  
Author(s):  
Mar Abad ◽  
Juana Ciudad ◽  
Manuel R. Rincon ◽  
Isabel Silva ◽  
José I. Paz-Bouza ◽  
...  

In the present study the prognostic value of both DNA ploidy and the proliferative activity of tomour cells were studied in a series of 76 consecutive patients suffering from gastric tumours. DNA ploidy and the proliferative index (as measured by the percentage of S-phase cells) were determined by flow cytometry using fresh tumour specimens.The presence of DNA aneuploid clones by flow cytometry was detected in 62% of the cases (mean DNA index of 1.63 ± 0.46; range 1.08–2.92), the mean proportion of S-phase cells being of 18.4 ± 11.5%. In comparison with diploid cases, aneuploid tumours showed a higher proliferative activity (cases with more than 15% S-phase cells: 18.4% versus 6.1%,p= 0.0001) as well as a higher incidence of node involvement (95% versus 68%,p= 0.001). By contrast, no significant differences were detected with respect to sex, age, histologic grade and type, clinical stage, tumour size and the incidence of extranodal involvement.Upon grouping the patients according to the proportion of S-phase cells no significant differences were observed for the clinical and biological parameters explored except for an association between a high percentage of S-phase cells and the presence of DNA aneuploidy (40% versus 96%,p= 0.0001). Regarding survival the presence of DNA aneuploidy was significantly associated with poor outcome as compared to the diploid cases (median of 15 versus 26 months,p= 0.005). By contrast, the proportion of S-phase cells did not predict patients’s outcome.Multivariate analysis of prognostic factors showed that the presence of DNA aneuploidy (p= 0.003) together with the histologic type (p= 0.03) and the existence of extranodal metastases (p= 0.05) were the best combination of prognostic factors for survival prediction.


Leukemias ◽  
1993 ◽  
pp. 23-26
Author(s):  
M. Danova ◽  
M. Giordano ◽  
G. Mazzini ◽  
A. Riccardi

1988 ◽  
Vol 24 (5) ◽  
pp. 873-880 ◽  
Author(s):  
Marco Danova ◽  
Alberto Riccardi ◽  
Paolo Gaetani ◽  
George D. Wilson ◽  
Giuliano Mazzini ◽  
...  

RSC Advances ◽  
2015 ◽  
Vol 5 (29) ◽  
pp. 22510-22526 ◽  
Author(s):  
Yuran Peng ◽  
Jingjing Li ◽  
Yicheng Sun ◽  
Judy Yuet-Wa Chan ◽  
Dekuan Sheng ◽  
...  

Andrographolide is bestowed with an interesting pharmacophore and has attracted numerous studies on the design and synthesis of andrographolide derivatives.


2005 ◽  
Vol 25 (1_suppl) ◽  
pp. S57-S57
Author(s):  
Ken-ichiro Kasura ◽  
Megumi Watanabe ◽  
Kumiko Takahashi ◽  
Genki Mizukoshi ◽  
Seiji Ohkubo ◽  
...  

1991 ◽  
Vol 65 (04) ◽  
pp. 432-437 ◽  
Author(s):  
A W J Stuttle ◽  
M J Powling ◽  
J M Ritter ◽  
R M Hardisty

SummaryThe anti-platelet monoclonal antibody P256 is currently undergoing development for in vivo detection of thrombus. We have examined the actions of P256 and two fragments on human platelet function. P256, and its divalent fragment, caused aggregation at concentrations of 10−9−3 × 10−8 M. A monovalent fragment of P256 did not cause aggregation at concentrations up to 10−7 M. P256–induced platelet aggregation was dependent upon extracellular calcium ions as assessed by quin2 fluorescence. Indomethacin partially inhibited platelet aggregation and completely inhibited intracellular calcium mobilisation. Apyrase caused partial inhibition of aggregation. Aggregation induced by the divalent fragment was dependent upon fibrinogen and was inhibited by prostacyclin. Aggregation induced by the whole antibody was only partially dependent upon fibrinogen, but was also inhibited by prostacyclin. P256 whole antibody was shown, by flow cytometry, to induce fibrinogen binding to indomethacin treated platelets. Monovalent P256 was shown to be a specific antagonist for aggregation induced by the divalent forms. In–111–labelled monovalent fragment bound to gel-filtered platelets in a saturable and displaceable manner. Monovalent P256 represents a safer form for in vivo applications


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