Low dose-rate irradiation with [H]-labelled valine to selectively target hypoxic cells in a human colorectal cancer xenograft model.

Background: Earlier in vitro studies show that irradiation with an ultra-low dose-rate of 15 mGy/h delivered with [H]-valine leads to loss of clonogenicity in hypoxic T-47D cells. Here, the aim was to determine if [H]-valine could be used to deliver low dose-rate irradiation in a colorectal cancer model.

Methods: Clonogenicity was measured in cultured cancer cell line HT29 irradiated with 15 mGy/h combined with intermittent hypoxia.

Hypothesis: Hypoxia induces de novo synthesis of NeuGc gangliosides in humans through CMAH domain substitute.

Immunotherapy is a growing field in cancer research. A privileged tumor-associated antigen that has received much attention is N-glycolyl (NeuGc) GM3. This ganglioside is present in several types of cancer, but is almost undetectable in human healthy tissues.

Separation of two sub-groups with different DNA content after treatment of T-47D breast cancer cells with low dose-rate irradiation and intermittent hypoxia.

Background Previous studies have shown that combined treatment with internal ultra-low dose-rate irradiation selectively inactivated hypoxic T-47D breast cancer cells after three to five weeks of treatment. However, 2-3% of the hypoxic cells were found to survive and restart proliferation upon re-oxygenation. Purpose To investigate the metastatic potential and characteristics of radiosensitivity of these surviving cells, named T - 47 D.

Hypoxia Strongly Affects Mitochondrial Ribosomal Proteins and Translocases, as Shown by Quantitative Proteomics of HeLa Cells.

Hypoxia is an important and common characteristic of many human tumors. It is a challenge clinically due to the correlation with poor prognosis and resistance to radiation and chemotherapy. Understanding the biochemical response to hypoxia would facilitate the development of novel therapeutics for cancer treatment.

Cell inactivation by combined low dose-rate irradiation and intermittent hypoxia.

Purpose: To investigate in detail the earlier observed combined effect of low dose-rate β-irradiation delivered at a dose-rate of 15 mGy/h and continued intermittent hypoxia that leads to extensive cell death after approximately 3-6 weeks.

Material And Methods: Continuous low dose-rate β-irradiation at a dose rate of 15, 1.5 or 0.

The roles of TGF-β3 and peroxynitrite in removal of hyper-radiosensitivity by priming irradiation.

Purpose: To investigate the mechanisms inducing and maintaining the permanent elimination of low dose hyper-radiosensitivity (HRS) in cells given a dose of 0.3 Gy at low dose-rate (LDR) (0.3 Gy/h).

The role of nitric oxide radicals in removal of hyper-radiosensitivity by priming irradiation.

In this study, a mechanism in which low-dose hyper-radiosensitivity (HRS) is permanently removed, induced by low-dose-rate (LDR) (0.2-0.3 Gy/h for 1 h) but not by high-dose-rate priming (0.

Low dose hyper-radiosensitivity is eliminated during exposure to cycling hypoxia but returns after reoxygenation.

Purpose: To investigate the effect of cycling hypoxia on low dose hyper-radiosensitivity (HRS).

Materials And Methods: Human breast tumor T-47D cells were grown in a hypoxia workstation operated at 4% O(2) for 3-6 weeks and the pericellular oxygen concentration was recorded every 20 minutes. The presence of HRS in response to subsequent challenge irradiation was measured by clonogenic survival.

Mechanisms of the elimination of low dose hyper-radiosensitivity in T-47D cells by low dose-rate priming.

Purpose: To investigate the mechanisms of elimination of low-dose hyper-radiosensitivity (HRS) in T-47D cells induced by 0.3 Gy low dose-rate (LDR) priming.

Materials And Methods: The mitotic ratio was measured using mitotic marker histone H3 phosphorylation in LDR primed as well as untreated T-47D cells.

The elimination of low-dose hyper-radiosensitivity by transfer of irradiated-cell conditioned medium depends on dose rate.

Irradiation of T-47D cells with 0.3 Gy delivered by a (60)Co source at a low dose rate of 0.3 Gy/h abolished low-dose hyper-radiosensitivity (HRS) for at least 14 months (with continuous cell culturing), while the same dose administered acutely (40 Gy/h) eliminated HRS for less than 24 h.