Dr Lisiane Meira

Lecturer in Toxicology

Qualifications: BSc, PhD

Email:
Phone: Work: 01483 68 6449
Room no: 13A AY 04

Office hours

9 am to 5 pm

Further information

Biography

  • 1984-1988     B.Sc., Biology. Federal University of Rio Grande do Sul, Porto Alegre/Brazil.
  • 1989-1994     Ph.D., Genetics and Molecular Biology. Curie Institute, Paris/France & UFRGS, Porto Alegre/Brazil.
  • 1995-2000     Postdoctoral Research Fellow/Instructor, UT Southwestern Medical Center, Texas, USA
  • 2001-2008     Research Scientist, Harvard School of Public Health/Massachusetts Institute of Technology, MA, USA
  • 2008-2009     Research Fellow, St. George’s University of London
  • 2009-current  Lecturer in Toxicology, University of Surrey

Research Interests

My research focuses on understanding the mechanisms by which exposures to endogenous and/or exogenous toxicants lead to pathology and disease. In particular, I am interested in understanding how defective repair of DNA damage can affect health, with implications to human degenerative diseases associated with aging such as cancer and neuronal degeneration.

Publications

Highlights

  • Calvo JA, Meira LB, Lee CY, Moroski-Erkul CA, Abolhassani N, Taghizadeh K, Eichinger LW, Muthupalani S, Nordstrand LM, Klungland A, Samson LD. (2012) 'DNA repair is indispensable for survival after acute inflammation.'. American Society for Clinical Investigation J Clin Invest., 122 (7), pp. 2680-2689.

    Abstract

    More than 15% of cancer deaths worldwide are associated with underlying infections or inflammatory conditions, therefore understanding how inflammation contributes to cancer etiology is important for both cancer prevention and treatment. Inflamed tissues are known to harbor elevated etheno-base (ε-base) DNA lesions induced by the lipid peroxidation that is stimulated by reactive oxygen and nitrogen species (RONS) released from activated neutrophils and macrophages. Inflammation contributes to carcinogenesis in part via RONS-induced cytotoxic and mutagenic DNA lesions, including ε-base lesions. The mouse alkyl adenine DNA glycosylase (AAG, also known as MPG) recognizes such base lesions, thus protecting against inflammation-associated colon cancer. Two other DNA repair enzymes are known to repair ε-base lesions, namely ALKBH2 and ALKBH3; thus, we sought to determine whether these DNA dioxygenase enzymes could protect against chronic inflammation-mediated colon carcinogenesis. Using established chemically induced colitis and colon cancer models in mice, we show here that ALKBH2 and ALKBH3 provide cancer protection similar to that of the DNA glycosylase AAG. Moreover, Alkbh2 and Alkbh3 each display apparent epistasis with Aag. Surprisingly, deficiency in all 3 DNA repair enzymes confers a massively synergistic phenotype, such that animals lacking all 3 DNA repair enzymes cannot survive even a single bout of chemically induced colitis.

  • Meira LB, Moroski-Erkul CA, Green SL, Calvo JA, Bronson RT, Shah D, Samson LD. (2009) 'Aag-initiated base excision repair drives alkylation-induced retinal degeneration in mice.'. Proc Natl Acad Sci U S A, United States: 106 (3), pp. 888-893.

    Abstract

    Vision loss affects >3 million Americans and many more people worldwide. Although predisposing genes have been identified their link to known environmental factors is unclear. In wild-type animals DNA alkylating agents induce photoreceptor apoptosis and severe retinal degeneration. Alkylation-induced retinal degeneration is totally suppressed in the absence of the DNA repair protein alkyladenine DNA glycosylase (Aag) in both differentiating and postmitotic retinas. Moreover, transgenic expression of Aag activity restores the alkylation sensitivity of photoreceptors in Aag null animals. Aag heterozygotes display an intermediate level of retinal degeneration, demonstrating haploinsufficiency and underscoring that Aag expression confers a dominant retinal degeneration phenotype.

