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Research Highlights

The vision of the NIEHS is to use environmental health sciences to understand human disease and improve human health.

2000-Present Research Highlights

  • illustration of DNADiscovered two new compounds derived from red tide that may treat mucus build-up associated with cystic fibrosis and similar lung diseases. Preliminary studies show these compounds improve the flow of mucus through the respiratory tract, allowing airways to clear more quickly and efficiently. These compounds offer new targets for the development of medications to help patients with cystic fibrosis and for individuals who may be affected during episodes of red tide algal blooms.1 (2005)
  • Demonstrated that benzene can significantly reduce white blood cell counts and platelet counts at or below the US occupational standard, particularly among susceptible subpopulations. Benzene exposed workers with genetic variants in two key metabolizing enzymes may be especially susceptible to benzene toxicity.2 (2005)
  • Demonstrated that nighttime exposure to artificial light can stimulate the growth of human breast tumors in mice by suppressing the levels of a key hormone called melatonin. Extended periods of nighttime darkness were shown to greatly slow the growth of these tumors. These results might explain why female night shift workers have a higher rate of breast cancer, and may offer an explanation for the rise in breast cancer incidence in industrialized countries.3 (2005)
  • Established a renowned fertility research program at NIEHS to understand the basic mechanisms underlying normal and abnormal development and reproduction. Among their recent findings, researchers demonstrate that fertility drugs did not improve ovulation rates in mice that were genetically engineered to lack estrogen receptor beta. The estrogen receptor beta was found to be important for moving the egg outside the ovary so it can be fertilized, providing the first definitive evidence of the role of this receptor in the ovary.4 (2005)
  • Researcher examining microarray display onscreenDemonstrated how researchers can get more consistent and reliable results when using a technology called microarrays or gene chips. Microarrays allow scientists to see how differences in gene expression are linked to specific diseases, and may allow for earlier detection of diseases like cancer. The researchers found that using a standardized process and commercially manufactured microarrays produced the best reproducible results.5 (2005)
  • Demonstrated that a gene known as paraoxonase 1 (PON1) may serve as an important disease indicator for pesticide exposure. The gene has been found to play a critical role in breaking down organophosphate insecticides. The high or low activity level of PON1 during pregnancy and early life development may either protect or leave individuals who are exposed to pesticides more vulnerable. (2004, 2006)6

    "Experience tells us that virtually all human diseases can be caused, modified, or altered by environmental agents...  The NIEHS is in a unique position to focus on the interplay between environmental exposures, vulnerable populations, human biology, genetics, and the common diseases that limit our longevity and quality of life."

