Fredric Jay Burns, Ph.D.

Mechanism of selenium-induced inhibition of arsenic-enhanced UVR carcinogenesis in mice
Burns, Fredric J; Rossman, Toby; Vega, Katherine; Uddin, Ahmed; Vogt, Stefan; Lai, Barry; Reeder, Richard J
2008 Jun;116(6):703-708, Environmental health perspectives
BACKGROUND: Hairless mice that ingested arsenite in drinking water exhibited more than a 5-fold enhancement of ultraviolet radiation (UVR) carcinogenesis, whereas arsenite alone was carcinogenically inactive. Dietary organoselenium blocked the cancer enhancement effect of arsenic but not cancer induction by UVR. OBJECTIVE: In this study we sought to explain selenium blockage of As enhancement by establishing the extent that As and Se tissue distributions are coincident or divergent. METHODS: We used the X-ray fluorescence microprobe at the Advanced Photon Source (Argonne National Laboratory) to probe sections of skin and liver from hairless mice exposed to a) UVR, b) UVR + As, c) UVR + organoselenium, or d) UVR + As + organoselenium. RESULTS: We found elevated levels of As in the skin epithelium (hair follicles and epidermis) and diffusely in the liver of mice exposed to UVR + As. Arsenic was entirely absent in skin in mice exposed to UVR + As + organoselenium, but a diffuse low level was seen in the liver. As and Se locations were consistently divergent in skin; As was more diffusely distributed, whereas Se was strongly associated with membranes. X-ray absorption near-edge spectra are consistent with the presence of the seleno-bis(S-glutathionyl) arsinium ion in the liver. CONCLUSIONS: Supplemental Se was uncommonly effective at preventing even a trace of As in skin at 14 or 196 days of continuous exposure to As in drinking water. Traces of the seleno-bis(S-glutathionyl) arsinium ion in the liver suggested that formation of this compound was more likely to be responsible for the As-blocking effect of Se than was a mechanism based on antioxidation
— id: 93323, year: 2008, vol: 116, page: 703, stat: Journal Article,

Mechanism of inhibition of arsenite co-carcinogenesis by supplemental selenium
Rossman, TG; Uddin, AN; Burns, FJ; Vega, K
2008 AUG ;49(7):557-557, Environmental & molecular mutagenesis
— id: 86809, year: 2008, vol: 49, page: 557, stat: Journal Article,

NASA Radiation Biomarker Workshop, September 27-28, 2007
Straume, Tore; Amundson, Sally A; Blakely, William F; Burns, Fredric J; Chen, Allen; Dainiak, Nicholas; Franklin, Stephen; Leary, Julie A; Loftus, David J; Morgan, William F; Pellmar, Terry C; Stolc, Viktor; Turteltaub, Kenneth W; Vaughan, Andrew T; Vijayakumar, Srinivasan; Wyrobek, Andrew J
2008 Sep;170(3):393-405, Radiation research
A summary is provided of presentations and discussions at the NASA Radiation Biomarker Workshop held September 27-28, 2007 at NASA Ames Research Center in Mountain View, CA. Invited speakers were distinguished scientists representing key sectors of the radiation research community. Speakers addressed recent developments in the biomarker and biotechnology fields that may provide new opportunities for health-related assessment of radiation-exposed individuals, including those exposed during long-duration space travel. Topics discussed included the space radiation environment, biomarkers of radiation sensitivity and individual susceptibility, molecular signatures of low-dose responses, multivariate analysis of gene expression, biomarkers in biodefense, biomarkers in radiation oncology, biomarkers and triage after large-scale radiological incidents, integrated and multiple biomarker approaches, advances in whole-genome tiling arrays, advances in mass spectrometry proteomics, radiation biodosimetry for estimation of cancer risk in a rat skin model, and confounding factors. A summary of conclusions is provided at the end of the report
— id: 95285, year: 2008, vol: 170, page: 393, stat: Journal Article,

Radiation carcinogenesis
Burns, Fred; et al
Environmental and occupational medicine Philadelphia : Wolters Kluwer/Lippincott Williams & Wilkins, 2007,
— id: 5370, year: 2007, vol: , page: ?, stat: Chapter,

Induction and prevention of carcinogenesis in rat skin exposed to space radiation
Burns, Fredric J; Tang, Moon-shong; Frenkel, Krystyna; Nadas, Arthur; Wu, Feng; Uddin, Ahmed; Zhang, Ronghe
2007 Jun;46(2):195-199, Radiation & environmental biophysics
Quantitative cancer incidence data exist for various laboratory animal models, but little of this information is usable for estimating human risks, primarily because of uncertainties about possible mechanistic differences among species. Acceptance and utilization of animal data for human risk assessment will require a much better understanding of the comparative underlying mechanisms than now exists. A dual-lesion, radiation-track model in rat skin has proven to be consistent with tumor induction data with respect to acute radiation doses ranging from 0.5 up to 10 Gy and higher, and average LETs ranging from 0.34 to 150 keV mum(-1) according to the form neoplastic risk (D,L) = CLD + BD(2). A recent result with the (56)Fe ion beam showed dose-response consistency for malignant (carcinomas) and benign (fibromas) tumor induction with earlier results utilizing argon and neon ion beams. A discrepancy between the model and experiment was found indicating that proportionality of cancer yield with LET did not occur at 150 versus 125 keV mum(-1), i.e. tumor yield did not increase in spite of a 20% increase of LET, which suggests that a LET response maximum exists at or within this dose range. Concordance between the model and tumor induction data in rat skin implies that potential intervening complexities of carcinogenic progression fail to obscure the basic radiobiological assumptions underpinning the model. Gene expression microarray analysis shows that vitamin A inhibits the expression of about 80% of the inflammation-related genes induced by the radiation and prevents about 46% of the neoplasms associated with (56)Fe ion radiation without appearing to interfere with the underlying dose and LET response patterns. Further validation is needed, but the model has the potential to provide quantitative estimates of cancer risk as a function of dose and LET for almost any type of radiation exposure and even for combinations of different radiations provided only three empirical parameters can be established for each type of radiation and organ system
— id: 72097, year: 2007, vol: 46, page: 195, stat: Journal Article,

Dietary chromium and nickel enhance UV-carcinogenesis in skin of hairless mice
Uddin, Ahmed N; Burns, Fredric J; Rossman, Toby G; Chen, Haobin; Kluz, Thomas; Costa, Max
2007 Jun 15;221(3):329-338, Toxicology & applied pharmacology
The skin cancer enhancing effect of chromium (in male mice) and nickel in UVR-irradiated female Skh1 mice was investigated. The dietary vitamin E and selenomethionine were tested for prevention of chromium-enhanced skin carcinogenesis. The mice were exposed to UVR (1.0 kJ/m(2) 3x weekly) for 26 weeks either alone, or combined with 2.5 or 5.0 ppm potassium chromate, or with 20, 100 or 500 ppm nickel chloride in drinking water. Vitamin E or selenomethionine was added to the lab chow for 29 weeks beginning 3 weeks before the start of UVR exposure. Both chromium and nickel significantly increased the UVR-induced skin cancer yield in mice. In male Skh1 mice, UVR alone induced 1.9+/-0.4 cancers/mouse, and 2.5 or 5.0 ppm potassium chromate added to drinking water increased the yields to 5.9+/-0.8 and 8.6+/-0.9 cancers/mouse, respectively. In female Skh1 mice, UVR alone induced 1.7+/-0.4 cancers/mouse, and the addition of 20, 100 or 500 ppm nickel chloride increased the yields to 2.8+/-0.9, 5.6+/-0.7 and 4.2+/-1.0 cancers/mouse, respectively. Neither vitamin E nor selenomethionine reduced the cancer yield enhancement by chromium. These results confirm that chromium and nickel, while not good skin carcinogens per se, are enhancers of UVR-induced skin cancers in Skh1 mice. Data also suggest that the enhancement of UVR-induced skin cancers by chromate may not be oxidatively mediated since the antioxidant vitamin E as well as selenomethionine, found to prevent arsenite-enhanced skin carcinogenesis, failed to suppress enhancement by chromate
— id: 72149, year: 2007, vol: 221, page: 329, stat: Journal Article,

Gene expression and cell cycle arrest in a rat keratinocyte line exposed to 56Fe ions
Wu, Feng; Zhang, Ronghe; Burns, Fredric J
2007 Mar;48(2):163-170, Journal of radiation research
The purpose of the present work was to examine gene expression patterns in a rat keratinocyte line exposed to a (56)Fe ion beam. The cells were exposed to 1.01 geV/nucleon (56)Fe ions generated by the NASA Space Radiation Laboratory facility. Data from Affymetrix rat microarrays (RAT 230_2) were processed by BRB ArrayTools 3.3.0 software, and the Gene Ontogeny (GO) database was utilized to categorize significantly responding genes. Cell cycle distribution was analyzed by flow cytometry, and cell survival was based on the colony survival assay. At 24 h after 3.0 Gy of (56)Fe ion radiation, 69 known genes were significantly (p <or= 0.001) altered (88% upregulated) and 16 of 97 categories of genes at level 7 in the GO hierarchy were significantly altered (p <or= 0.01) including 'mitosis', 'DNA repair' and 'positive regulation of cell cycle' in comparison to control. Flow cytometry revealed that 60% of irradiated cells versus 10% of control cells were in G(2)/M phase of the cell cycle at 24 h after (56)Fe ion radiation. Colony survival rate for rat keratinocytes irradiated with 3.0 Gy of (56)Fe ion was 6.6% versus control at 24 h after irradiation. The results in the present study suggest a link between the increased expression of cell cycle genes and cell death
— id: 72413, year: 2007, vol: 48, page: 163, stat: Journal Article,

Arsenic as a co-carcinogen
Rossman, TG; Uddin, AN; Burns, FJ
2006 DEC ;19(12):1700-1700, Chemical research in toxicology
— id: 71052, year: 2006, vol: 19, page: 1700, stat: Journal Article,

