S possible that NaPaC administrated early was capable to inactivate, at the least in component, this growth issue and consequently to prevent vessel dilation. Due to the fact vessels are present even within the early treated tumours, it might be that A431 cells surround and co-opt, instantly following inoculation, the existing subcutaneous vessels as it was described in the case of non-small-cell-lung carcinoma (Pezzela et al, 1997) and melanoma (Leenders et al, 2002). Furthermore, NaPaC appears to have no effect, administrated early or late, on this phenomenon. Even so, we cannot discard that in our experimental model the formation of neo-vessels occurs extremely early and that NaPaC is just not able to inhibit it absolutely. Altogether, our benefits showed that NaPaC inhibited the A431 tumour growth acting on both endothelial and tumour cells. The extent of this impact was dependent on the outset of NaPaC treatment. Because the period of NaPaC action on A431 cell proliferation was precisely the same (5 weeks) and since the endothelial cell HIV-1 gp160 Proteins Purity & Documentation density was decreased in the same manner in each early and late treated tumours, by far the most probable is that the distinction in tumour development inhibition was due to changes in intratumour vascular network top towards the boost in tumour cell death observed above. Altogether, our data indicate that A431 xenograft model may be utilised to study the influence of vascular network in tumour development and to screen possible antiangiogenic agents. In conclusion, we demonstrated that NaPaC potently inhibits fast-growing epidermoid carcinoma by acting on tumour cells and intratumour endothelial cells what ever the state of xenograft improvement. Nontoxic at effective doses, NaPaC provides fascinating clues for therapies of solid tumours stopping the vascular network evolution in malignant lesions, as a result inhibiting the rapid expansion from modest tumours to late-stage tumours. Moreover, its direct inhibitory action on tumour cell proliferation argues for its usefulness in late-stage tumour remedy.ACKNOWLEDGEMENTS` We thank Grant sponsors: Ministere de l’Education Nationale; Association pour la Recherche contre le Cancer (Grant no. 9721), La Ligue Nationale contre le Cancer and Biodex Laboratory. We are grateful to Professor A Martin for beneficial discussions regarding the histological tumour analysis, Professor M Frojmovic for English corrections, O Sainte-Catherine for superb technical assistance and L Correa for NaPaC preparation. We thank Professor PM Martin for A431 cell present.
PO Box 2345, Beijing AKT Serine/Threonine Kinase 3 (AKT3) Proteins Accession 100023, China Fax: +86-10-85381893 E-mail: [email protected] www.wjgnet.comWorld J Gastroenterol 2004;ten(23):3414-3418 Globe Journal of Gastroenterology Copyright 2004 by The WJG Press ISSN 1007-LIVER CANCER Expressions of cysteine-rich61, connective tissue development element and Nov genes in hepatocellular carcinoma and their clinical significanceZhi-Jun Zeng, Lian-Yue Yang, Xiang Ding, Wei WangZhi-Jun Zeng, Lian-Yue Yang, Xiang Ding, Wei Wang, Liver Cancer Laboratory, Department of Surgery, Xiangya Hospital, Central South University, Changsha 410008, Hunan Province, China Supported by the National Important Technologies R and D Plan, No. 2001BA703BO4 and the National All-natural Science Foundation of China, No.30371595 Correspondence to: Lian-Yue Yang, Liver Cancer Laboratory, Department of Surgery, Xiangya Hospital, Central South University, Changsha 410008, Hunan Province, China. [email protected] Phone: +86-731-4327326 Fax: +86-731-4327332 Received: 2004-02-28 Accepted:.