  • Discovered that a gene which plays an important role in immune function, known as toll-like receptor 4 (TLR4), may also play a critical role in suppressing chronic lung inflammation and tumor development in mice.7 (2005)
  • Demonstrated that lifetime lead exposure may increase the risk of developing cataracts, the leading cause of blindness. Men with high levels of lead in the tibia, the larger of the two leg bones below the knee, had a 2.5-fold increased risk for cataracts.8 (2004)
  • Researchers identified a unique cooperative role for certain hormones and proteins in the body, specifically glucocorticoids and tumor necrosis factor alpha, in regulating adaptive immunity and inflammation. Inflammation has been implicated as a contributing factor in several human cancers, including lung cancer. These results have important implications for immune responses to agents such as bacterial lipopolysaccharides, as well as to numerous other environmental agents. A better understanding of the body's immune system will provide us with new ways to fight off many diseases.9 (2004)
  • Discovered how a heavy metal environmental toxicant, cadmium can inactivate an important cellular repair system. Cadmium was found to cause mutations in DNA by inhibiting DNA mismatch repair. This mismatch repair system is important for keeping mutations from occurring during DNA synthesis.10 (2003)
  • Identified an enzymatic protein complex that repairs double stranded DNA breaks that are caused by long inverted DNA repeats. This study addresses important issues of environmental impact on the genome and the role of genome organization in genome stability. Studies on how chromosomes break and rearrange may lead to breakthroughs on ways to prevent or treat many inherited diseases.11 (2002)
  • Identified a brain protein known as transthyretin that may block the progression of Alzheimer's disease by inhibiting the effects of another protein, beta-amyloid peptide.12 (2004) It was NIEHS scientists who discovered that beta-amyloid peptide, found in patients with Alzheimer's disease, can disrupt brain signals that may contribute to the memory loss associated with the disease.13 (2001)
  • Identified a key molecule called the aryl hydrocarbon receptor (AhR), enabling scientists to develop a better understanding of how dioxin affects human cells. From this finding, researchers discover the superfamily of receptors (PAS) that mediate response to various forms of environmental stress, including circadian rhythm and controlling basic physiologic processes, such as vascular development and learning.14 (2000-1997)
  • Discovered that years of exposure to high concentrations of tiny particles of soot and dust from cars, power plants and factories can increase a person's risk of dying from lung cancer and heart disease to a level that is comparable to the risk associated with prolonged exposure to second-hand tobacco smoke.15 (2002)
  • Demonstrated that children playing an abundance of outdoor sports in areas where ozone levels are high may be three times more likely to develop asthma than children who do not take part in outdoor sporting activities.16 (2002)
  • Produced two lines of genetically altered mice that will have a significant impact on the study of cancer development. Research with these mice has shown that removal of two genes, COX-1 and COX-2, leads to a significant decrease in development of colon, skin and intestinal cancers in laboratory animals.17 (2002)
  • Analyzed more than 450 thousand birth records and discovered that men and women with birth defects have a higher risk of passing that defect on to their children. While children of mothers are not at increased risk for defects other than the one carried by the mother, children of fathers with birth defects have a significantly higher risk of birth defects of any kind.18 (2001)
  • Examined data from five large studies of women in the northeastern United States and revealed no link between exposure to the pesticide DDT and the widespread industrial chemical PCB, and elevated rates of breast cancer.19 (2001)
  • Identified the mechanism by which aflatoxin, a toxin produced by fungus found on corn, peanuts and other crops in Africa and Asia, causes hepatocellular carcinoma or liver cancer.20 (2000)
  • Researchers from NIEHS and the U.S. Department of Housing and Urban Development find that indoor dust samples collected from randomly-selected U.S. bedrooms contain unexpectedly high levels of dust mite and cockroach allergens that could pose a significant risk for the development of allergic diseases and asthma.21 (2000)

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The National Toxicology Program

The National Toxicology Program is an interagency program that conducts toxicological and human health hazard evaluations of substances in our environment and develops improved toxicological testing methods. The NTP is headquartered at NIEHS, and the NIEHS Director serves as its Director.

The Report on Carcinogens (The RoC)

Information produced by the National Toxicology Program (NTP) is used widely by government agencies, medical and scientific communities and the public. Probably one of the NTP's most visible products is the Report on Carcinogens (RoC), which the NTP prepares on behalf of the Secretary of the Department of Health and Human Services. Over 1,000,000 people visited the NTP Web site during the first two days of the release of the 11th RoC on January 31, 2005.

The RoC is an informational scientific and public health document that identifies and discusses agents that may pose a hazard to human health by virtue of their carcinogenicity. It lists these agents in two categories -- "known to be human carcinogens" and "reasonably anticipated to be human carcinogens." Some examples of substances identified by the RoC as "known" to be carcinogenic include benzene, asbestos, "dioxin" such as 2,3,7,8- Tetrachlorodibenzo-p-dioxin, and environmental tobacco smoke and tobacco smoking.

The ROC has evolved since the first edition was published in 1980 and included 26 listings. The 2005 edition includes 246 listings, with 58 of them "known to be human carcinogens."

The NTP is currently reviewing additional nominations for possible listing in or removal from the 12th RoC. The NTP has identified additional nominations that it may consider for review as either a new listing in or changing the current listing in the 12th RoC. For detailed information regarding these nominations visit the RoC web page and select "12th RoC".