Alterations in gene expression in rat skin exposed to 56Fe ions and dietary vitamin A acetate
Zhang, Ronghe; Burns, Fredric J; Chen, Haobin; Chen, Shuaili; Wu, Feng
2006 May;165(5):570-581, Radiation research
The purpose of the present work was to examine gene expression patterns in rat skin exposed to a beam of (56)Fe ions, a surrogate for the high-energy, heavy-ion galactic radiation background, as a basis for obtaining a better understanding of the possible mechanism(s) behind the radioprotective activity of vitamin A. A 2 x 4-cm rectangle of dorsal rat skin was exposed to 1.01 GeV/nucleon (56)Fe ions generated by the Alternating Gradient Synchrotron at Brookhaven National Laboratory. Gene expression patterns were monitored in either the presence or absence of a 250-ppm dietary supplement of vitamin A acetate in powdered lab chow. Although vitamin A and other retinoids show anti-carcinogenic activity in several animal models, the underlying changes in gene expression have not been examined extensively. At either 1 or 7 day after irradiation, a 1-cm square of irradiated and control rat skin was excised and analyzed using the Affymetrix rat microarray (RG_U34A) system. Microarray responses were displayed and processed by GeneSpring 7.0 and GOTree software. At 1 day after 3 Gy of (56)Fe-ion irradiation, the expression of 110 genes was significantly up-regulated (P < = 0.05) in comparison to levels in control rat skin, while no genes were altered by the vitamin A acetate supplement alone. Combined with (56)Fe-ion radiation, the vitamin A acetate supplement blocked the expression of 88 (80%) of the 110 genes and eliminated 16 of 18 gene categories that were significantly altered (all increased) by the (56)Fe-ion radiation. Categories with large numbers of genes eliminated by the retinoid included response to stress, 33 genes; response to biotic stimulus, 38 genes; signal transduction, 35 genes; and regulation of cellular/physiological process, 40 genes. Even for immune response and response to biotic stimulus, the only two categories that remained significantly altered in the presence of the vitamin, the combined number of altered genes was reduced from 74 to 13. No significant alterations in gene expression were found at 7 days relative to the numbers in controls. The results indicate that at 1 day dietary vitamin A acetate strongly interfered with (56)Fe-ion-induced gene expression within the broad categories of stimulus- and stress-related genes, implying that the latter gene categories likely play a role in the radioprotective action of the vitamin
— id: 64657, year: 2006, vol: 165, page: 570, stat: Journal Article,

Ionizing radiation synergistic induction of cyclooxygenase-2 with benzo[a]pyrene diol-epoxide through nuclear factor of activated T cells in mouse epidermal Cl 41 cells
Zhang, Ronghe; Li, Jingxia; Burns, Fredric J; Huang, Chuanshu
2006 Mar;15(3):721-727, Oncology reports
Carcinogenic effects of ionizing radiation and benzo[a]pyrene-7,8-diol-9,10-epoxide (B[a]PDE), a major metabolite of benzo[a]pyrene (B[a]P), have been well demonstrated both in vitro and in vivo. Two-stage carcinogenesis results indicate that mouse skin is highly susceptible to both ionizing radiation and benzo[a]pyrene-7,8-diol-9,10-epoxide (B[a]PDE), a major metabolite of benzo[a]pyrene (B[a]P). It is believed that signaling pathways leading to the regulation of gene expression play a significant role in the development of skin cancers. The NFAT family of proteins are important transcription factors involved in the regulation of various target genes, such as IL-1 and TNF-alpha, which play key roles in the regulation of inflammation and carcinogenesis. Thus, the effect of ionizing radiation and B[a]PDE on COX-2 induction and NFAT3 activation, and their relationship, was investigated in mouse epidermal Cl 41 cells. We found that B[a]PDE exposure induced a very high level of NFAT activation in mouse epidermal Cl 41 cells. Ionizing radiation exhibited a synergistic effect with B[a]PDE on NFAT activation and COX-2 induction, while ionizing radiation alone had no effect. By stably knocking down NFAT3 protein expression by means of the specific interfering RNA (siRNA) technique, we found that COX-2 induction by B[a]PDE and the synergistic effect of ionizing radiation with B[a]PDE was totally blocked. These results indicate that ionizing radiation acts synergistically with B[a]PDE on COX-2 induction, and the synergism is dependent on the NFAT3 pathway
— id: 63739, year: 2006, vol: 15, page: 721, stat: Journal Article,

Vitamin E and organoselenium prevent the cocarcinogenic activity of arsenite with solar UVR in mouse skin
Uddin, Ahmed N; Burns, Fredric J; Rossman, Toby G
2005 Dec;26(12):2179-2186, Carcinogenesis
Arsenic-induced carcinogenesis is a worldwide problem for which there is currently limited means for control. Recently, we showed that arsenite in drinking water greatly potentiates solar ultraviolet radiation (UVR) induced skin cancer in mice, at concentrations as low as 1.25 mg/l. In this study, we examined the protective efficacy of vitamin E and 1,4-phenylenebis(methylene)selenocyanate (p-XSC) against tumors induced by UVR and UVR + arsenite. Hairless mice were exposed to UVR alone (1.0 kJ/m(2) x 3 times weekly) or UVR + sodium arsenite (5 mg/l in drinking water) and fed lab chow supplemented or not with vitamin E (RRR-alpha-tocopheryl acetate, 62.5 IU/kg diet) or p-XSC (10 mg/kg) for 26 weeks. The tumor yield for mice receiving UVR alone was 3.6 tumors/mouse and the addition of arsenite to the drinking water increased the yield to 7.0 tumors/mouse (P < 0.005). Vitamin E and p-XSC reduced the tumor yield in mice given UVR + arsenite by 2.1-fold (P < 0.001) and 2-fold (P < 0.002), respectively. Vitamin E, but not p-XSC, reduced the tumor yield induced by UVR alone by 30% (P < 0.05). No significant difference in tumor types or grade of malignancy was observed in mice treated with or without chemopreventives. Immunostaining of mouse skin for 8-oxo-2'-deoxyguanosine (8-oxo-dG) revealed a significant reduction of 8-oxo-dG formation in mice treated with vitamin E or p-XSC compared with those treated with UVR + arsenite. These results show that vitamin E and p-XSC protect strongly against arsenite-induced enhancement of UVR carcinogenesis
— id: 61332, year: 2005, vol: 26, page: 2179, stat: Journal Article,

Arsenite-induced alterations of DNA photodamage repair and apoptosis after solar-simulation UVR in mouse keratinocytes in vitro
Wu, Feng; Burns, Fredric J; Zhang, Ronghe; Uddin, Ahmed N; Rossman, Toby G
2005 Aug;113(8):983-986, Environmental health perspectives
Our laboratory has shown that arsenite markedly increased the cancer rate caused by solar-simulation ultraviolet radiation (UVR) in the hairless mouse skin model. In the present study, we investigated how arsenite affected DNA photodamage repair and apoptosis after solar-simulation UVR in the mouse keratinocyte cell line 291.03C. The keratinocytes were treated with different concentrations of sodium arsenite (0.0, 2.5, 5.0 microM) for 24 hr and then were immediately irradiated with a single dose of 0.30 kJ/m2 UVR. At 24 hr after UVR, DNA photoproducts [cyclobutane pyrimidine dimers (CPDs) and 6-4 photoproducts (6-4PPs)] and apoptosis were measured using the enzyme-linked immunosorbent assay and the two-color TUNEL (terminal deoxynucleotide transferase dUTP nick end labeling) assay, respectively. The results showed that arsenite reduced the repair rate of 6-4PPs by about a factor of 2 at 5.0 microM and had no effect at 2.5 microM. UVR-induced apoptosis at 24 hr was decreased by 22.64% at 2.5 microM arsenite and by 61.90% at 5.0 microM arsenite. Arsenite decreased the UVR-induced caspase-3/7 activity in parallel with the inhibition of apoptosis. Colony survival assays of the 291.03C cells demonstrate a median lethal concentration (LC50) of arsenite of 0.9 microM and a median lethal dose (LD50) of UVR of 0.05 kJ/m2. If the present results are applicable in vivo, inhibition of UVR-induced apoptosis may contribute to arsenite's enhancement of UVR-induced skin carcinogenesis
— id: 62598, year: 2005, vol: 113, page: 983, stat: Journal Article,

The action of a dietary retinoid on gene expression and cancer induction in electron-irradiated rat skin
Burns, Fredric J; Chen, Shuaili; Xu, Guijuan; Wu, Feng; Tang, Moon-Shong
2002 Dec;43 Suppl:S229-S232, Journal of radiation research
Current models of radiation carcinogenesis generally assume that the DNA is damaged in a variety of ways by the radiation and that subsequent cell divisions contribute to the conversion of the damage to heritable mutations. Cancer may seem complex and intractable, but its complexity provides multiple opportunities for preventive interventions. Mitotic inhibitors are among the strongest cancer preventive agents, not only slowing the growth rate of preneoplasias but also increasing the fidelity of DNA repair processes. Ionizing radiation, including electrons, is a strong inducer of cancer in rat skin, and dietary retinoids have shown potent cancer preventive activity in the same system. A non-toxic dietary dose of retinyl acetate altered gene expression levels 24 hours after electron irradiation of rat skin. Of the 8740 genes on an Affymetrix rat expression array, the radiation significantly (5 fold or higher) altered 188, while the retinoid altered 231, including 16 radiation-altered genes that were reversely altered. While radiation strongly affected the expression of stress response, immune/inflammation and nucleic acid metabolism genes, the retinoid most strongly affected proliferation-related genes, including some significant reversals, such as, keratin 14, retinol binding protein, and calcium binding proteins. These results point to reversal of proliferation-relevant genes as a likely basis for the anti-radiogenic effects of dietary retinyl acetate
— id: 72110, year: 2002, vol: 43 Suppl, page: S229, stat: Journal Article,

