Anticancer research
-
Anticancer research · Mar 2000
Growth inhibition of Ph+ progenitor cells from CML patients using the tyrosine kinase inhibitor CGP57148B.
Different methods have been investigated for their purging capacity of contaminating CML cells in autologous stem cell products. CGP57148B, a tyrphostin, has been shown to be efficient in the reduction of cell proliferation of CML cell lines and primary CML cells, as well as in the inhibition of bcr/abl-related tumor formation in animal models. ⋯ Our results support the observation that CGP57148B can selectively inhibit proliferation of Ph+/bcr/abl+ primary CML cells under serum-free cytokine-supplemented culture conditions.
-
Anticancer research · Mar 2000
Vascular endothelial growth factor expression in progression of cervical cancer: correlation with thymidine phosphorylase expression, angiogenesis, tumor cell proliferation, and apoptosis.
Vascular endothelial growth factor (VEGF) has been linked not only to angiogenic activity but also to thymidine phosphorylase (TP), rapid tumor growth, and inhibition of apoptotic cell death. Our purpose was to examine how VEGF expression affect these factors in cervical cancer at varying stages of progression. ⋯ VEGF expression may stimulate tumor cell proliferation in the early stages of cervical cancer, and may be responsible for cervical tumorigenesis.
-
Anticancer research · Jan 2000
Comparative StudyExpression of nitric oxide synthase isozymes (NOS I-III) by immunohistochemistry and DNA in situ hybridization. Correlation with macrophage presence, vascular endothelial growth factor (VEGF) and oedema volumetric data in 220 glioblastomas.
Nitric oxide (NO) is synthesized from arginine by three different isozymes of nitric oxide synthase (NOS I-III). NO has been identified as a powerful metabolite of vascular smooth muscle cell function, cerebral blood circulation and oedema induction. NOS induction by different cytokines has been shown previously in glioblastoma cell cultures and NOS III expression due to astrocytoma grading has been shown in several tumors recently. The aim of the present study was to study the coexpression of NOS I-III, macrophage and capillary presence with VEGF, EGF and their receptors and to investigate a possible mechanism in peritumoral oedema generation. ⋯ The main source of NO is NOS I and NOS III. The latter is located in endothelial cells and glioblastoma cells. The expression of NOS II in glioblastomas is restricted to infiltrating macrophages. NOS II and III expressions were observed significantly together with that of VEGF-R1. Neither NOS I-III nor VEGF-R expression could be correlated with the extension of the peritumoral oedema.
-
Anticancer research · Jan 2000
Clinical TrialLiposomal doxorubicin (Caelyx) in advanced pretreated soft tissue sarcomas: a phase II study of the Italian Sarcoma Group (ISG).
Doxorubicin remains one of the few drugs with consistent single agent activity in advanced Soft Tissue Sarcomas (STS), with a demonstrated dose-response relationship. Liposomal-encapsulated Doxorubicin (LED) has been shown to be at least as active as free doxorubicin in experimental models, and phase I and II human studies indicate that this novel strategy of drug delivery my have less myocardial toxicity. Few clinical trials in adult STS have been published until now, with disappointing and often contrasting results. ⋯ This study shows that Caelyx has some activity in advanced, anthracycline-pretreated STS, with favourable toxic profile. From the analysis of available experiences it emerges that liposomal doxorubicin has not been tested at doses adequate to exploit the antitumor effects of the drug, being the reached dose-intensity being even lower than those deemed critical for obtaining optimal responses to free doxorubicin. We suggest that further and better addressed studies be performed in STS, including patients with less advanced stages of disease, focused on attempting to delivery the drug at optimal doses.
-
Anticancer research · Nov 1999
Early effects of retinoic acid on proliferation, differentiation and apoptosis in non-small cell lung cancer cell lines.
Retinoids represent a potentially useful class of drugs in the chemoprevention and treatment of cancer, due to their ability to regulate cell proliferation and differentiation. However, there is controversy in the literature about the effects of all-trans retinoic acid (ATRA) in non- small cell lung cancer (NSCLC). In this study we examined the effects of ATRA on apoptotic death in NSCLC. ⋯ These results indicate the possibility of the early growth-inhibitory and apoptotic effects of ATRA in NSCLC which may result in selection of ATRA-resistant cells.