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1990-1999 Research Highlights

  • Demonstrated that early smoking may alter a young person's DNA, possibly increasing the risk of lung cancer years later, even after the smoker quits.22 (1999)
  • Discovered that lead which has accumulated in a woman's bones from earlier exposures can be released during pregnancy and transferred to breast milk during lactation.23 (1998)
  • Identified a key protein called tristetraprolin which may help researchers find drugs to treat inflammatory diseases such as rheumatoid arthritis, Crohn's disease, and graft-versus-host disease. (1998)24 While development of these drugs will require years of additional research and testing, preliminary screening programs are already underway. (2006)
  • A study funded jointly by NIEHS and the European Commission's Climate Research Programme finds some developmental delays in 7-year-old Faroe Islands children of mothers whose diets of fish and whale exposed them to methylmercury during pregnancy.25 (1998) NIEHS-funded researchers, in collaboration with scientists from the Danish Medical Research Council, also noted similar cognitive deficits in these children when tested at 14 years of age.26 (2005)
  • Discovered that calorie-restricted diets can slow the development of bladder cancer in mice by reducing the level of a key hormone called insulin-like growth factor 1. This research established the role of caloric restriction in the prevention of certain cancers, and identified insulin-like growth factor 1 as a key risk factor in the development and progression of cancer.27 (1997)
  • Demonstrated that children who are exposed to relatively small amounts of polychlorinated biphenyls (PCBs) before birth have higher rates of low-normal IQ scores, poor reading comprehension, and memory problems.28 (1996)
  • Discovered that boys with relatively high levels of lead in their bones are more likely to engage in aggressive acts and delinquent behavior than boys with lower bone lead levels.29 (1996) Follow-up studies also associated high blood lead levels with antisocial acts. (2001)
  • In 1994, Dr. Martin Rodbell, an NIEHS scientist emeritus and former Scientific Director, was bestowed with the highest honor a scientist could receive, the Nobel Prize in Medicine. Pioneering studies by Dr. Rodbell and his colleagues at the NIH, laid the ground work for the discovery of "G-proteins" and their role in signal transduction, which regulates the human body's cellular "communication" activities. This discovery informed us about hormone function. It also played a role in demonstrating how light and odors are perceived, how signals travel between neurons in the brain, and how some diseases affect the function of our vital organs.
  • Identified and cloned a gene that suppresses the spread of prostate cancer in animals.30 (1995)
  • Recognized with one of the highest honors in science, when NIEHS' Dr. Martin Rodbell was named a co-recipient of the Nobel Prize in medicine for discoveries about the communication system that regulates cellular activity.31 (1994)
  • Isolated a tumor-suppressor gene, BRCA1, which is known to play a critical role in the development of hereditary breast and ovarian cancer.32 (1994)
  • Discovered a strong association between exposure to fine particles, sulfur dioxide, and acid aerosols, and an increase in respiratory symptoms, reduced lung capacity, and risk of early death.33 (1993)

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Key Pre-1990 Research Highlights

  • image of cellDemonstrated that exposure to very low levels of lead during early childhood can lead to significant delays in cognitive and behavioral development. (1979)
  • Developed an animal model that predicts and confirms that exposure to diethylstilbestrol (DES), a drug that was prescribed during pregnancy for women from 1938 to 1971 to prevent miscarriages and premature deliveries, can result in various reproductive abnormalities in both male and female offspring. (1975)
  • Linked asbestos exposure to an increased incidence of lung tumors and mesotheliomas, and found that asbestos-exposed workers who smoke cigarettes have a risk of lung cancer more than ten times as great as asbestos-exposed individuals who do not smoke. (1967)

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Future Directions

Although the National Institute of Environmental Health Sciences and the National Toxicology Program have done much to understand the role that environmental exposures can have on human health, the future promises to bring even more pioneering advances:

  • Researchers will develop new technologies to more accurately and efficiently detect, measure, and track toxicants in people and the environment.
  • Researchers will use the tools and accomplishments in the new field of environmental genomics to understand the interactions between environmental exposures and genes in the development and progression of human diseases.
  • NIEHS will translate new environmental health sciences knowledge into effective prevention, intervention and treatment strategies.
  • Scientists will use new basic science knowledge about how environmental agents affects targets at the molecular, cellular or tissue levels to inform us about how diseases develop and progress.
  • The NTP will continue to expand the scientific basis for making public health decisions on the potential toxicity of environmental agents.