Arsenite cocarcinogenesis: an animal model derived from genetic toxicology studies
Rossman, Toby G; Uddin, Ahmed N; Burns, Fredric J; Bosland, Maarten C
2002 Oct;110 Suppl 5(4):749-752, Environmental health perspectives
Although epidemiologic evidence shows an association between inorganic arsenic in drinking water and increased risk of skin, lung, and bladder cancers, no animal model for arsenic carcinogenesis has been successful. This lack has hindered mechanistic studies of arsenic carcinogenesis. Previously, we and others found that low concentrations (< or =5 microm) of arsenite (the likely environmental carcinogen), which are not mutagenic, can enhance the mutagenicity of other agents, including ultraviolet radiation (UVR) and alkylating agents. This enhancing effect appears to result from inhibition of DNA repair by arsenite, but not via inhibition of DNA repair enzymes. Rather, low concentrations of arsenite disrupt p53 function and upregulate cyclin D1. Failure to find an animal model for arsenic carcinogenesis might be because arsenite is not a carcinogen per se but acts as an enhancing agent (cocarcinogen) with a genotoxic partner. We tested this hypothesis with solar UVR in hairless but immunocompetent Skh1 mice. Mice were given 10 mg/L sodium arsenite in drinking water (or not) and irradiated with 1.7 KJ/m(2) solar UVR 3 times weekly. As expected, no tumors appeared in any organs in control mice or in mice given arsenite alone. After 26 weeks irradiated mice given arsenite had a 2.4-fold increase in skin tumor yield compared with mice given UVR alone. The tumors were mostly squamous cell carcinomas, and those occurring in mice given UVR plus arsenite were much larger and more invasive. These results are consistent with the hypothesis that arsenic acts as a cocarcinogen with a second (genotoxic) agent by inhibiting DNA repair and/or enhancing positive growth signaling. Skin cancers in populations drinking water containing arsenic may be caused by the enhancement by arsenic compounds of carcinogenesis induced by UVR (or other environmental agents). It is possible that lung and bladder cancers associated with arsenic in drinking water may also require a carcinogenic partner
— id: 34894, year: 2002, vol: 110 Suppl 5, page: 749, stat: Journal Article,

Fibroma induction in rat skin following single or multiple doses of 1.0 GeV/nucleon 56Fe ions from the Brookhaven Alternating Gradient Synchrotron (AGS)
Burns FJ; Zhao P; Xu G; Roy N; Loomis C
2001 ;17 Suppl 1(8):194-195, Physica medica
Rat skin was exposed to the plateau region of the 1.0 GeV/nucleon 56Fe beam at the Brookhaven AGS. Rats were irradiated or not with single of split doses of 56Fe or argon; some 56Fe-exposed rats were fed 250 ppm retinyl acetate continuously in the lab chow beginning 1 week before irradiation. All lesions were noted, photographed and identified for eventual histological diagnosis. The preponderance of the tumors so far are fibromas. The data show that single doses of 56Fe ions are 2 or 3 fold more effective than argon in producing tumors at 4.5 Gy but are about equally effective at 3.0 Gy and 9.0 Gy. The presence of 250 ppm retinyl acetate in the lab chow reduced the incidence of tumors by about 50-60% in comparison to groups exposed only to the radiation. These are preliminary findings based on only about one-fourth the eventual number of tumors expected
— id: 32228, year: 2001, vol: 17 Suppl 1, page: 194, stat: Journal Article,

Arsenite is a cocarcinogen with solar ultraviolet radiation for mouse skin: an animal model for arsenic carcinogenesis
Rossman TG; Uddin AN; Burns FJ; Bosland MC
2001 Oct 1;176(1):64-71, Toxicology & applied pharmacology
Although epidemiological evidence shows an association between arsenic in drinking water and increased risk of skin, lung, and bladder cancers, arsenic compounds are not animal carcinogens. The lack of animal models has hindered mechanistic studies of arsenic carcinogenesis. Previously, this laboratory found that low concentrations of arsenite (the likely environmental carcinogen) which are not mutagenic can enhance the mutagenicity of other agents, including ultraviolet radiation (UVR). This enhancing effect appears to result from inhibition of DNA repair by arsenite. Recently we found that low concentrations of arsenite disrupted p53 function and upregulated cyclin D1. These results suggest that the failure to find an animal model for arsenic carcinogenesis is because arsenite is not a carcinogen per se, but rather acts as an enhancing agent (cocarcinogen) with a genotoxic partner. We tested this hypothesis with solar UVR as carcinogenic stimulus in hairless Skh1 mice. Mice given 10 mg/l sodium arsenite in drinking water for 26 weeks had a 2.4-fold increase in yield of tumors after 1.7 KJ/m(2) UVR three times weekly compared with mice given UVR alone. No tumors appeared in mice given arsenite alone. The tumors were mostly squamous cell carcinomas, and those occurring in mice given UVR plus arsenite appeared earlier and were much larger and more invasive than in mice given UVR alone. These results are consistent with the hypothesis that arsenic acts as a cocarcinogen with a second (genotoxic) agent by inhibiting DNA repair and/or enhancing positive growth signaling
— id: 32229, year: 2001, vol: 176, page: 64, stat: Journal Article,

A model of repair for tumor induction by high and low LET radiation
Hiz, Z; Burns, F J
Advances in DNA damage and repair: Oxygen radical effects, cellular protection, and biological consequences Dordrecht: Kluwer Academic Publishers, 1999,
— id: 2565, year: 1999, vol: , page: 489, stat: Chapter,

XP-A mutations in basal cell carcinomas (BCCs) from X-irradiated tinea capitis patients with multiple BCCs
Zhao, P; Shore, R E; Roy, N; Burns, F
1999 Apr 10-14;40:283-283, Proceedings (American Association for Cancer Research)
— id: 15918, year: 1999, vol: 40, page: 283, stat: Journal Article,

Oxidative stress suppresses transcription factor activities in stimulated lymphocytes
Flescher E; Tripoli H; Salnikow K; Burns FJ
1998 May;112(2):242-247, Clinical & experimental immunology
Effects of oxidative stress on stimulation-dependent signal transduction, leading to IL-2 expression, were studied. Purified quiescent human blood T lymphocytes were subjected to: (i) acute exposure to hydrogen peroxide; (ii) chronic exposure to hydrogen peroxide; and (iii) acute exposure to ionizing radiation. The cells were then stimulated for 6 h. DNA-binding activities (determined by the electrophoretic mobility shift assay) of three transcription factors: NFkappaB, AP-1 and NFAT, were abolished in the lymphocytes by all three modes of oxidative stress. The lymphocytes exhibited lipid peroxidation only upon exposure to the lowest level of hydrogen peroxide used (20 microM). All three modes of oxidative stress induced catalase activity in the lymphocytes. The only exception was hydrogen peroxide at 20 microM, which did not induce catalase activity. We conclude that: (i) suppression of specific transcription factor functions can potentially serve as a marker of exposure to oxidative stress and its effects on human lymphocytes; (ii) lipid peroxidation is only detectable in human lymphocytes upon exposure to weak oxidative stress which does not induce catalase activity; (iii) therefore, transcription factor DNA-binding activities are more sensitive to oxidative stress than lipid peroxidation
— id: 7564, year: 1998, vol: 112, page: 242, stat: Journal Article,

Interaction of nickel with UV-light in the induction of cytogenetic effects in human peripheral lymphocytes
Katsifis SP; Shamy M; Kinney LP; Burns FJ
1998 Dec 3;422(2):331-337, Mutation research
Chemical interaction is of major concern in the assessment of risk by regulatory agencies. In the present study, treatment of human lymphocytes with NiSO4 (1-100 microM) or UV-light (200, 1000 ergs/mm2) induced micronuclei (MN) in a dose-dependent fashion. Statistical analysis of the interaction factor (IF), showed that combined treatments of Ni(II) (1-100 microM) with UV-light (200, or 1000 ergs/mm2) interacted antagonistically for the induction of MN. Recently we reported that Ni(II) (0.5-10 microM) with UV-light (200 or 1000 ergs/mm2) or Cr(VI) or X-rays interacted antagonistically for the induction of sister chromatid exchanges (SCE), in peripheral human lymphocytes. These observations suggest that nickel present in complex mixtures may reduce the response, even in the presence of strong MN or SCE inducers, and may lead, therefore, to an underestimate of chemical exposure as assessed by these assays. Furthermore, metals affecting certain microsteps in the process of DNA replication or repair (e.g., histones, polymerases, ligases) may have similar antagonistic effects. Further studies are therefore recommended.
— id: 7365, year: 1998, vol: 422, page: 331, stat: Journal Article,

Solar ultraviolet radiation and skin damage: an epidemiological study among a Chinese population
Zhao, P; Zhu, X; Liu, Y; Wang, B; Wang, C; Burns, F J
1998 Nov-Dec;53(6):405-409, Archives of environmental health
To explore skin damage resulting from solar ultraviolet radiation on Mongoloid people, we investigated 470 healthy people in northeast China. We assessed their skin texture and elastic fibers, number of Langerhans cells, and the incidence of p53 gene mutations. The results showed that solar ultraviolet radiation played a significant role in aging of skin in Chinese people; aging began at 30 y of age (i.e., 20 y later than in Caucasians). In the high-exposure group, aging of skin was twice as severe and occurred 10 y earlier than in the low-exposure group. The counts of Langerhans cells had a tendency to decrease in the high-exposure group. Neither p53 mutations nor solar keratosis were found in individuals of any age-findings that indicated a qualitative different pattern than that of Caucasians
— id: 113686, year: 1998, vol: 53, page: 405, stat: Journal Article,

Effect of antioxidants on UV-induced DNA breakage in human peripheral lymphocytes
E, X F; Liu, Y; Burns, F J; Wang, B X
1997 Dec;59(6):888-893, Bulletin of environmental contamination & toxicology
— id: 113687, year: 1997, vol: 59, page: 888, stat: Journal Article,

Rare activation of ras oncogenes in radiation induced rat skin tumors
Felber, M; Burns, F; Garte, S
1997 JAN-FEB ;4(1):131-133, Oncology reports
We examined a large panel of radiation induced rat skin tumors for activation of the H- or K-ras oncogenes. Using oligonucleotide hybridization analysis of tumor DNA we found that only 1 out of 96 tumors tested had an activated K-ras gene, and none of the 78 tumors examined for H-ras mutations were positive. Tumors were induced by high and low LET, and included lesions of various sizes and histologic type. DNA sequencing of tumors and NIH3T3 transfectants from a previous study gave results consistent with a rare occurence of ras activation in this system
— id: 53366, year: 1997, vol: 4, page: 131, stat: Journal Article,

Histamine release from rat peritoneal mast cells and human basophils induced by the free radical generator 2,2'-azobis (2-amidinopropane) dihydrochloride (AAPH)
Burrows, M S; Burns, F J; Ennis, M
1996 Mar;45 Suppl 1:S9-10, Inflammation research
— id: 113688, year: 1996, vol: 45 Suppl 1, page: S9, stat: Journal Article,

