Predicting the sensitivity to ion therapy based on the response to photon irradiation--experimental evidence and mathematical modelling.

Background/aim: The use of ion radiation therapy is growing due to the continuously increasing positive clinical experience obtained. Therefore, there is a high interest in radio-biological experiments comparing the relative efficiency in cell killing of ions and photons as photons are currently the main radiation modality used for cancer treatment. This comparison is particularly important since the treatment planning systems (TPSs) used at the main ion therapy Centers make use of parameters describing the cellular response to photons, respectively ions, determined in vitro.

Investigation of the dose- and time-dependence of the induction of different types of cell death in a small‑cell lung cancer cell line: Implementation of the repairable-conditionally repairable model.

The purpose of this study was to quantify and model various types of cell death for a small-cell lung cancer (SCLC) cell line (U1690) after exposure to a 137Cs source and as well as to compare the linear-quadratic (LQ) and repairable-conditionally repairable model (RCR). This study is based on four different experiments that were taken place at Cancer Centrum Karolinska (CCK). A human small-cell lung cancer (SCLC) cell line after the exposure to a 137Cs source was used for the extraction of the clonogenic cell survival curve.

Chelation of lysosomal iron protects against ionizing radiation.

Ionizing radiation causes DNA damage and consequent apoptosis, mainly due to the production of hydroxyl radicals (HO•) that follows radiolytic splitting of water. However, superoxide (O2•-) and H2O2 also form and induce oxidative stress with resulting LMP (lysosomal membrane permeabilization) arising from iron-catalysed oxidative events. The latter will contribute significantly to radiation-induced cell death and its degree largely depends on the quantities of lysosomal redox-active iron present as a consequence of autophagy and endocytosis of iron-rich compounds.

Metronomic scheduling of imatinib abrogates clonogenicity of neuroblastoma cells and enhances their susceptibility to selected chemotherapeutic drugs in vitro and in vivo.

Imatinib is currently in early clinical trials as targeted therapy for relapsed neuroblastomas and other childhood solid tumors expressing platelet-derived growth factor receptors (PDGFR) or c-Kit. Short-term treatment with imatinib in clinically achievable concentrations is ineffective in neuroblastoma in vitro. However, clinically, imatinib is administered daily over long time periods.

Different G2/M accumulation in M059J and M059K cells after exposure to DNA double-strand break-inducing agents.

Purpose: To investigate and compare the cell cycle progression in relation to cell death in the human glioma cell lines, M059J and M059K, after exposure to DNA double-strand break-inducing agents.

Methods And Materials: The M059J and M059K cells, deficient and proficient in the catalytic subunit of the DNA-dependent protein kinase, respectively, were exposed to 1 and 4 Gy of photons or accelerated nitrogen ions. In addition, M059J and M059K cells were treated with 10 and 40 mug/mL of bleomycin for 30 min, respectively.

Radiation-induced cell cycle response in lymphocytes is not related to clinical side-effects in breast cancer patients.

Background: We examined whether development of radiation-induced lung injury after irradiation for breast cancer correlates with lymphocyte radiosensitivity (LRS) in vitro.

Materials And Methods: Patients were selected from a cohort of 177 patients, who were treated with adjuvant postoperative radiotherapy (RT) for loco-regional breast cancer, and included 14 patients who had severe early lung injury measured as respiratory symptoms caused by RT and treated with corticosteroids (i.e.

X-ray-induced DNA double-strand breaks in mouse l1210 cells: a new computational method for analyzing neutral filter elution data.

The aim of this article is to present a method for studying the shape of the dose and repair responses for X-ray-induced double-strand breaks (DSBs) as measured by neutral filter elution (NFE). The approach is closely related to a method we developed for the use of specific molecular size markers and used for determination of the absolute number of randomly distributed radiation-induced DSBs by pulsed-field gel electrophoresis (PFGE). Mouse leukemia L1210 cells were X-irradiated with 0-50 Gy.