A considerable amount of patients undergoing radio/chemotherapy, experience tumor relapse after some time. The reason for this is that minor cell populations from the primary tumor or metastases survive the harsh chemical- and/or radiation treatment. Surviving cells even grow more aggressively, eventually destroying tissue and organ function. Combining chemotherapy with radiotherapy sometimes is more successful killing aggressive cells which otherwise would resist radiotherapy. One fundamental principle why some cells are resistant to radiotherapy and others are not are specific signaling patterns. Such signaling patterns set apart the cellular reactions to certain environmental stimuli. For example, a specific molecular program predisposes cells to undergo programmed cell death (apoptosis) if environmental or/and cell damage is too high. In some populations of cancer cells the ability to undergo apoptosis is often impaired which renders them resistant to radiation from the beginning. Other cell populations however are still able to harness this program if certain stimuli are given which mostly makes them more sensitive to radiation. However, if apoptotic signals for some reason are incapacitated aberrant cells will continue to grow despite beeing damaged. For this reason it is important to know how the combination of radiation induced signaling events and chemotherapy induced events affect cellular behaviour and eventually, how, on the molecular level, combination therapy makes aberrant cells more prone to radiation.
Our scientific interest focuses on the action of chemotherapeutic reagents on cellular signaling cascades and whether these actions in combination with processes triggered by radiation either facilitate or weaken the ability of cells to survive therapeutic tumor treatment.