Influence of p53 and bcl-2 on chemosensitivity in benign and malignant prostatic cell lines.

The administration of cancer chemotherapeutic agents results in an increase in the apoptotic cells in the tumor: therefore, it has been assumed that anticancer drugs exhibit their cytotoxic effects via apoptotic signaling pathways. Characteristics that confer sensitivity to drug-induced apoptosis are, a functional p53 protein and expression of the apoptosis-promoting protein, bax. The role of p53 and bax/bcl-2 in drug-induced apoptosis was assessed in six prostate cell lines, 1532T, 1535T, 1542T, 1542N, BPH-1 and LNCaP using TD(50) concentrations of etoposide, vinblastine and estramustine.

Changes in G1-phase populations in human glioblastoma and neuroblastoma cell lines influence p66/Be neutron-induced micronucleus yield.

Some photon resistant tumours are sensitive to neutrons but no predictive methods exist which could identify such tumours. In a recent study addressing this clinically important issue, we demonstrated that relative biologic effectiveness (RBE) values for p(66)/Be neutrons estimated from micronucleus (MN) data correlate positively with RBE values obtained from conventional clonogenic survival data. However, not all photon-resistant cell lines showed high RBE values when the MN endpoint was used.

Micronucleus response of human glioblastoma and neuroblastoma cells toward low-LET photon and high-LET p(66)/Be neutron irradiation.

The identification of photon resistant tumors that are sensitive to neutrons is still an unresolved problem, and no radiobiological criteria have been developed that could help the selection of patients for neutron therapy. The micronucleus (MN) assay has been evaluated for this purpose in a panel of human glioblastoma and neuroblastoma cell lines spanning a wide range of photon sensitivities defined by mean inactivation doses ([Latin capital letter D with macron above][gamma]) of 1.25-3.

Studies on the influence of DNA repair on radiosensitivity in prostate cell lines.

The relationship between radiosensitivity and DNA repair was investigated in six human prostate cell lines, 1542-NPTX, BPH-1, 1542-CP(3)TX, 1532-CP(2)TX, 1535-CP(1)TX and LNCaP. Except for LNCaP, these cell lines are new and were derived from primary prostate tumours and normal non-tumourigenic prostate tissue. Cell survival was assessed by clonogenic assay.

Drug resistance in prostate cancer cell lines is influenced by androgen dependence and p53 status.

Chemotherapeutic drug resistance remains a significant obstacle in the control of prostate cancer. The influence of p53 and androgen status on the drug response of new cell lines from normal, benign and primary tumour epithelium was investigated. The prostate cell lines 1542-NPTX, BPH-1, 1542-CP(3)TX, 1532-CP(2)TX, 1535-CP(1)TX and LNCaP were exposed to TD(50) doses of etoposide, vinblastine and estramustine for a period of 24 h and re-incubated for a further 4 days before measuring the cell viability by crystal violet vital dye staining assay.

Influence of irradiation and pentoxifylline on histone H3 phosphorylation in human tumour cell lines.

Phosphorylation of histone H3 at Ser-10 correlates with chromatin condensation and this amino terminal modification is now recognized as a specific marker of mitosis. We have monitored the appearance of cells showing histone H3 phosphorylation in four human tumour cell lines to identify cell cycle progression after irradiation. In the human melanoma cell lines Be11 and MeWo and in the squamous cell carcinoma lines 4197 and 4451 a dose of 7 Gy of Co-gamma irradiation increases the number of cells binding anti-histone H3-P antibody 1-8-fold in a p53-independent manner.