Interaction of nickel with mutagens in the induction of sister chromatid exchanges in human lymphocytes
Katsifis SP; Kinney PL; Hosselet S; Burns FJ; Christie NT
1996 Jan 16;359(1):7-15, Mutation research
In this study, individual treatments of human lymphocytes with Ni(II) [0.5-25 microM], Cr(VI) [0.65-1.30 microM], UV-light or X-rays induced SCEs in a dose-dependent fashion, and combined treatments of Ni(II) with Cr(VI), UV-light or X-rays interacted antagonistically. Nickel, at environmentally relevant exposure levels, can have the effect in complex mixtures of reducing an otherwise positive SCE response and could lead to underestimating human exposures to certain classes of chemicals or radiation. Furthermore, our data indicate that antagonism may occur when human lymphocytes are exposed simultaneously to Ni(II) and Cr(VI), suggesting an explanation for epidemiological studies reporting conflicting results for cytogenetic effects in lymphocytes of workers exposed to chromium and nickel
— id: 6920, year: 1996, vol: 359, page: 7, stat: Journal Article,

DNA fingerprinting analysis of radiation-induced rat skin tumors
Felber M; Burns FJ; Garte SJ
1994 Oct;14(3):163-170, Cancer biochemistry biophysics
DNA fingerprinting analysis was performed on rat skin tumors induced by high linear energy transfer neon ion radiation. Most of these tumors (13/15) showed DNA-fingerprint variability between independently isolated tumors from the same animal. These changes include multiple band shifts and extra bands. Comparisons of DNA fingerprints were also made on successive biopsy samples from the same tumor. Each of 3 neon-induced tumors and 2 of 8 electron (low LET) induced tumors showed progressive loss of amplified sequences, gain of amplified sequences, deletions, band shifts, and the appearance of extra bands in progressive biopsies. These results provide evidence for LET-specific effects on genomic instability in radiation-induced rat skin tumors
— id: 6615, year: 1994, vol: 14, page: 163, stat: Journal Article,

The low carcinogenicity of electron radiation relative to argon ions in rat skin
Burns FJ; Jin Y; Koenig KL; Hosselet S
1993 Aug;135(2):178-188, Radiation research
The carcinogenicity of electron radiation relative to argon ions in rat skin was examined, specifically investigating whether the linear-quadratic model is useful for predicting cancer yield for one type of radiation based on yields observed for a different type. Three experiments were conducted to obtain information on the relationship between cancer yield and the dose of electron radiation: (1) a conventional dose-response protocol where the number of rats per group was based on the expected tumor yield; (2) a multiple-fraction protocol designed to take advantage of yield additivity as a way to estimate carcinogenicity at lower doses; and (3) a protocol to examine the effect of age at the time of irradiation on the dose-response relationship for cancer induction. Published data on the induction of skin cancer in rats irradiated with electrons were reanalyzed and combined with results of the new experiments. Skin cancer yield versus dose for argon ions was consistent with the linear-quadratic model, but the cancer yield for electrons was considerably lower (by a factor of 6.7 at 10 Gy) than the prediction based on the linear-quadratic model. The cancer yield for electron radiation was better fitted by a dose-cubed power function than a linear-quadratic function. The results indicate a substantially lower carcinogenic effectiveness for electron radiation, especially at lower doses, in comparison to argon ions and suggest that electrons may cause cancer by a three-event pathway instead of the two-event pathway that is consistent with the results for argon ions
— id: 8237, year: 1993, vol: 135, page: 178, stat: Journal Article,

Amplification of the c-myc oncogene in radiation-induced rat skin tumors as a function of linear energy transfer and dose
Felber M; Burns FJ; Garte SJ
1992 Sep;131(3):297-301, Radiation research
The c-myc oncogene was previously shown to be amplified in large, later-stage carcinomas of the rat skin induced by 0.8-MeV electrons. In a panel of 70 tumors induced by neon ions (45 keV/microns), c-myc amplification was rare, and in contrast to the data for tumors induced by low-linear-energy transfer (LET) (0.3 keV/microns) radiation, showed no correlation with tumor size, growth period, or time, but was associated with radiation dose. The tissue specificity for c-myc amplification seen in tumors induced by electrons was not seen in tumors induced by neon ions. These results suggest that quite distinct molecular mechanisms operate even in late stages of carcinogenesis that depend on the LET of the inducing radiation. Furthermore, the results suggest that c-myc amplification observed in tumors induced by low-LET radiation is not a general property of rat skin carcinomas, but is linked mechanistically to the inducing radiation, even though it is not detectable until many months after exposure and tumor appearance
— id: 13455, year: 1992, vol: 131, page: 297, stat: Journal Article,

Oncogene amplification detected by in situ hybridization in radiation-induced skin cancers in rats
Jin Y; Burns FJ; Garte SJ
1992 Nov;132(2):193-199, Radiation research
Amplification of the c-myc oncogene has been detected by Southern blotting in the DNA of radiation-induced skin cancers in the rat. In the current work the localization of oncogene amplification within specific cells in the different cancers and in multiple biopsies of the same cancer was studied by in situ hybridization. The amount of amplification was measured by counting grains on tissue sections hybridized in situ to biotin-labeled human c-myc third exon, rat v-H-ras, and rat v-Ki-ras probes. The in situ estimates of c-myc amplification were generally correlated with previous findings using the Southern blot method, but within each cancer only a fraction of cells exhibited amplification. Multiple biopsies of a squamous carcinoma showed amplification of v-H-ras and c-myc but not v-Ki-ras during tumor growth, but none of these oncogenes were amplified during tumor regression. The c-myc-positive cells were distributed uniformly within the cancers and exhibited a more uniform nuclear structure in comparison to the more vacuolated c-myc-negative cells. A high [3H]thymidine labeling index was found in irradiated epidermal cells on Day 7 after exposure, and yet no evidence of c-myc oncogene amplification was found in situ. No c-myc amplification was found in unirradiated normal epidermis or in irradiated epidermal cells in the vicinity of radiation-induced cancers. The data indicate that c-myc amplification is cell-specific within radiation-induced carcinomas and does not occur in epidermal cells proliferating in response to radiation exposure
— id: 8414, year: 1992, vol: 132, page: 193, stat: Journal Article,

Progression and multiple events in radiation carcinogenesis of rat skin
Burns FJ; Hosselet S; Jin Y; Dudas G; Garte SJ
1991 Dec;32 Suppl 2:202-216, Journal of radiation research
The multistage theory of carcinogenesis specifies that cells progress to cancer through a series of discrete, irreversible genetic alterations, but data on radiation-induced cancer incidence in rat skin suggests that an intermediate repairable alteration may occur. Data are presented on cancer induction in rat skin exposed to the following radiations: 1. an electron beam (LET = 0.34 kev/mu), 2. a neon ion beam (LET = 45 kev/mu) and 3. an argon ion beam (LET = 125 kev/mu). The latter 2 beams were generated by the Bevalac at the Lawrence Berkeley Laboratory, Berkeley, CA. About 6.0 cm2 of skin was irradiated per rat. The rats were observed every 6 weeks for at least 78 weeks and tumors were scored at first occurrence. Several histological types of cancer, including squamous and basal cell carcinomas, were induced. The total cancer yield was fitted by the quadratic equation, and the equation parameters were estimated by linear regression for each type of radiation. Analysis of the DNA from the electron-induced carcinomas indicated that K-ras and/or c-myc oncogenes were activated in all tumors tested. In situ hybridization indicated that the cancers contain subpopulations of cells with differing amounts of c-myc and H-ras amplification. The results are consistent with the idea that ionizing radiation produces stable, carcinogenetically relevant lesions via 2 repairable events at low LET and via a non-repairable, linked event pathway at high LET; either pathway may advance the cell by 1 stage in the multistage model
— id: 8236, year: 1991, vol: 32 Suppl 2, page: 202, stat: Journal Article,

Oncogenes and radiation carcinogenesis
Garte SJ; Burns FJ
1991 Jun;93:45-49, Environmental health perspectives
Current research indicates a role for several oncogenes in radiation-induced carcinogenesis in vivo and cell transformation in vitro. Certain oncogenes are probably also involved in some cases of human cancer caused by exposure to nonionizing radiation and may play a mechanistic role in the phenomenon of radioresistance seen in later stages of tumor progression. The mechanisms of oncogene activation seen in radiation-induced tumors include point mutations, gene amplification, and changes in gene expression. Genetic factors associated with target species, strain, and tissue type play an important role in determining the specific nature of oncogene activation by radiation exposure. Using the rat skin as a model for cancer induction by ionizing radiation, we found concurrent activation of K-ras and c-myc oncogenes in end-stage tumors. Amplification of the myc gene proved to occur during a late stage of tumor progression and is not an early initiating event resulting from the direct action of radiation on target cells. The importance of tissue specificity, tumor cell heterogeneity, and physical characteristics of the radiation exposure are discussed
— id: 14010, year: 1991, vol: 93, page: 45, stat: Journal Article,

Promotion and progression in carcinogenesis
Burns, F J
1990 ;340D:65-80, Progress in clinical & biological research
— id: 113690, year: 1990, vol: 340D, page: 65, stat: Journal Article,

Amplification of the c-myc oncogene during progression of radiation-induced rat skin tumors
Garte, S J; Burns, F J; Ashkenazi-Kimmel, T; Felber, M; Sawey, M J
1990 May 15;50(10):3073-3077, Cancer research
Evaluation of a large panel of radiation-induced rat skin tumors of diverse size and histological type revealed a correlation between c-myc copy number and tumor size. Both the frequency and degree of c-myc gene amplification were increased in large compared to small carcinomas, but none of the sarcomas examined showed c-myc amplification. Serial biopsies of individual tumors exhibited similar trends of increasing c-myc copy number in later biopsies. In one regressing tumor, the c-myc gene copy number paralleled the growth rate of the tumor during growth and regression. The average time required from tumor appearance to significant gene amplification was close to the average period between tumor appearance and the onset of rapid growth. The data suggest that, rather than being a target gene for the direct early effects of ionizing radiation, c-myc functions as a late-stage progression-related oncogene in this model system
— id: 113689, year: 1990, vol: 50, page: 3073, stat: Journal Article,