  • Klapacz J, Meira LB, Luchetti DG, Calvo JA, Bronson RT, Edelmann W, Samson LD. (2009) 'O-6-methylguanine-induced cell death involves exonuclease 1 as well as DNA mismatch recognition in vivo'. NATL ACAD SCIENCES PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 106 (2), pp. 576-581.
  • Meira LB, Bugni JM, Green SL, Lee C-W, Pang B, Borenshtein D, Rickman BH, Rogers AB, Moroski-Erkul CA, McFaline JL, Schauer DB, Dedon PC, Fox JG, Samson LD. (2008) 'DNA damage induced by chronic inflammation contributes to colon carcinogenesis in mice'. AMER SOC CLINICAL INVESTIGATION INC JOURNAL OF CLINICAL INVESTIGATION, 118 (7), pp. 2516-2525.
  • Ringvoll J, Moen MN, Nordstrand LM, Meira LB, Pang B, Bekkelund A, Dedon PC, Bjelland S, Samson LD, Falnes PO, Klungland A. (2008) 'AlkB homologue 2-mediated repair of ethenoadenine lesions in mammalian DNA'. AMER ASSOC CANCER RESEARCH CANCER RESEARCH, 68 (11), pp. 4142-4149.

Journal articles

  • Meira LB, Calvo JA, Shah D, Klapacz J, Moroski-Erkul CA, Bronson RT, Samson LD. (2014) 'Repair of endogenous DNA base lesions modulate lifespan in mice.'. DNA Repair (Amst), Netherlands: 21, pp. 78-86.

    Abstract

    The accumulation of DNA damage is thought to contribute to the physiological decay associated with the aging process. Here, we report the results of a large-scale study examining longevity in various mouse models defective in the repair of DNA alkylation damage, or defective in the DNA damage response. We find that the repair of spontaneous DNA damage by alkyladenine DNA glycosylase (Aag/Mpg)-initiated base excision repair and O(6)-methylguanine DNA methyltransferase (Mgmt)-mediated direct reversal contributes to maximum life span in the laboratory mouse. We also uncovered important genetic interactions between Aag, which excises a wide variety of damaged DNA bases, and the DNA damage sensor and signaling protein, Atm. We show that Atm plays a role in mediating survival in the face of both spontaneous and induced DNA damage, and that Aag deficiency not only promotes overall survival, but also alters the tumor spectrum in Atm(-/-) mice. Further, the reversal of spontaneous alkylation damage by Mgmt interacts with the DNA mismatch repair pathway to modulate survival and tumor spectrum. Since these aging studies were performed without treatment with DNA damaging agents, our results indicate that the DNA damage that is generated endogenously accumulates with age, and that DNA alkylation repair proteins play a role in influencing longevity.

  • Brignull LM, Czimmerer Z, Saidi H, Daniel B, Villela I, Bartlett NW, Johnston SL, Meira LB, Nagy L, Nohturfft A. (2013) 'Reprogramming of lysosomal gene expression by interleukin-4 and Stat6'. BIOMED CENTRAL LTD BMC GENOMICS, 14 Article number ARTN 853
  • Bordin DL, Lima M, Lenz G, Henriques JAP, Saffi J, Meira LB, Mésange P, Soares DG, Larsen AK, Escargueil AE. (2013) 'DNA alkylation damage and autophagy induction'. Mutation Research - Reviews in Mutation Research, 753 (2), pp. 91-99.

    Abstract

    Many alkylating agents are used as chemotherapeutic drugs and have a long history of clinical application. These agents inflict a wide range of DNA damage resulting in a complex cellular response. After DNA damage, cells trigger a series of signaling cascades promoting cellular survival and cell cycle blockage which enables time for DNA repair to occur. More recently, induction of autophagy has been observed in cancer cells after treatment with different DNA-targeted anticancer drugs, including alkylating agents. Several studies have demonstrated that induction of autophagy after DNA damage delays apoptotic cell death and may therefore lead to chemoresistance, which is the limiting factor for successful chemotherapy. On the other hand, depending on the extent of damage and the cellular context, the induction of autophagy may also contribute to cell death. Given these conflicting results, many studies have been conducted to better define the role of autophagy in cancer cells in response to chemotherapy. In this review, we describe the main alkylating agents used in clinical oncology as well as the cellular response they evoke with emphasis on autophagy. © 2013 Elsevier B.V.

  • Polycarpou E, Carrington S, Tyrrell E, Carew MA, Meira LB, Modjtahedi H. (2013) 'Resveratrol 3-O-d-glucuronide and resveratrol 4′-O-d-glucuronide inhibit colon cancer cell growth: Evidence for a role of A3 adenosine receptors, cyclin D1 depletion, and G1 cell cycle arrest'. Molecular Nutrition and Food Research, 57 (10), pp. 1708-1717.