Strategic Plan

In May 2006, the NIEHS unveiled a new strategic plan aimed at challenging and energizing the scientific community to use environmental health sciences to understand the causes of disease and to improve human health. The plan, "New Frontiers in Environmental Sciences and Human Health" emphasizes research focused on complex human disease, and calls for inter-disciplinary teams of scientists to investigate a broad spectrum of disease factors, including environmental agents, genetics, age, diet, and activity levels. Recent advances in technology make this emphasis on human health and new integrative approach possible.

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  1. Abraham WM, Bourdelais AJ, Sabater JR, Ahmed A, Lee TA, Serebriakov I, Baden DG. Airway responses to aerosolized brevetoxins in an animal model of asthma. Am J Respir Crit Care Med. 2005 Jan 1;171(1):26-34. Abstract ( Exit NIEHS Website

  2. Lan Q, Zhang L, Li G, Vermeulen R, Weinberg RS, Dosemeci M, Rappaport SM, Shen M, Alter BP, Wu Y, Kopp W, Waidyanatha S, Rabkin C, Guo W, Chanock S, Hayes RB, Linet M, Kim S, Yin S, Rothman N, Smith MT. Hematotoxicity in workers exposed to low levels of benzene. Science. 2004 Dec 3;306(5702):1774-6. Abstract ( Exit NIEHS Website

  3. Blask DE, Brainard GC, Dauchy RT, Hanifin JP, Davidson LK, Krause JA, Sauer LA, Rivera-Bermudez MA, Dubocovich ML, Jasser SA, Lynch DT, Rollag MD, Zalatan F. Melatonin-depleted blood from premenopausal women exposed to light at night stimulates growth of human breast cancer xenografts in nude rats. Cancer Res. 2005 Dec 1;65(23):11174-84. Abstract ( Exit NIEHS Website

  4. Couse JF, Yates MM, Deroo BJ, Korach KS. Estrogen receptor-beta is critical to granulosa cell differentiation and the ovulatory response to gonadotropins. Endocrinology. 2005 Aug;146(8):3247-62. Abstract ( Exit NIEHS Website

  5. Members of the Toxicogenomics Research Consortium. Standardizing global gene expression analysis between laboratories and across platforms. Nat Methods. 2005 May;2(5):351-6. Abstract ( Exit NIEHS Website

  6. Furlong CE, Holland N, Richter RJ, Bradman A, Ho A, Eskenazi B. PON1 status of farmworker mothers and children as a predictor of organophosphate sensitivity. Pharmacogenet Genomics. 2006 Mar;16(3):183-190. Abstract ( Exit NIEHS Website

    Berkowitz GS, Wetmur JG, Birman-Deych E, Obel J, Lapinski RH, Godbold JH, Holzman IR, Wolff MS. In utero pesticide exposure, maternal paraoxonase activity, and head circumference. Environ Health Perspect. 2004 Mar;112(3):388-91. Abstract ( Exit NIEHS Website

  7. Bauer AK, Dixon D, DeGraff LM, Cho HY, Walker CR, Malkinson AM, Kleeberger SR. Toll-Like Receptor 4 in Butylated Hydroxytoluene-Induced Mouse Pulmonary Inflammation and Tumorigenesis. Journal of the National Cancer Institute. 2005 Dec 7;97(23):1778-81. Abstract ( Exit NIEHS Website

  8. Schaumberg DA, Mendes F, Balaram M, Dana MR, Sparrow D, Hu H. Accumulated lead exposure and risk of age-related cataract in men. JAMA. 2004 Dec 8;292(22):2750-4. Abstract ( Exit NIEHS Website

  9. Hermoso MA, Matsuguchi T, Smoak K, Cidlowski JA. Glucocorticoids and tumor necrosis factor alpha cooperatively regulate toll-like receptor 2 gene expression. Mol Cell Biol. 2004 Jun;24(11):4743-56. Abstract ( Exit NIEHS Website