Cancer risk associated with therapeutic irradiation of skin [see comments]
Burns FJ
1989 Jul;125(7):979-981, Archives of dermatology
— id: 10565, year: 1989, vol: 125, page: 979, stat: Journal Article,

Mouse skin papillomas as a stage in cancer progression
Burns FJ
1989 ;298:81-93, Progress in clinical & biological research
— id: 10768, year: 1989, vol: 298, page: 81, stat: Journal Article,

Multiple stages in radiation carcinogenesis of rat skin
Burns FJ; Albert RE; Garte SJ
1989 May;81:67-72, Environmental health perspectives
Epithelial cell cancers are induced in rat skin by ionizing radiation in a manner that is consistent with the dual action (i.e., two alterations) hypothesis of radiation effects on DNA. This hypothesis states simply that two initial alterations, presumably in the DNA, are necessary to start a normal cell on the pathway to cancer. The initial radiation-induced alteration in the DNA is repairable as indicated by the reduction in tumor incidence with increasing time between dose fractions; the repair halftime is estimated to be 3.0 +/- 1.0 hr. Theoretical predictions of a specific dependence of tumor incidence on linear energy transfer (LET) have been verified experimentally for two specific LET values. However, the theoretical formulation provides no guidance regarding the observed reduction in the carcinogenic action of radiation with age at the time of exposure. Analysis of the tumor DNA for oncogene activation indicated k-ras and c-myc oncogenes were activated in highly anaplastic rat skin cancers, whereas only one of these oncogenes, usually c-myc, was activated in comparatively benign basal cell carcinomas and in squamous cell carcinomas
— id: 10648, year: 1989, vol: 81, page: 67, stat: Journal Article,

Radiation-induced cancer in rat skin
Burns FJ; Albert RE; Garte SJ
1989 ;11:293-319, Carcinogenesis: a comprehensive survey
— id: 10800, year: 1989, vol: 11, page: 293, stat: Journal Article,

An experimental model for oncogene activation during tumor progression in vivo
Garte SJ; Burns FJ; Ashkenazi-Kimmel T; Cosma GN; Sawey MJ
1989 Sep-Oct;9(5):1439-1446, Anticancer research
Tumor progression usually involves a complex pattern of molecular alterations. In many human tumors oncogene amplification or activation has been associated with advanced stages of cancer. Transfection studies have demonstrated the ability of several cellular oncogenes to induce a more malignant phenotype in transformed cells. We have examined the role of c-myc in tumor progression in rat tracheal cell culture, and in rat skin tumors induced by ionizing radiation. In the latter in vivo model, c-myc amplification was found to occur as a function of tumor size. Serial biopsies of growing tumors confirmed the trend toward increased gene copy number with time and stage of progression. This effect was specific for the c-myc gene, in epithelial tumors. Evidence was found for a role of tumor heterogeneity and evolution of tumor cell subpopulations in determining the oncogene activation profile of individual tumors
— id: 10505, year: 1989, vol: 9, page: 1439, stat: Journal Article,

Failure of the tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA) to inhibit cell-cell coupling in newborn mouse epidermal cells and Chinese hamster V79 cells under non-standard culture conditions
Miller, D R; Istone, L; Burkart, W; Young, W; Blight, A R; Burns, F J
1987 Jun;8(6):847-850, Carcinogenesis
The function of the skin tumor promoter 12-O-tetradecanoyl-phorbol-13-acetate (TPA) during two-stage carcinogenesis in mice remains obscure because of TPA's numerous phenotypic effects. In vitro studies under established conditions have generated substantial interest in TPA's ability to inhibit, although transiently in some cases, direct cell-cell coupling in several permanent cell lines, by analogy allowing latent 'initiated cells' to escape homeostatic controls in vivo. Using different culture conditions designed to improve the growth of newborn mouse epidermal cells, we examined dye coupling in these cells, and metabolic co-operation in V79 cells, finding no effect of TPA on coupling. It appears that this effect of TPA is overly sensitive to in vitro conditions. Since a corresponding physiological effect has not yet been demonstrated in vivo, future studies should be directed to establish that coupling inhibition by TPA actually does occur and plays some role during tumor promotion in vivo, and is not merely a characteristic of certain culture systems
— id: 113692, year: 1987, vol: 8, page: 847, stat: Journal Article,

Radioautographic measurement of electron-induced epidermal kinetic effects in different aged rats
Sargent, E V; Burns, F J
1987 Mar;88(3):320-323, Journal of investigative dermatology
We have previously shown that the ability of rat epidermal cells to repair electron-induced DNA damage decreases as a function of age. The present investigation was performed to examine the relationship between this finding and sensitivity of epidermal cells to the cytotoxic effects of the radiation. Male CD rats at ages 2, 28, 100, 200, 420, and 728 days were injected with [3H]-thymidine [( 3H]Thd) at a dose of 2 mu Ci/g body weight. One hour later, the rats were anesthetized and the dorsal skin irradiated with various doses of 0.8 meV electrons at a dose rate of 660 rads/min. At 24 h after irradiation, radioautographs were made of a sheet of epidermis that was separated by trypsinization from the underlying dermis. Labeled cells were scored either as singlets or doublets (adjacent labeled cells). The percent labeled cells and percent labeled cells as doublets were determined. The estimated labeling index (the proportion of cells labeled by a single exposure to [3H]Thd) of the epidermal basal layer decreased as a function of age. The slope of the semilog plot of the percent labeled cells as doublets as a function of electron dose indicates that the Do value decreases with increasing age. The results show, however, that the greatest difference in sensitivity occurs between 2-day (neonatal) and 28-day (pubescent) animals and again between 420-day (adult) and 728-day (senescent) animals
— id: 113693, year: 1987, vol: 88, page: 320, stat: Journal Article,

The early and late effect of ultraviolet light exposure on the induction and repair of electron-induced DNA damage in rat epidermis
Sargent, E V; Burns, F J
1987 Aug;39(3):233-243, Mechanisms of aging & development
Experiments were performed to determine the early and late effects of ultraviolet light (UVL) on induction and repair of DNA damage in rat epidermis by electron radiation. The dorsal skin of 28-day-old rats was irradiated with 8.0 X 10(5) or 13.6 X 10(5) ergs/mm2 UVL or weekly exposures of 0.4 X 10(5) ergs/mm2 UVL for 23 or 48 weeks. At 1, 48, 100, 200, or 400 days after single UVL doses or 28 days after last weekly UVL dose, the animals were irradiated with 1200 rads of electrons and the resultant alkaline labile DNA damage and repair quantitated by the S1 nuclease assay. The cytotoxic effect of UVL on basal epidermal cells was assessed by the labeled doublets technique. Single UV doses were capable of inhibiting repair of electron induced DNA damage for up to 5 h, but did not have any measurable late effect (greater than 20 days) on the rate or extent of DNA repair. The rate of DNA repair in epidermal cells from animals exposed to weekly doses of UVL was more rapid than in age-matched controls. The UV doses used on these experiments were shown to be cytotoxic to a large proportion of the basal epidermal cells. The results indicate that exposure of the rat skin to single cytotoxic or multiple exposures of UVL did not accelerate the age related loss of DNA repair capacity
— id: 113691, year: 1987, vol: 39, page: 233, stat: Journal Article,

Activation of c-myc and c-K-ras oncogenes in primary rat tumors induced by ionizing radiation
Sawey, M J; Hood, A T; Burns, F J; Garte, S J
1987 Feb;7(2):932-935, Molecular & cellular biology
An activated K-ras oncogene was detected by transfection in NIH 3T3 cells and by Southern blot analysis in 6 of 12 rat skin tumors induced by ionizing radiation. The DNA from 10 of the 12 tumors also showed c-myc gene amplification and restriction polymorphisms. Evidence for tissue specificity was observed in patterns of oncogene activation, with each of three clear cell carcinomas exhibiting activation of both c-myc and K-ras oncogenes
— id: 113694, year: 1987, vol: 7, page: 932, stat: Journal Article,

SPECIFIC ALTERATIONS IN RADIATION-INDUCED ACTIVATION OF THE C- MYC ONCOGENE
Sawey, MJ; Burns, FJ; Garte, SJ
1987 Mar;28(3):147-147, Proceedings (American Association for Cancer Research)
— id: 31219, year: 1987, vol: 28, page: 147, stat: Journal Article,

Radiation carcinogenesis and DNA alterations
Burns, F. J.; Upton, Arthur C.; Silini, G
New York : Plenum Press, c1986,
— id: 375, year: 1986, vol: , page: , stat: ,

Radiation induction of cancer of the skin
Fry, R J; Storer, J B; Burns, F J
1986 ;19:58-60, British journal of radiology. Supplement
— id: 113695, year: 1986, vol: 19, page: 58, stat: Journal Article,

Radiation carcinogenesis
Upton, Arthur C.; Albert, Roy E.; Burns, Fredric J.; Shore, Roy E
New York : Elsevier, c1986,
— id: 417, year: 1986, vol: , page: , stat: ,

Expression of long terminal repeat (LTR) sequences in carcinogen-induced murine skin carcinomas
Housey, G M; Kirschmeier, P; Garte, S J; Burns, F; Troll, W; Weinstein, I B
1985 Feb 28;127(1):391-398, Biochemical & biophysical research communications
RNA sequences homologous to the Long Terminal Repeat (LTR) sequence of Moloney Murine Leukemia Virus proviral DNA are expressed in murine squamous cell carcinomas of the skin induced by chemical carcinogens. These transcripts range in size from 8.2 to less than 2.4 kb but their size profile varies between individual tumors. These RNAs are not detected in the poly A+ RNA fraction obtained from the epidermis of control mice or carcinogen induced skin papillomas. The poly A+ RNAs from the livers and spleens of some of the mice with skin carcinomas also revealed LTR related sequences, whereas these RNAs were not detected in the livers and spleens of control mice or of carcinogen-treated mice that did not develop carcinomas. Thus, chemical carcinogenesis in mouse skin is associated with constitutive expression of endogenous retrovirus related sequences in the carcinomas as well as in certain apparently normal host tissues
— id: 108447, year: 1985, vol: 127, page: 391, stat: Journal Article,

