Page 21 - 2014 Printable Abstract Book
P. 21
respond to a wide range of irradiation conditions in different cell types and tissues. Negatively modulated
genes revealed a dominant signature of mitotic cell cycle regulation which appears both dose and time-
dependent, but this signature is prominent in cancer cells and highly proliferating tissues but it is strongly
attenuated in non-cancer cells, thus posing a fundamental question how to correctly evaluate the tissue
transcriptional responses to irradiation as compared with what has been observed in cell lines. To this
scope, the skin's reaction to irradiation is a key in vivo model to focus. High-throughput gene expression
analyses have been performed to identify patterns of molecular changes following exposure of the skin
to irradiation. In particular, the leptin gene resulted up-regulated upon exposure to 14 MeV neutron
irradiation and the regulative mechanisms of production, circulation, and tissues receptors have been
dissected to gain an inside view of changes of leptin regulatory network in response to radiation.
Discussion will be open to interpretate on significant variations between in vitro vs in vivo models.
TR12. RADIATION-INDUCED SECONDARY CANCERS
(TR1201) Radiation-induced secondary cancers. Cecile M. Ronkers, Emma Children's Hospital,
Amsterdam, Netherlands
Cancer patients who received radiotherapy in the past are at increased risk of a second, new
cancer diagnosis, which represents a serious and high-impact treatment complication in terms of quality
of life, morbidity, and mortality. Because a radiotherapy field mostly involves part of the body, large
cohorts of cancer survivors harbor a variety of radiation doses at particular risk organs. Moreover, such
cohorts often can be followed relatively easily through the medical system, in comparison to other
radiation-exposed populations. Thus, from an epidemiologic point of view, long-term follow-up studies
among cancer survivors represent an important source of information on radiation dose response
relationships across a wide spectrum of dose levels and for a wide range of health outcomes, including
cancer. The first part of this topical review will be oriented towards etiologic research, i.e., addressing
recent findings on radiotherapy dose and second cancer risk, including the role of other treatment- and
patient characteristics. The second part will focus on clinical implications: how can such research findings
be translated for meaningful use in clinical practice, for screening recommendations in cancer survivors
who had radiotherapy and for future radiotherapy treatment planning.
TR13. RADIATION MITIGATORS, POTENTIAL, PITFALLS, AND HOPE FOR NEW SMALL MOLECULES
(TR1301) Radiation Mitigators, small molecules, hope for the future and possible pitfalls. Colin K. Hill,
USC Keck School of Medicine, Los Angeles, CA
For many years the conventional wisdom was that radiation damage could only be prevented if a
chemical compound was present to mop up free radicals during the radiation exposure. This thought
spawned the area of research in radiobiology known as radio-protector research. Several free radical
scavengers were extensively studied and eventually used in humans. However there had been almost no
compounds available that could “mitigate” the effects of radiation on normal tissue when given after the
radiation exposure. Over the last several decades this has become a more and more urgent issue with
both nuclear accidents and possible nuclear terrorism likely to cause radiation damage in members of the
population who need a remedy after the fact. In the last two decades and particularly since the events of
19 | P a g e
genes revealed a dominant signature of mitotic cell cycle regulation which appears both dose and time-
dependent, but this signature is prominent in cancer cells and highly proliferating tissues but it is strongly
attenuated in non-cancer cells, thus posing a fundamental question how to correctly evaluate the tissue
transcriptional responses to irradiation as compared with what has been observed in cell lines. To this
scope, the skin's reaction to irradiation is a key in vivo model to focus. High-throughput gene expression
analyses have been performed to identify patterns of molecular changes following exposure of the skin
to irradiation. In particular, the leptin gene resulted up-regulated upon exposure to 14 MeV neutron
irradiation and the regulative mechanisms of production, circulation, and tissues receptors have been
dissected to gain an inside view of changes of leptin regulatory network in response to radiation.
Discussion will be open to interpretate on significant variations between in vitro vs in vivo models.
TR12. RADIATION-INDUCED SECONDARY CANCERS
(TR1201) Radiation-induced secondary cancers. Cecile M. Ronkers, Emma Children's Hospital,
Amsterdam, Netherlands
Cancer patients who received radiotherapy in the past are at increased risk of a second, new
cancer diagnosis, which represents a serious and high-impact treatment complication in terms of quality
of life, morbidity, and mortality. Because a radiotherapy field mostly involves part of the body, large
cohorts of cancer survivors harbor a variety of radiation doses at particular risk organs. Moreover, such
cohorts often can be followed relatively easily through the medical system, in comparison to other
radiation-exposed populations. Thus, from an epidemiologic point of view, long-term follow-up studies
among cancer survivors represent an important source of information on radiation dose response
relationships across a wide spectrum of dose levels and for a wide range of health outcomes, including
cancer. The first part of this topical review will be oriented towards etiologic research, i.e., addressing
recent findings on radiotherapy dose and second cancer risk, including the role of other treatment- and
patient characteristics. The second part will focus on clinical implications: how can such research findings
be translated for meaningful use in clinical practice, for screening recommendations in cancer survivors
who had radiotherapy and for future radiotherapy treatment planning.
TR13. RADIATION MITIGATORS, POTENTIAL, PITFALLS, AND HOPE FOR NEW SMALL MOLECULES
(TR1301) Radiation Mitigators, small molecules, hope for the future and possible pitfalls. Colin K. Hill,
USC Keck School of Medicine, Los Angeles, CA
For many years the conventional wisdom was that radiation damage could only be prevented if a
chemical compound was present to mop up free radicals during the radiation exposure. This thought
spawned the area of research in radiobiology known as radio-protector research. Several free radical
scavengers were extensively studied and eventually used in humans. However there had been almost no
compounds available that could “mitigate” the effects of radiation on normal tissue when given after the
radiation exposure. Over the last several decades this has become a more and more urgent issue with
both nuclear accidents and possible nuclear terrorism likely to cause radiation damage in members of the
population who need a remedy after the fact. In the last two decades and particularly since the events of
19 | P a g e