  10. Jin YH, Clark AB, Slebos RJ, Al-Refai H, Taylor JA, Kunkel TA, Resnick MA, Gordenin DA. Cadmium is a mutagen that acts by inhibiting mismatch repair. Nat Genet. 2003 Jul;34(3):326-9. Abstract ( Exit NIEHS Website

  11. Lobachev KS, Gordenin DA, Resnick MA. The Mre11 complex is required for repair of hairpin-capped double-strand breaks and prevention of chromosome rearrangements. Cell. 2002 Jan 25;108(2):183-93. Abstract ( Exit NIEHS Website

  12. Stein TD, Anders NJ, DeCarli C, Chan SL, Mattson MP, Johnson JA. Neutralization of transthyretin reverses the neuroprotective effects of secreted amyloid precursor protein (APP) in APPSW mice resulting in tau phosphorylation and loss of hippocampal neurons: support for the amyloid hypothesis. J Neurosci. 2004 Sep 1;24(35):7707-17. Abstract ( Exit NIEHS Website

  13. Pettit DL, Shao Z, Yakel JL. beta-Amyloid(1-42) peptide directly modulates nicotinic receptors in the rat hippocampal slice. J Neurosci. 2001 Jan 1;21(1):RC120. Abstract ( Exit NIEHS Website

  14. Gu YZ, Hogenesch JB, Bradfield CA. The PAS superfamily: sensors of environmental and developmental signals. Annu Rev Pharmacol Toxicol. 2000;40:519-61. Abstract ( Exit NIEHS Website

    Bunger MK, Wilsbacher LD, Moran SM, Clendenin C, Radcliffe LA, Hogenesch JB, Simon MC, Takahashi JS, Bradfield CA. Mop3 is an essential component of the master circadian pacemaker in mammals. Cell. 2000 Dec 22;103(7):1009-17. Abstract ( Exit NIEHS Website

    Hahn ME, Karchner SI, Shapiro MA, Perera SA. Molecular evolution of two vertebrate aryl hydrocarbon (dioxin) receptors (AHR1 and AHR2) and the PAS family. Proc Natl Acad Sci U S A. 1997 Dec 9;94(25):13743-8. Abstract ( Exit NIEHS Website

    Hogenesch JB, Gu YZ, Jain S, Bradfield CA. The basic-helix-loop-helix-PAS orphan MOP3 forms transcriptionally active complexes with circadian and hypoxia factors. Proc Natl Acad Sci U S A. 1998 May 12;95(10):5474-9. Abstract ( Exit NIEHS Website

  15. Pope CA 3rd, Burnett RT, Thun MJ, Calle EE, Krewski D, Ito K, Thurston GD. Lung cancer, cardiopulmonary mortality, and long-term exposure to fine particulate air pollution. JAMA. 2002 Mar 6;287(9):1132-41. Abstract ( Exit NIEHS Website

  16. McConnell R, Berhane K, Gilliland F, London SJ, Islam T, Gauderman WJ, Avol E, Margolis HG, Peters JM. Asthma in exercising children exposed to ozone: a cohort study. Lancet. 2002 Feb 2;359(9304):386-91. Abstract ( Exit NIEHS Website

  17. Tiano HF, Loftin CD, Akunda J, Lee CA, Spalding J, Sessoms A, Dunson DB, Rogan EG, Morham SG, Smart RC, Langenbach R. Deficiency of either cyclooxygenase (COX)-1 or COX-2 alters epidermal differentiation and reduces mouse skin tumorigenesis. Cancer Research 2002 Jun 15;62(12):3395-401. Abstract ( Exit NIEHS Website

  18. Lie RT, Wilcox AJ, Skjaerven R. Survival and reproduction among males with birth defects and risk of recurrence in their children. JAMA. 2001 Feb 14;285(6):755-60. Abstract ( Exit NIEHS Website