Repair of radiation-induced DNA damage in rat epidermis as a function of age
Sargent, E V; Burns, F J
1985 May;102(2):176-181, Radiation research
The rate of repair of radiation-induced DNA damage in proliferating rat epidermal cells diminished progressively with increasing age of the animal. The dorsal skin was irradiated with 1200 rad of 0.8 MeV electrons at various ages, and the amount of DNA damage was determined as a function of time after irradiation by the method of alkaline unwinding followed by S1 nuclease digestion. The amount of DNA damage immediately after irradiation was not age dependent, while the rate of damage removal from the DNA decreased with increasing age. By fitting an exponential function to the relative amount of undamaged DNA as a function of time after irradiation, DNA repair halftimes of 20, 27, 69 and 107 min were obtained for 28, 100-, 200-, and 400-day-old animals, respectively
— id: 113696, year: 1985, vol: 102, page: 176, stat: Journal Article,

TRANSFORMING ACTIVITY OF DNA FROM RADIATION-INDUCED RAT SKIN TUMORS
Sawey, MJ; Garte, SJ; Hood, AT; Burns, FJ
1985 ;26(MAR):69-69, Proceedings (American Association for Cancer Research)
— id: 30889, year: 1985, vol: 26, page: 69, stat: Journal Article,

Approach to risk assessment for genotoxic carcinogens based on data from the mouse skin initiation-promotion model
Burns, F; Albert, R; Altshuler, B; Morris, E
1983 Apr;50:309-320, Environmental health perspectives
Tumor induction data in the mouse skin initiation-promotion system were found to be consistent with a quadratic function where the coefficient of the linear term depended on the dose of the promoter. The model implies that the existence of promoters may be more important at low doses of the carcinogen than at high doses where most testing is performed. Experiments are described showing that the initiating effect of carcinogenic chemicals, such as benzo(a)pyrene, 7,12-dimethyl-benz(a)anthracene, nitroquinoline oxide and beta-propiolactone, accumulates in a linear, irreversible manner at low doses. Even when 7,12-dimethylbenz(a)anthracene was applied intragastrically to pregnant females, initiating activity was found in the skins of exposed offspring about in proportion to dose applied and number of cells at risk. The initiated cells essentially represent a potential for cancer that has a high probability for expression in the presence of a promoter. Risk then can be interpreted in terms of the accumulated dose of initiator which alone presents a small risk of cancer. However, a promoter may substantially expand the overall risk, possibly by clonally expanding the initiated cells. Promotion needs to be sustained since there is a reduction of cancer risk if promotion is ended early. Some tissues, such as mouse bladder, may be intrinsically promoted more than others so that comparisons between tissues and between species are best made when the combination of intrinsic promotion and response to extrinsic promotion are comparable
— id: 123141, year: 1983, vol: 50, page: 309, stat: Journal Article,

Transplacental skin tumor initiation of Ha/ICR mice at different fetal ages
Morris, E P; Burns, F J; Albert, R E
1983 Sep;43(9):4271-4274, Cancer research
The initiation of cells in fetal skin was studied by exposing pregnant Ha/ICR mice intragastrically to single doses of a carcinogen at different times during gestation. For comparison, adult mice were exposed to the same carcinogen in a similar manner. The carcinogen, 7,12-dimethylbenz(a)anthracene (DMBA), was given at a dose of about 120 mg/kg in 0.2 ml sesame oil by gavage to 7-week-old pregnant females. The presence of initiated cells in the adult offspring was determined by topical application of 5.0 micrograms in 0.2 ml acetone of the skin tumor promoter tetradecanoyl-12-phorbol-13-acetate to the skin three times weekly beginning at 9 weeks of age. The yield of tumors was determined as a function of time during continuous promotion. Evidence of initiated cells was found in adults exposed transplacentally to DMBA as early as Day 9 of fetal development. The histological characteristics of the tumors and their temporal pattern of development were essentially the same for mice exposed at different stages of fetal development as they were for mice exposed to DMBA as adults. Male and female offspring exhibited approximately the same tumor yields. The use of [3H]DMBA and autoradiographs provided evidence that the cellular dose of DMBA was approximately equivalent at each stage of gestation and in adult skin. The results suggest that the number of initiated cells produced by a given dose of DMBA to the epidermis or fetal ectoderm is proportional to the number of cells in the tissue at the time of exposure
— id: 113697, year: 1983, vol: 43, page: 4271, stat: Journal Article,

Relationship of benign papillomas to cancer induction in mouse skin
Burns, F J; Albert, R E
1981 ;4(1-4):99-107, Cancer detection & prevention
An analysis is presented for evaluating the potency of initiators, promoters, and carcinogens based on the number of tumors that occur as a function of dose and time when compounds are applied topically in an appropriate solvent to mouse skin. A given compound was tested as an initiator (a single dose followed by prolonged promotion), as a whole carcinogen (multiple applications for a prolonged period of time), and as a cocarcinogen (multiple applications for a prolonged period of time in combination with promotion). Compounds tested were 7,12 dimethylbenz(a)anthracene (DMBA), benzo(a)pyrene (B(a)P), 4-nitroquinoline-1-oxide (4-NQO), and betapropriolactone (BPL). The results indicated that various types of papillomas were produced in proportion to the dose applied to DMBA, B(a)P, and BPL. Certain of these papillomas were nonregressible and progressed readily to carcinomas; others regressed and did not progress to cancer. Multiple doses of DMBA and B(a)P produced carcinomas without an antecedent papilloma stage. The latter cancers were produced in proportion to the 2nd or 3rd power of applied carcinogen dose and were accelerated strongly by concomitant action of a promoter. Certain nonregressible papillomas probably represent the first step in a two or three step progression to cancer, although cancers from papillomas occur in proportion to dose
— id: 113700, year: 1981, vol: 4, page: 99, stat: Journal Article,

The induction and repair of DNA breaks in rat epidermis irradiated with electrons
Burns, F J; Sargent, E V
1981 Jul;87(1):137-144, Radiation research
— id: 113698, year: 1981, vol: 87, page: 137, stat: Journal Article,

Inhibition of benz[a]pyrene-induced mammary carcinogenesis by retinyl acetate
McCormick, D L; Burns, F J; Albert, R E
1981 Mar;66(3):559-564, Journal of the National Cancer Institute
The administration of a 250-ppm retinyl acetate dietary supplement for various periods relative to intragastric administration of 50 mg benzo[a]pyrene (BP) significantly inhibited the induction of mammary cancers in virgin female inbred LEW/Mai rats. with day of BP administration taken as time 0, groups receiving the retinoid from weeks -2 to +1, +1 to +90, +20 to +90, and -2 to +90 showed a significant reduction in tumor response as compared to controls. The inhibition of carcinogenesis achieved by a +1 to +20 administration schedule was temporary; the tumor yield was suppressed initially but returned to control levels by week 60. Autoradiographic analysis of mammary glands from 50-day-old rats indicated that a 2-week exposure to supplemental retinyl acetate significantly reduced the mammary gland parenchymal cell labeling index in ductal, alveolar, and terminal end bud structures. Beginning the retinyl acetate supplement 1 week after the administration of BP significantly reduced the number of terminal ductal hyperplasias. The inhibition of carcinogenesis achieved by a short period of retinyl acetate administration before and during the period of carcinogen availability as well as the inhibition achieved by long-term postcarcinogen retinoid exposure may involve an antiproliferative effect on the rat mammary gland
— id: 113699, year: 1981, vol: 66, page: 559, stat: Journal Article,

Dose-dependent size increases of aortic lesions following chronic exposure to 7,12-dimethylbenz(a)anthracene
Penn, A; Batastini, G; Soloman, J; Burns, F; Albert, R
1981 Feb;41(2):588-592, Cancer research
The prevalence, size, and patterns of distribution of arterial lesions (plaques) were investigated in cockerels exposed chronically to 7,12-dimethylbenz(a)anthracene (DMBA). Animals, from 5 to 20 weeks of age, received weekly i.m. injections of 5, 10, or 20 mg of DMBA per kg, dissolved in dimethyl sulfoxide. Control animals received weekly injections of dimethyl sulfoxide. All animals were sacrificed at 21 weeks of age. The entire aorta from each animal was cut transversely into 5-mm segments starting at the iliac trifurcation. The cross-sectional area of plaques was determined by light microscopic analysis of sections taken from the face of each segment. Plaque frequency was similar in DMBA-treated and control groups. However, mean plaque cross-sectional area was 7- to 11-fold higher for the treatment groups than for the controls. The distribution of plaque areas in both treated animals and controls was consistent with a log normal distribution. Median cross-sectional area and plaque volume index each increased in a linear fashion with DMBA dose. Small plaques were present in all groups. Large plaques were present only in DMBA-treated animals. Labeling indices of plaques, although low, were 2.3- to 26-fold higher than for underlying medial smooth muscle cells. The data indicate that the primary response to chronic DMBA exposure is a dose-dependent size increase of spontaneous aortic lesions and not the induction of new lesions
— id: 123140, year: 1981, vol: 41, page: 588, stat: Journal Article,

LINEAR DOSE-RESPONSE RELATIONSHIPS FOR CO-CARCINOGENESIS IN THE MOUSE SKIN
Albert, RE; Burns, F; Altshuler, B
1980 ;21(MAR):106-106, Proceedings (American Association for Cancer Research)
— id: 27993, year: 1980, vol: 21, page: 106, stat: Journal Article,

Synchronous and metachronous malignancies of the colon and rectum
Burns, F J
1980 Nov-Dec;23(8):578-579, Diseases of the colon & rectum
In a brief survey of the literature on colorectal malignancy, the incidence of multiple primary (synchronous and metachronous) malignancies is reviewed. A changing pattern of incidence is noted, with decrease in incidence of rectal malignancies and increasing incidence of colonic malignancies, especially in the right colon. The author recommends stool screening for blood and more roentgenographic and endoscopic studies of the colon for earlier diagnosis of colonic malignancies
— id: 113701, year: 1980, vol: 23, page: 578, stat: Journal Article,

THE DOSE-RESPONSE FOR RAT SKIN TUMOR-INDUCTION ESTIMATED FROM MULTIPLE DOSES
Burns, FJ; Sargent, EV; Albert, RE
1980 ;83(2):435-435, Radiation research
— id: 27978, year: 1980, vol: 83, page: 435, stat: Journal Article,

