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Radiotherapy (RT) is a form of local treatment used mainly for malignant tumors. Such tumors originate from mutated stem cells. During their development they do attract a variety of host cells, coined tumor-associated host cells. Malignant tumors are characterized by uncontrolled growth, invasion and metastasis, the latter being the major cause of death of patients, even when their primary tumor is under control. RT inhibits growth. There are, however, clinical data suggesting that, under some circumstances, it may stimulate metastasis. DNA is a target of ionizing radiation (IR), though not the only one. IR produces cascades of growth factors and chemokines; it activates molecules initiating multiple signaling pathways that modulate several cellular functions. We consider cancer as a network of ecosystems, including at least the founder primary tumor, the site of metastasis and the bone marrow. As these ecosystems are in continuous communication, it is not surprising that RT of the primary tumor influences metastasis. Indeed, experiments with cells in culture and with animal tumors have shown that IR stimulates invasion and metastasis and activates pro-invasive and prometastatic cellular activities through upregulation of key molecules. At certain doses and within certain time frames, IR enhances the activities of the tumor-associated host cells that support invasion and metastasis, namely: endothelial cells building new vessels; leucocytes and macrophages causing inflammation; myofibroblasts initiating desmoplasia; osteoblasts and osteoclasts establishing bone metastasis; nerve cells producing efferent growth- and invasion-promoting molecules. Techniques such as spatially fractioned radiotherapy and hadron therapy may have different effects on metastasis. Taking into consideration the dose- and time-dependency of the IR-induced tumor-associated host cell reactions, these techniques, as well as the conventional ones, should be combined with repetitive biological imaging, reevaluation of planning and eventual replanning during the course of the treatment.

Radiation-induced lung injury (RILI) is the most common, dose-limiting complication of thoracic radio- and radiochemotherapy. Unfortunately, predicting which patients will suffer from this complication is extremely difficult. Ideally, individual phenotype- and genotype-based risk profiles should be able to identify patients who are resistant to RILI and who could benefit from dose escalation in chemoradiotherapy. This could result in better local control and overall survival. We review the risk predictors that are currently in clinical use--dosimetric parameters of radiotherapy such as normal tissue complication probability, mean lung dose, V20 and V30--as well as biomarkers that might individualize risk profiles. These biomarkers comprise a variety of proinflammatory and profibrotic cytokines and molecules including transforming growth factor beta1 that are implicated in development and persistence of RILI. Dosimetric parameters of radiotherapy show a low negative predictive value of 60% to 80%. Depending on the studied molecule, negative predictive value of biomarkers is approximately 50%. The predictive power of biomarkers might be increased if they are coupled with radiogenomics, e.g., genotyping analysis of single nucleotide polymorphisms in transforming growth factor beta1, transforming growth factor beta1 pathway genes, and other cytokines. Genetic variability and the complexity of RILI and its underlying molecular mechanisms make identification of biological risk predictors challenging. Further investigations are needed to develop more effective risk predictors of RILI.

Charcoal meat grill workers are one of the many occupational groups that are subject to carbon monoxide exposure. This group have often been overlooked and not investigated. Carboxyhemoglobin (%COHb) levels in 100 male workers were assessed before work and after work the same day. Carboxyhemoglobin levels increased significantly after work in both smoking and nonsmoking workers. The mean COHb levels for smoking workers before work was 3.8% and for nonsmokers was 2.4%, whereas after work, the mean COHb level for smokers increased to 8.1% and for nonsmokers to 6.2%. These elevated mean COHb levels exceed the 5% COHb level recommended by WHO and NIOSH. With respect to smokers only, 36 (81.8%) workers after work exceed 5%, whereas the nonsmokers, 29 (51.8%) of the workers exceed 5%. These results indicate that charcoal meat grilling workers are exposed to significant levels of carbon monoxide. Several control measures have been suggested to mitigate exposure to carbon monoxide.