Br J Dermatol 1996 Jan;134(1):77-84 
<b>UVA-induced immune suppression in human skin: protective effect of vitamin E in human epidermal cells in vitro.</b> 
Clement-Lacroix P, Michel L, Moysan A, Morliere P, Dubertret L. Laboratoire de Dermatologie, INSERM U312, Hopital Saint-Louis, Paris, France. 
<b>UVA (320-400 nm) radiation damage to membranes, proteins, DNA and other cellular targets is predominantly related to oxidative processes. In the present study, we demonstrated that cutaneous UVA-induced immunosuppression can be related, at least in part, to the appearance of these oxidative processes.</b> The UVA-induced oxidative processes in freshly isolated epidermal cells were monitored by measuring the thiobarbituric acid reactive substances (TBARS) as an index of peroxidation. The in vitro immunosuppressive effects of UVA were demonstrated by measuring the allogeneic lymphocyte proliferation induced by epidermal cells or purified Langerhans cells in the mixed epidermal cell-lymphocyte reaction (MECLR). In addition, the effects of a potent antioxidant (vitamin E) on these two UVA-induced processes were analysed. Our results showed that the antigen-presenting function of Langerhans cells measured in the MECLR is dose-dependently decreased by UVA radiation (up to 20J/cm2). <b>Overnight incubation of epidermal cells with vitamin E (400 mumol/l) before irradiation partially protected epidermal cells from the immunosuppressive effects of UVA radiation,</b>and decreased TBARS release into the supernatant (a decrease of 35% compared with a control without vitamin E). <b>Our results suggest that UVA radiation may alter cell-presenting antigen function partly via the generation of reactive oxygen species which trigger peroxidative processes, and these data contribute to the understanding of the role of oxidative mechanisms in immune suppression induced by UVA radiation. Our in vitro model can be used to quantify UV-mediated epidermal cell damage and the degree of immune photoprotection provided by various agents.</b> 
&&url PMID: 8745890 


Radiat Res 1983 Apr;94(1):10-40 
<b>Radiation biology: the conceptual and practical impact on radiation therapy.</b> 
Suit HD. 
Radiation biology has had an important impact on clinical radiation therapy by providing a rationale for implementation of new treatment strategies and for clinical concepts or practices thereby increasing their acceptance. The observed rather narrow range of D0 and n values for mammalian cells contributed to successful trials of radiation treatment of several "radiation-resistant" tumors, e.g., carcinoma of prostate, color-rectum, and <b>sarcoma of soft tissue.</b> Attention of clinicians was forcibly directed to assessment of local results (local failure, treatment complications) and not merely survival at 5 years by the extensive literature of cell survival curves (in vivo and in vitro) and dose-response assays on normal and tumor tissues. Upon these same laboratory results a scientific rationale was developed for use of shrinking field technique, low dose for subclinical disease, and the combination of moderate dose radiation therapy and conservative surgery. The entire area of clinical research into altered dose fractionation schedules is based upon research on cell proliferation kinetics and repair of radiation damage. The understanding that the time for complete regression of tumor depends not only upon cell kill but also on the pattern of cell proliferation of the progeny of lethally irradiated cells and the abundance of stroma provided a basis for accepting patients with slowly responding tumors for treatment. There remains a wide field of need in research in this area as even today a large proportion of patients who die of cancer die with their cancer uncontrolled at the primary site. Publication Types: Historical article 
&&url PMID: 6344129 


Cancer 1978 Mar;41(3):991-5 ??????

Am J Roentgenol 1976 Dec;127(6):1027-32 
<b>Inherent cellular radiosensitivity of human tumors of varying clinical curability.</b> 
Weichselbaum RR, Epstein J, Little JB, Kornblith P. 
It is well known that radiation therapy can be successfully used to cure or control some types of human tumors, while consistently failing in others. This has been ascribed to several factors including differences in the intrinsic sensitivity of the tumor cells and in their ability to recover from radiation damage. In this study, human tumor cells from an osteogenic sarcoma, a glioblastoma, and two medulloblastomas, as well as cells from human skin, were established in tissue culture, and the in vitro x-ray survival and DNA repair parameters determined. No significant differences in either clonogenic survival or DNA strand rejoining ability could be detected among these human tumors or skin cells, despite the wide variability in their radiocurability in vivo. In addition, skin cell strains derived from patients exhibiting markedly sensitive or resistant skin reactions during fractionated radiotherapy showed no differences in survival characteristics from normal controls. It is therefore suggested that the wide range of radiocurabilities seen among various human tumors cannot be explained on the basis of inherent cellular factors responsible for the survival of tumor cells after x-irradiation. 
&&url PMID: 1069484 


Indian J Exp Biol 1989 Nov;27(11):1005-7
<b>2-Deoxy-D-glucose induced modification of chromosomal damage in UV-irradiated peripheral human leukocytes.</b> 
Kalia VK, Jain VK. 
UV-irradiation (0.6 J/m2) of peripheral human leukocytes 27 hr after PHA-stimulation induced a considerable mitotic delay in the cultures. Approximately two thirds of the chromosomal aberrations induced by UV were gaps of the chromatid and isochromatid types. Treatment with glucose antimetabolite 2-deoxy-D-glucose (2-DG) alone did not induce any chromosomal damage. Presence of 2-DG (5 mM, equimolar with glucose) for 2 hr after UV-irradiation resulted in a significant reduction in the frequency of cells with aberrations. Decrease in the total aberrations per cell was also observed. The data are consistent with earlier observations that 2-DG reduces the manifestation of radiation damage in normal proliferating cells. 
&&url PMID: 2620927 