Inhibition of rat mammary carcinogenesis by short dietary exposure to retinyl acetate
McCormick, D L; Burns, F J; Albert, R E
1980 Apr;40(4):1140-1143, Cancer research
— id: 113702, year: 1980, vol: 40, page: 1140, stat: Journal Article,

INDUCTION OF DNA STRAND BREAKS BY ELECTRON-RADIATION IN RAT EPIDERMIS TREATED WITH THE SENSITIZER 5-BROMO-2'-DEOXYURIDINE
Sargent, EV; Burns, FJ
1980 ;83(2):427-427, Radiation research
— id: 27977, year: 1980, vol: 83, page: 427, stat: Journal Article,

ATHEROGENICITY OF THE CARCINOGEN 7,12 DIMETHYLBENZ(A)ANTHRACENE (DMBA) - DOSE-RESPONSE STUDY
Penn, A; Batastini, GG; Burns, FJ; Albert, RE
1979 ;20(MAR):187-187, Proceedings (American Association for Cancer Research)
— id: 30100, year: 1979, vol: 20, page: 187, stat: Journal Article,

Dose response for benzo(a)pyrene adducts in mouse epidermal DNA
Pereira, M A; Burns, F J; Albert, R E
1979 Jul;39(7 Pt 1):2556-2559, Cancer research
The dose dependency of the binding of benzo(a)pyrene (BaP) with DNA of mouse epidermis was investigated. BaP-conjugated epidermal DNA was isolated and enzymatically degraded to deoxyribonucleosides. The BaP-DNA adducts were separated by Sephadex LH-20 column or high-performance liquid chromatography. Two major BaP-DNA adducts were found. One was in the region of the elution profile that contained polycyclic aromatic hydrocarbons adducted to deoxyribonucleosides. The other adduct was eluted from Sephadex LH-20 and high-performance liquid chromatography columns before the deoxyribonucleosides and after deoxyribonucleotides. Both adducts of BaP in epidermal DNA reached a maximum 7 hr after a single skin application, and subsequently little, if any, loss of adducts was observed for 49 hr. Both adducts varied as a linear function for topical doses in the range from 0.01 to 300 microgram/mouse. The formation of DNA adducts by BaP occurred in proportion to dose at doses several orders of magnitude below those that are feasible to test for carcinogenicity
— id: 113704, year: 1979, vol: 39, page: 2556, stat: Journal Article,

Induction of skin tumors in the rat by single exposure to ultraviolet radiation
Strickland, P T; Burns, F J; Albert, R E
1979 Dec;30(6):683-688, Photochemistry & photobiology
— id: 113703, year: 1979, vol: 30, page: 683, stat: Journal Article,

Rat skin tumor incidence following single and fractionated exposures to proton radiation
Burns, F J; Strickland, P; Vanderlaan, M; Albert, R E
1978 Apr;74(1):152-158, Radiation research
— id: 113705, year: 1978, vol: 74, page: 152, stat: Journal Article,

QUANTITATIVE CARCINOGENESIS IN RAT SKIN WITH 7,12- DIMETHYLBENZ(A)ANTHRACENE (DMBA) AND IONIZING-RADIATION
Burns, FJ; Strickland, PT; Albert RE
1978 ;19(MAR):237-237, Proceedings (American Association for Cancer Research)
— id: 129587, year: 1978, vol: 19, page: 237, stat: Journal Article,

SKIN CANCER IN RATS AFTER SINGLE AND FRACTIONATED DOSES OF HIGH-ENERGY AR-40 IONS
Burns, FJ; Strickland, PT; Albert RE
1978 ;74(3):550-550, Radiation research
— id: 129588, year: 1978, vol: 74, page: 550, stat: Journal Article,

BENZO(A)PYRENE AND 7,12 DIMETHYLBENZ(A)ANTHRACENE ADDUCTS IN MOUSE EPIDERMAL DNA
Pereira, M; Burns, FJ; Albert, RE
1978 ;19(MAR):207-207, Proceedings (American Association for Cancer Research)
— id: 29795, year: 1978, vol: 19, page: 207, stat: Journal Article,

INDUCTION OF SKIN TUMORS IN RAT BY SINGLE EXPOSURE TO ULTRAVIOLET-RADIATION
STRICKLAND PT; BURNS FJ; ALBERT RE
1978 ;74(3):552-552, Radiation research
— id: 49951, year: 1978, vol: 74, page: 552, stat: Journal Article,

Effect of carcinogens on chicken atherosclerosis
Albert, R E; Vanderlaan, M; Burns, F J; Nishizumi, M
1977 Jul;37(7 Pt 1):2232-2235, Cancer research
Weekly i.m. injections of the polycyclic hydrocarbon carcinogens, 7,12-dimethylbenz(a,h)anthracene (DMBA; 25 mg/kg/injection) and benzo(a)pyrene (50 mg/kg/injection) were given for a period of up to 22 weeks to chickens (SC strain) beginning at age 4 weeks. Atherosclerotic lesions of the abdominal aorta occurred more frequently and were larger in the DMBA- and benzo(a)pyrene-treated birds than in controls. These lesions were proliferative in character as indicated by a higher [3H]thymidine autoradiographic labeling index compared to the underlying medial cells of the aorta. Measurements of serum cholesterol in DMBA-treated birds showed no differences from controls. Although both carcinogens accelerated the development of atherosclerotic plaques, DMBA was more potent than benzo(a)pyrene
— id: 113708, year: 1977, vol: 37, page: 2232, stat: Journal Article,

Split-dose recovery for radiation-induced tumours in rat skin
Burns, F J; Vanderlaan, M
1977 Aug;32(2):135-144, International journal of radiation biology & related studies in physics, chemistry, & medicine
Tumour-related recovery in rat skin was estimated from the dependence of tumour yield on time between split doses of electron radiation. Tumour yield versus dose was established at nine dose points, and at three points the dose was split into two equal fractions spaced 0-25, 3-2 or 6-3 hours apart. After irradiation the rats were observed periodically for at least 64 weeks, and at death the tumours were examined histologically. The dependence of yield on dose for single doses was consistent with a quadratic function up to a peak yield at about 1600 rad. The effect of split doses on tumour yield depended on the position on the dose--response curve. At the lowest split dose, the yield declined with a half-time of about 1-8 hours. At the intermediate split dose, an initial increase was followed by a decline with a half-time of about 3-9 hours. At the highest split dose, the tumour yield increased with time between exposures. Fractionation-induced increases in tumour yield were explained as a sparing effect on cell lethality, whereas tumour-related recovery per se was indicated at the lower two doses
— id: 113706, year: 1977, vol: 32, page: 135, stat: Journal Article,

Hepatic cell loss and proliferation induced by N-2-fluorenylacetamide, diethylnitrosamine, and aflatoxin B1 in relation to hepatoma induction
Nishizumi, M; Albert, R E; Burns, F J; Bilger, L
1977 Aug;36(2):192-197, British journal of cancer
Three hepatic carcinogens (aflatoxin B1, diethylnitrosamine (DEN) and N-2-fluorenylacetamide (FAA)) were compared for carcinogenicity, early cell toxicity and parenchymal cell proliferation. The carcinogens were administered to rats for 15 weeks as follows: aflatoxin B1, 1 in 10(6) in pelleted food; DEN, 2 in 10(5) in drinking water; FAA, 3 in 10(4) in pelleted food. The loss of prelabelled DNA and the [H3] TdR pulse-labelling indices (LI) of parenchymal and nonparenchymal cells were determined at various times during the period of carcinogen availability. On a molar basis, aflatoxin B1 was 90 times as carcinogenic as FAA and 24 times as carcinogenic as DEN. However, for about equal magnitudes of hepatic cell proliferation and loss, aflatoxin B1 was the least potent carcinogen. For a given level of carcinogenicity, FAA was more potent than DEN in causing loss of hepatic DNA and in increasing the parenchymal cell labelling index. DEN and aflatoxin B1 produced about the same degree of DNA loss and parenchymal cell labelling, but the former was a more potent carcinogen. When carcinogenicity was compared for approximately equal levels of early hepatic cell destruction and proliferation, the 3 chemicals in the present study could be ranked in descending order of potency as DEN, FAA and aflatoxin B1
— id: 113707, year: 1977, vol: 36, page: 192, stat: Journal Article,

EARLY EFFECTS OF SINGLE AND FRACTIONATED DOSES OF HIGH-ENERGY AR-40 IONS ON SKIN OF RATS
STRICKLAND PT; BURNS FJ; ALBERT RE
1977 ;70(3):673-673, Radiation research
— id: 49851, year: 1977, vol: 70, page: 673, stat: Journal Article,

Tumor and injury responses of rat skin after sieve pattern x irradiation
Albert, R E; Burns, F J
1976 Jul;67(1):142-148, Radiation research
— id: 113710, year: 1976, vol: 67, page: 142, stat: Journal Article,

Tumor induction and hair follicle damage for different electron penetrations in rat skin
Burns, F J; Sinclair, I P; Albert, R E; Vanderlaan, M
1976 Sep;67(3):474-481, Radiation research
— id: 113709, year: 1976, vol: 67, page: 474, stat: Journal Article,

Regression kinetics of mouse skin papillomas
Burns, F J; Vanderlaan, M; Sivak, A; Albert, R E
1976 Apr;36(4):1422-1427, Cancer research
The persistence and proliferation rate of mouse skin papillomas were studied in HA/ICR mice initiated with 7,12-dimethylbenz(a)anthracene and promoted three times weekly with phorbol myristate acetate. When the promoter treatments were stopped, rapid (half-time, 24 days) and slow (half-time, greater than 140 days) components of papilloma regression were observed. When the promoter dose was increased, the major effect was an increase among the rapidly regressing papillomas. Increases in the epidermal pulse-labeling index and the number of dermal inflammatory cells produced by phorbol myristate acetate in normal skin were reversible when the phorbol myristate acetate was stopped, but high pulse-labeling index values in papillomas were not reversible. Antithymocyte serum had no effect on regression, although ethylphenylpropriolate, a nonpromoting irritant, slowed the regression sufficiently to increase the half-time from 24 to 57 days. The action of the promoter in overcoming the regression tendency of the papillomas may explain certain features of the role of nonspecific irritation and the importance of promotion frequency in determining tumor yield
— id: 113711, year: 1976, vol: 36, page: 1422, stat: Journal Article,

