Acridine orange (AO) demonstrates several biological activities. When exposed to low doses of X-ray radiation, AO increases the production of reactive radicals (radiodynamic therapy (AO-RDT)). We elucidated the efficacy of AO-RDT in breast and prostate cancer cell lines, which are likely to develop bone metastases. We used the mouse osteosarcoma cell line LM8, the human breast cancer cell line MDA-MB-231, and the human prostate cancer cell line PC-3. Cultured cells were exposed to AO and radiation at various concentrations followed by various doses of irradiation. The cell viability was then measured. In vivo, each cell was inoculated subcutaneously into the backs of mice. In the AO-RDT group, AO (1.0 μg) was locally administered subcutaneously around the tumour followed by 5 Gy of irradiation. In the radiation group, 5 Gy of irradiation alone was administered after macroscopic tumour formation. The mice were killed on the 14th day after treatment. The change in tumour volume by AO-RDT was primarily evaluated.Aims
Methods
Bone metastasis ultimately occurs due to a complex multistep process, during which the interactions between cancer cells and bone microenvironment play important roles. Prior to colonization of the bone, cancer cells must succeed through a series of steps that will allow them to gain migratory and invasive properties; epithelial-to-mesenchymal transition (EMT) is known to be integral here. The aim of this study was to determine the effects of G protein subunit alpha Q (GNAQ) on the mechanisms underlying bone metastasis through EMT pathway. A total of 80 tissue samples from patients who were surgically treated during January 2012 to December 2014 were used in the present study. Comparative gene analysis revealed that the GNAQ was more frequently altered in metastatic bone lesions than in primary tumour sites in lung cancer patients. We investigated the effects of GNAQ on cell proliferation, migration, EMT, and stem cell transformation using lung cancer cells with GNAQ-knockdown. A xenograft mouse model tested the effect of GNAQ using micro-CT analyses and histological analyses.Aims
Methods
Pathological fractures in children can occur
as a result of a variety of conditions, ranging from metabolic diseases and
infection to tumours. Fractures through benign and malignant bone
tumours should be recognised and managed appropriately by the treating
orthopaedic surgeon. The most common benign bone tumours that cause pathological
fractures in children are unicameral bone cysts, aneurysmal bone
cysts, non-ossifying fibromas and fibrous dysplasia. Although pathological
fractures through a primary bone malignancy are rare, these should
be recognised quickly in order to achieve better outcomes. A thorough
history, physical examination and review of plain radiographs are
crucial to determine the cause and guide treatment. In most benign
cases the fracture will heal and the lesion can be addressed at
the time of the fracture, or after the fracture is healed. A step-wise
and multidisciplinary approach is necessary in caring for paediatric
patients with malignancies. Pathological fractures do not have to
be treated by amputation; these fractures can heal and limb salvage
can be performed when indicated.
