Update on clinical radiobiology

Abstract

Radiation therapy is an important local cytotoxic modality for cancer treatment whose aim is to control the disease while minimising damage to normal tissue. The combination of different treatment modalities offers a more effective cure and reduction in normal tissue toxicity. However, the differences in genetic profiles can cause diverse treatment outcomes. Multidisciplinary research, where technologies and knowledge from different areas are integrated, is necessary to design the optimal regimen for individualised cancer treatment. This paper offers an overview of some new cancer treatment strategies; the impact of molecular imaging on radiation oncology; and a computer simulation model to optimise treatment planning based on patient information. It briefly discusses molecular targeted therapy, tumour microenvironment and bioreductive agents, and evidence for making individualised medicine a reality. Using DNA microarrays and proteomic technologies, information on defined molecular targets and genetic profiling for individual patients can be obtained and new algorithms for radiation oncology-related diagnosis, treatment response and prognosis can be developed.

Cervical Cancer: A Perspective on Recent Patents

“…Now, degradative Matrix Metallo Proteinases (MMP's) are released into the surrounding tissue by the activated endothelial cells. The MMP's degrade the extracellular matrix causing endothelial cell migration, division and organization to form a new blood vessel network (Chawapun, 2006).…”

“…Epidermal Growth Factor (EGF) and its receptor (EGFR) are involved in growth regulation. The EGFR belongs to a family of four receptors-EGFR (HER1/ErbB1), ErbB2 (HER2/neu), ErbB3 (HER3) and ErbB4 (HER4) (Chawapun, 2006). These cell membrane located receptors contain external binding domains which facilitate factor binding.…”

“…These cell membrane located receptors contain external binding domains which facilitate factor binding. This process results in receptor dimerization and activation of the Ras-Raf-mitogen activated protein kinase (MAPK) or phosphatidylinositol-3-kinase (PI3K) pathway causing angiogenesis, cell proliferation and cell migration (Baumann and Krause, 2004;Chawapun, 2006;Santarpia et al, 2012).…”