COMBINED EFFECT OF IONIZING-RADIATION AND ULTRAVIOLET-LIGHT ON TUMOR INDUCTION IN RAT SKIN
Burns, FJ; Strickland, P; Vanderlaan, M; Albert, RE
1976 ;67(3):629-629, Radiation research
— id: 28731, year: 1976, vol: 67, page: 629, stat: Journal Article,

Massive pseudoproteinuria caused by nafcillin
Line, D E; Adler, S; Fraley, D S; Burns, F J
1976 Mar 22;235(12):1259-1259, JAMA
— id: 113712, year: 1976, vol: 235, page: 1259, stat: Journal Article,

A model describing the effects of dose and dose rate on tumour induction by radiation in rat skin
Vanderlaan, M.; Burns, F.J.; Albert, R.E.
Biological and environmental effects of low-level radiation : proceedings of a symposium ... Vienna : International Atomic Energy Agency, 1976,
A model is proposed for analysing the effects of dose rate on tumour induction from dose-response and fractionation data. The model assumes that tumours can result from either one or two dose-dependent steps. Equations were derived which provide relationships between the number of cells in the irreversible state and dose and dose rate. The model predicts that for acute exposure the tumour yield I will have the form I=A/sub 1/D+A/sub 2/D/sup 2/ where A/sub 1/ is derived from the one-step mode and A/sub 2/ is derived from the two-step mode. The dose-rate implications of the model are summarized in terms of a dose rate factor which is defined as the ratio of the acute dose to the protracted dose needed to produce the same tumour yield
— id: 5017, year: 1976, vol: , page: 253, stat: Chapter,

AGE-DEPENDENCE OF ONCOGENICITY OF IONIZING-RADIATION IN RAT SKIN
Vanderlaan, M; Strickland, P; Albert, RE; Burns, FJ
1976 ;67(3):629-629, Radiation research
— id: 28732, year: 1976, vol: 67, page: 629, stat: Journal Article,

EFFECT OF CARCINOGENS ON ATHEROSCLEROSIS IN CHICKEN AORTA
Albert, RE; Nishizumi, M; Burns, F
1975 ;16(MAR):25-25, Proceedings (American Association for Cancer Research)
— id: 28547, year: 1975, vol: 16, page: 25, stat: Journal Article,

The effect of 24-hour fractionation interval on the induction of rat skin tumors by electron radiation
Burns, F J; Albert, R E; Sinclair, I P; Vanderlaan, M
1975 Jun;62(3):478-487, Radiation research
— id: 113713, year: 1975, vol: 62, page: 478, stat: Journal Article,

DOSE-RESPONSE CURVE FOR TUMOR INDUCTION WITH SINGLE AND SPLIT DOSES OF 10 MEV PROTONS
Burns, FJ; Albert, RE; Vanderlaan, M; Strickland, P
1975 ;62(3):598-599, Radiation research
— id: 28529, year: 1975, vol: 62, page: 598, stat: Journal Article,

REGRESSION OF MOUSE SKIN PAPILLOMAS DURING TREATMENT WITH ANTITHYMOCYTE-SERUM OR ETHYLPHENYLPROPRIOLATE
Burns, FJ; Vanderlaan, M; Albert, RE
1975 ;16(MAR):110-110, Proceedings (American Association for Cancer Research)
— id: 28553, year: 1975, vol: 16, page: 110, stat: Journal Article,

RECOVERY RATE FOR TUMOR INDUCTION IN RAT SKIN WITH SPLIT DOSES OF ELECTRONS
Vanderlaan, M; Burns, FJ; Albert, RE
1975 ;62(3):598-598, Radiation research
— id: 28528, year: 1975, vol: 62, page: 598, stat: Journal Article,

COMPARISON OF CONTINUOUS AND INTERMITTENT DIETARY 2-FAA FOR HEPATIC CARCINOGENICITY IN RATS
Albert, RE; Burns, FJ; Bilger, L
1974 ;15(MAR):137-137, Proceedings (American Association for Cancer Research)
— id: 28393, year: 1974, vol: 15, page: 137, stat: Journal Article,

EFFECT OF RADIATION PENETRATION AND GROWTH STAGE OF HAIR FOLLICLES ON SKIN TUMOR INDUCTION
Albert, RE; Burns, FJ; Vanderla[...], M
1974 ;59(1):17-18, Radiation research
— id: 28367, year: 1974, vol: 59, page: 17, stat: Journal Article,

PROLIFERATION OF EARLY TUMOR FOCI IN IRRADIATED RAT SKIN
Burns, FJ; Vanderla[...], M; Albert, RE
1974 ;59(1):18-18, Radiation research
— id: 28368, year: 1974, vol: 59, page: 18, stat: Journal Article,

REGRESSION KINETICS OF CHEMICALLY-INDUCED PAPILLOMAS IN MOUSE SKIN
Burns, FJ; Vanderla[...], M; Sivak, A
1974 ;15(MAR):89-89, Proceedings (American Association for Cancer Research)
— id: 28391, year: 1974, vol: 15, page: 89, stat: Journal Article,

COMPARISON OF HEPATIC CELL-KINETICS IN PRECANCEROUS STAGES INDUCED BY SOME HEPATOCARCINOGENS
Nishizum[...], M; Albert, RE; Burns, FJ
1974 ;15(MAR):96-96, Proceedings (American Association for Cancer Research)
— id: 28392, year: 1974, vol: 15, page: 96, stat: Journal Article,

The effect of fractionation on tumor induction and hair follicle damage in rat skin
Burns, F J; Albert, R E; Sinclair, I P; Bennett, P
1973 Feb;53(2):235-240, Radiation research
— id: 113714, year: 1973, vol: 53, page: 235, stat: Journal Article,

Radiation-induced hair-follicle damage and tumor formation in mouse and rat skin
Albert, R E; Burns, F J; Bennett, P
1972 Oct;49(4):1131-1137, Journal of the National Cancer Institute
— id: 113715, year: 1972, vol: 49, page: 1131, stat: Journal Article,

Cell loss and proliferation induced by N-2-fluorenylacetamide in the rat liver in relation to hepatoma induction
Albert, R E; Burns, F J; Bilger, L; Gardner, D; Troll, W
1972 Oct;32(10):2172-2177, Cancer research
— id: 108494, year: 1972, vol: 32, page: 2172, stat: Journal Article,

Tumor incidence in rat skin after proton irradiation in a sieve pattern
Burns, F J; Albert, R E; Bennett, P; Sinclair, I P
1972 Apr;50(1):181-190, Radiation research
— id: 113716, year: 1972, vol: 50, page: 181, stat: Journal Article,

The technique of hemorrhoidectomy
Burns, F J
1971 Feb;68(2):114-115, Missouri medicine
— id: 113717, year: 1971, vol: 68, page: 114, stat: Journal Article,

Complications of colostomy
Burns, F J
1970 Nov-Dec;13(6):448-450, Diseases of the colon & rectum
— id: 113718, year: 1970, vol: 13, page: 448, stat: Journal Article,

On the existence of a G 0 -phase in the cell cycle
Burns, F J; Tannock, I F
1970 Oct;3(4):321-334, Cell & tissue kinetics
— id: 113719, year: 1970, vol: 3, page: 321, stat: Journal Article,

Condylomata acuminata of the rectum with associated malignancy
Burns, F J; Van Goidsenhoven, G E
1970 ;63 Suppl:119-120, Proceedings of the Royal Society of Medicine
— id: 113720, year: 1970, vol: 63 Suppl, page: 119, stat: Journal Article,

The morphology and growth characteristics of radiation-induced epithelial skin tumors in the rat
Albert, R E; Phillips, M E; Bennett, P; Burns, F; Heimbach, R
1969 Mar;29(3):658-668, Cancer research
— id: 123136, year: 1969, vol: 29, page: 658, stat: Journal Article,

An evaluation by alpha-particle Bragg peak radiation of the critical depth in the rat skin for tumor induction
Heimbach, R D; Burns, F J; Albert, R E
1969 Aug;39(2):332-344, Radiation research
— id: 113721, year: 1969, vol: 39, page: 332, stat: Journal Article,

The RBE for skin tumors and hair follicle damage in the rat following irradiation with alpha particles and electrons
Burns, F J; Albert, R E; Heimbach, R D
1968 Nov;36(2):225-241, Radiation research
Rat skin was irradiated with cyclotron-accelerated alpha particles with doses ranging from 210 rads to 6850 rads and monoenergetic electrons with doses ranging from 810 rads to 12,300 rads. The beams were modified so that the depth-dose curves were approximately identical with penetrations of about 1.0 mm. Tumors were counted every 4 weeks for 80 weeks, and at death or sacrifice the hair follicle damage was assessed by using 'whole mounts' of separated epithelium. The RBE values determined from a comparison of the dose response curves were: acute skin injury, RBE = 3.0+/-1.0; hair follicle survival, RBE = 2.1 +/- 0.7; hair follicle damage, RBE = 2.6 = 0.4; tumor induction, RBE = 2.9+/- 0.5. Within the experimental error, these values were independent of the dose. For both types of radiation, the tumor incidence increased approximately as the square of time and at low doses approximately as the 4th power of dose. The histological characteristics of the tumors and the correlation between the incidence of tumors and damaged hair follicles were independent of the type of radiation. The results were consistent with the hypothesis that structural damage to the hair follicles is a factor in the tumor induction process
— id: 71868, year: 1968, vol: 36, page: 225, stat: Journal Article,

Skin damage and tumor formation from grid and sieve patterns of electron and beta radiation in the rat
Albert, R E; Burns, F J; Heimbach, R D
1967 Mar;30(3):525-540, Radiation research
— id: 113723, year: 1967, vol: 30, page: 525, stat: Journal Article,

The association between chronic radiation damage of the hair follicles and tumor formation in the rat
Albert, R E; Burns, F J; Heimbach, R D
1967 Mar;30(3):590-599, Radiation research
— id: 113722, year: 1967, vol: 30, page: 590, stat: Journal Article,

The effect of penetration depth of electron radiation on skin tumor formation in the rat
Albert, R E; Burns, F J; Heimbach, R D
1967 Mar;30(3):515-524, Radiation research
— id: 113724, year: 1967, vol: 30, page: 515, stat: Journal Article,