  19. Gammon MD, Neugut AI, Santella RM, Teitelbaum SL, Britton JA, Terry MB, Eng SM, Wolff MS, Stellman SD, Kabat GC, Levin B, Bradlow HL, Hatch M, Beyea J, Camann D, Trent M, Senie RT, Garbowski GC, Maffeo C, Montalvan P, Berkowitz GS, Kemeny M, Citron M, Schnabe F, Schuss A, Hajdu S, Vincguerra V, Collman GW, Obrams GI. The Long Island Breast Cancer Study Project: description of a multi-institutional collaboration to identify environmental risk factors for breast cancer. Breast Cancer Res Treat. 2002 Jun;74(3):235-54. Abstract ( Exit NIEHS Website

  20. Wang JS, Shen X, He X, Zhu YR, Zhang BC, Wang JB, Qian GS, Kuang SY, Zarba A, Egner PA, Jacobson LP, Munoz A, Helzlsouer KJ, Groopman JD, Kensler TW. Protective alterations in phase 1 and 2 metabolism of aflatoxin B1 by oltipraz in residents of Qidong, People's Republic of China. J Natl Cancer Inst. 1999 Feb 17;91(4):347-54. Abstract ( Exit NIEHS Website

    Wogan GN. Aflatoxin as a human carcinogen. Hepatology. 1999 Aug;30(2):573-5. Abstract ( Exit NIEHS Website

  21. Vojta PJ, Friedman W, Marker DA, Clickner R, Rogers JW, Viet SM, Muilenberg ML, Thorne PS, Arbes SJ Jr, Zeldin DC. First National Survey of Lead and Allergens in Housing: survey design and methods for the allergen and endotoxin components. Environ Health Perspect. 2002 May;110(5):527-32. Abstract ( Exit NIEHS Website

  22. Wiencke JK, Thurston SW, Kelsey KT, Varkonyi A, Wain JC, Mark EJ, Christiani DC. Early age at smoking initiation and tobacco carcinogen DNA damage in the lung. J Natl Cancer Inst. 1999 Apr 7;91(7):614-9. Abstract ( Exit NIEHS Website

  23. Gulson BL, Jameson CW, Mahaffey KR, Mizon KJ, Patison N, Law AJ, Korsch MJ, Salter MA. Relationships of lead in breast milk to lead in blood, urine, and diet of the infant and mother. Environ Health Perspect. 1998 Oct;106(10):667-74. Abstract ( Exit NIEHS Website

  24. Carballo E, Lai WS, Blackshear PJ. Feedback inhibition of macrophage tumor necrosis factor-alpha production by tristetraprolin. Science. 1998 Aug 14;281(5379):1001-5. Abstract ( Exit NIEHS Website

  25. Davidson PW, Myers GJ, Cox C, Axtell C, Shamlaye C, Sloane-Reeves J, Cernichiari E, Needham L, Choi A, Wang Y, Berlin M, Clarkson TW. Effects of prenatal and postnatal methylmercury exposure from fish consumption on neurodevelopment: outcomes at 66 months of age in the Seychelles Child Development Study. JAMA. 1998 Aug 26;280(8):701-7. Abstract ( Exit NIEHS Website

  26. Murata K, Weihe P, Budtz-Jorgensen E, Jorgensen PJ, Grandjean P. Delayed brainstem auditory evoked potential latencies in 14-year-old children exposed to methylmercury. J Pediatr. 2004 Feb;144(2):177-83. Abstract ( Exit NIEHS Website

  27. Hursting SD, Switzer BR, French JE, Kari FW. The growth hormone: insulin-like growth factor 1 axis is a mediator of diet restriction-induced inhibition of mononuclear cell leukemia in Fischer rats. Cancer Res. 1993 Jun 15;53(12):2750-7. Abstract ( Exit NIEHS Website

    Doll R, Peto R. The causes of cancer: quantitative estimates of avoidable risks of cancer in the United States today. J Natl Cancer Inst. 1981 Jun;66(6):1191-308. Abstract ( Exit NIEHS Website

  28. Jacobson JL, Jacobson SW. Intellectual impairment in children exposed to polychlorinated biphenyls in utero. N Engl J Med. 1996 Sep 12;335(11):783-9. Abstract ( Exit NIEHS Website