Int J Radiat Biol 1989 Dec;56(6):963-73 
<b>Nuclear lysate sedimentation measurements of peripheral blood lymphocytes from radiotherapy patients.</b> 
Deeley JO, Moore JL. South Wales Radiotherapy and Oncology Service, Velindre Hospital, Cardiff, U.K. 
When isolated nuclei of human lymphocytes are challenged with 2 M NaCl a histone-free-DNA-protein (HF-DNA) complex is released. In a linear sucrose gradient (pH 8.0) the sedimentation distance of HF-DNA is reduced when immediately isolated from cells irradiated in vitro. At low doses, if irradiated cells are incubated at 37 degrees C the sedimentation behaviour approaches that of unirradiated cells (i.e. repair). In the present study such repair was usually complete within 1 h. The radiation damage to lymphocytes from a healthy donor group and three patient groups consisting of new patients (before radiotherapy), well patients (2 to 6 years post-radiotherapy) and patients with complications attributed to radiotherapy was similar. The lymphocytes from most healthy donors and new patients demonstrated complete repair of radiation damage following an incubation of 1 h at 37 degrees C. However, 2/29 (6.9 per cent) healthy donors and 2/25 (8 per cent) new patients demonstrated poor repair. Of those patients now attending with 'bowel complications' attributed to radiotherapy 7/16 (44 per cent) demonstrated poor repair. In contrast, all those (11/11) described as 'well and complication-free' showed good repair. 
&&url PMID: 2574224


Hautarzt 1990 Aug;41(8):448-50
<b>[Exacerbation of progressive scleroderma following roentgen therapy].</b> [Article in German] 
Haustein UF. Klinik und Poliklinik fur Hautkrankheiten des Bereichs Medizin, Karl-Marx-Universitat Leipzig. 
In a 38-year-old female patient suffering from progressive scleroderma and breast carcinoma the clinical features were exacerbated and became generalized after radiotherapy, and unfortunately regressed only transiently during aggressive polychemotherapy. Links between progressive scleroderma and carcinoma and the immune system are discussed. The risk of post-irradiation worsening of progressive scleroderma is pointed out. 
&&url PMID: 2177048 


Cancer 1977 Feb;39(2 Suppl):987-98 
<b>Chemical modification of radiation effects</b>
Phillips TL.
A number of powerful chemical compounds that modify radiation effects have been discovered and tested both in the laboratory and clinically over the past 25 years. There are four major classes of compounds: aminothiol radio-protectors which act on well vascularized euoxic cells and concentrate in tissues such as skin, gut and marrow; nitromidazole radiosensitizers which act on hypoxic tumor cells; pyrimidine analogues which are incorporated into the DNA of cycling cells and cause radiosensitization; and cancer themotherapy agents which, in addition to their ability to kill tumor cells directly, also may sensitize tumor and normal cells to radiation. The mechanism of action, experimental activity, and clinical results or the potential for each of these agents are reviewed. 
&&url PMID: 319901


CRC Crit Rev Clin Radiol Nucl Med 1975 Jul;6(3):425-39
<b>A survey of the benefits and risks in the practice of radiology.</b> 
Payne JT, Loken MK. 
The findings from both animal and human studies on the radiation risk at low doses and low dose rates are far from conclusive, primarily due to statistical limitations. However, to arrive at some estimate of radiation risk, a conservative approach has been taken, and a linear extrapolation of radiation effects from high doses to low doses has been made. Thus, it is assumed that any exposure to radiation carries some risk of somatic or genetic damage and that there is no threshold or safe dose. In medical practice, diagnostic radiological procedures should be performed only if useful clinical information will be derived. In addition, this information should be obtained at the least possible risk to the patient. For mass chest X-rays, mammography, and lung scans, a quantitative determination of benefit to risk is developed. This approach, though possible desirable, is exceedingly difficult to establish for most diagnostic radiological procedures. Thus, good clinical judgement should be employed in radiological practice, just as it should be employed in all aspects of medical practice. 
&&url PMID: 1097189 


Radiat Res 2000 Sep;154(3):342-6 
<b>Identification of potential mRNA biomarkers in peripheral blood lymphocytes for human exposure to ionizing radiation.</b> 
Amundson SA, Do KT, Shahab S, Bittner M, Meltzer P, Trent J, Fornace AJ Jr. National Institutes of Health, National Cancer Institute, Bethesda, MD 20892, USA. 
Since early in the Atomic Age, biological indicators of radiation exposure have been sought, but currently available methods are not entirely satisfactory. Using cDNA microarray hybridization to discover new potential biomarkers, we have identified genes expressed at increased levels in human peripheral blood lymphocytes after ex vivo irradiation. We recently used this technique to identify a large set of ionizing radiation-responsive genes in a human cell line (Oncogene 18, 3666-3672, 1999). The present set of radiation markers in peripheral blood lymphocytes was identified 24 h after treatment, and while the magnitude of mRNA induction generally decreased over time, many markers were still significantly elevated up to 72 h after irradiation. In all donors, the most highly responsive gene identified was DDB2, which codes for the p48 subunit of XPE, a protein known to play a crucial role in repair of ultraviolet (UV) radiation damage in DNA. Induction of DDB2, CDKN1A (also known at C1P1/WAF1) and XPC showed a linear <b>dose-response relationship between 0.2 and 2 Gy at 24 and 48 h after irradiation, with less linearity at earlier or later times. These results suggest that relative levels of gene expressions in peripheral blood cells may provide estimated of environmental radiation exposures.</b> 
&&url PMID: 11012342