  29. Needleman HL, Riess JA, Tobin MJ, Biesecker GE, Greenhouse JB. Bone lead levels and delinquent behavior. JAMA. 1996 Feb 7;275(5):363-9. Abstract ( Exit NIEHS Website

    Dietrich KN, Ris MD, Succop PA, Berger OG, Bornschein RL. Early exposure to lead and juvenile delinquency. Neurotoxicol Teratol. 2001 Nov-Dec;23(6):511-8. Abstract ( Exit NIEHS Website

  30. Dong JT, Lamb PW, Rinker-Schaeffer CW, Vukanovic J, Ichikawa T, Isaacs JT, Barrett JC. KAI1, a metastasis suppressor gene for prostate cancer on human chromosome 11p11.2. Science. 1995 May 12;268(5212):884-6. Abstract ( Exit NIEHS Website

  31. Birnbaumer L, Pohl SL, Rodbell M. The glucagon-sensitive adenyl cyclase system in plasma membranes of rat liver. II. Comparison between glucagon- and fluoride-stimulated activities. J Biol Chem. 1971 Mar 25;246(6):1857-60. Abstract ( Exit NIEHS Website

    Cooper DM, Schlegel W, Lin MC, Rodbell M. The fat cell adenylate cyclase system. Characterization and manipulation of its bimodal regulation by GTP. J Biol Chem. 1979 Sep 25;254(18):8927-31. Abstract ( Exit NIEHS Website

    Londos C, Salomon Y, Lin MC, Harwood JP, Schramm M, Wolff J, Rodbell M. 5'-Guanylylimidodiphosphate, a potent activator of adenylate cyclase systems in eukaryotic cells. Proc Natl Acad Sci U S A. 1974 Aug;71(8):3087-90. Abstract ( Exit NIEHS Website

    Pohl SL, Birnbaumer L, Rodbell M. The glucagon-sensitive adenyl cyclase system in plasma membranes of rat liver. I. Properties. J Biol Chem. 1971 Mar 25;246(6):1849-56. Abstract ( Exit NIEHS Website

    Rodbell M, Krans HM, Pohl SL, Birnbaumer L. The glucagon-sensitive adenyl cyclase system in plasma membranes of rat liver. IV. Effects of guanylnucleotides on binding of 125I-glucagon. J Biol Chem. 1971 Mar 25;246(6):1872-6. Abstract ( Exit NIEHS Website

    Rodbell M, Birnbaumer L, Pohl SL, Krans HM. The glucagon-sensitive adenyl cyclase system in plasma membranes of rat liver. V. An obligatory role of guanylnucleotides in glucagon action. J Biol Chem. 1971 Mar 25;246(6):1877-82. Abstract ( Exit NIEHS Website

    Rodbell M, Krans HM, Pohl SL, Birnbaumer L. The glucagon-sensitive adenyl cyclase system in plasma membranes of rat liver. 3. Binding of glucagon: method of assay and specificity. J Biol Chem. 1971 Mar 25;246(6):1861-71. Abstract ( Exit NIEHS Website

    Yamamura H, Lad PM, Rodbell M. GTP stimulates and inhibits adenylate cyclase in fat cell membranes through distinct regulatory processes.J Biol Chem. 1977 Nov 25;252(22):7964-6. Abstract ( Exit NIEHS Website

    Rodbell M. The role of hormone receptors and GTP-regulatory proteins in membrane transduction. Nature. 1980 Mar 6;284(5751):17-22. Abstract ( Exit NIEHS Website

  32. Miki Y, Swensen J, Shattuck-Eidens D, Futreal PA, Harshman K, Tavtigian S, Liu Q, Cochran C, Bennett LM, Ding W, et al. A strong candidate for the breast and ovarian cancer susceptibility gene BRCA1. Science. 1994 Oct 7;266(5182):66-71. Abstract ( Exit NIEHS Website

  33. Dockery DW, Pope CA 3rd, Xu X, Spengler JD, Ware JH, Fay ME, Ferris BG Jr, Speizer FE. An association between air pollution and mortality in six U.S. cities. N Engl J Med. 1993 Dec 9;329(24):1753-9. Abstract ( Exit NIEHS Website

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