    Abstract

    Scope: Resveratrol is a plant-derived polyphenol with chemotherapeutic properties in animal cancer models and many biochemical effects in vitro. Its bioavailability is low and raises the possibility that the metabolites of resveratrol have biological effects. Here we investigate the actions of resveratrol 3-O-d-glucuronide, resveratrol 4′-O-d-glucuronide, and resveratrol 3-O-d-sulfate on the growth of colon cancer cells in vitro. Methods and results: The growth of Caco-2, HCT-116, and CCL-228 cells was measured using the neutral red and MTT assays. Resveratrol and each metabolite inhibited cell growth with IC50 values of 9.8-31 μM. Resveratrol caused S phase arrest in all three cell lines. Resveratrol 3-O-d-glucuronide and resveratrol 4′-O-d-glucuronide caused G1 arrest in CCL-228 and Caco-2 cells. Resveratrol 3-O-d-sulfate had no effect on cell cycle. Growth inhibition was reversed by an inhibitor of AMP-activated protein kinase (compound C) or an adenosine A3 receptor antagonist (MRS1191). The A3 receptor agonist 2Cl-IB-MECA inhibited growth and A3 receptors were detected in all cell lines. The resveratrol glucuronides also reduced cyclin D1 levels but at higher concentrations than in growth experiments and generally did not increase phosphorylated AMP-activated protein kinase. Conclusion: Resveratrol glucuronides inhibit cell growth by G1 arrest and cyclin D1 depletion, and our results strongly suggest a role for A3 adenosine receptors in this inhibition. © 2013 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.

  • Calvo JA, Moroski-Erkul CA, Lake A, Eichinger LW, Shah D, Jhun I, Limsirichai P, Meira LB, Samson LD, Bronson RT, Christiani DC. (2013) 'Aag DNA Glycosylase Promotes Alkylation-Induced Tissue Damage Mediated by Parp1'. PLoS Genetics, 9 (4)

    Abstract

    Alkylating agents comprise a major class of front-line cancer chemotherapeutic compounds, and while these agents effectively kill tumor cells, they also damage healthy tissues. Although base excision repair (BER) is essential in repairing DNA alkylation damage, under certain conditions, initiation of BER can be detrimental. Here we illustrate that the alkyladenine DNA glycosylase (AAG) mediates alkylation-induced tissue damage and whole-animal lethality following exposure to alkylating agents. Aag-dependent tissue damage, as observed in cerebellar granule cells, splenocytes, thymocytes, bone marrow cells, pancreatic β-cells, and retinal photoreceptor cells, was detected in wild-type mice, exacerbated in Aag transgenic mice, and completely suppressed in Aag mice. Additional genetic experiments dissected the effects of modulating both BER and Parp1 on alkylation sensitivity in mice and determined that Aag acts upstream of Parp1 in alkylation-induced tissue damage; in fact, cytotoxicity in WT and Aag transgenic mice was abrogated in the absence of Parp1. These results provide in vivo evidence that Aag-initiated BER may play a critical role in determining the side-effects of alkylating agent chemotherapies and that Parp1 plays a crucial role in Aag-mediated tissue damage. © 2013 Calvo et al.

  • Barazzuol L, Jena R, Burnet NG, Meira LB, Jeynes JC, Kirkby KJ, Kirkby NF. (2013) 'Evaluation of poly (ADP-ribose) polymerase inhibitor ABT-888 combined with radiotherapy and temozolomide in glioblastoma.'. Radiat Oncol, England: 8

    Abstract

    The cytotoxicity of radiotherapy and chemotherapy can be enhanced by modulating DNA repair. PARP is a family of enzymes required for an efficient base-excision repair of DNA single-strand breaks and inhibition of PARP can prevent the repair of these lesions. The current study investigates the trimodal combination of ABT-888, a potent inhibitor of PARP1-2, ionizing radiation and temozolomide(TMZ)-based chemotherapy in glioblastoma (GBM) cells.

  • Bordin DL, Lima M, Lenz G, Henriques JAP, Saffi J, Meira LB, Mésange P, Soares DG, Larsen AK, Escargueil AE. (2013) 'DNA alkylation damage and autophagy induction'. Mutation Research - Reviews in Mutation Research,

    Abstract

    Many alkylating agents are used as chemotherapeutic drugs and have a long history of clinical application. These agents inflict a wide range of DNA damage resulting in a complex cellular response. After DNA damage, cells trigger a series of signaling cascades promoting cellular survival and cell cycle blockage which enables time for DNA repair to occur. More recently, induction of autophagy has been observed in cancer cells after treatment with different DNA-targeted anticancer drugs, including alkylating agents. Several studies have demonstrated that induction of autophagy after DNA damage delays apoptotic cell death and may therefore lead to chemoresistance, which is the limiting factor for successful chemotherapy. On the other hand, depending on the extent of damage and the cellular context, the induction of autophagy may also contribute to cell death. Given these conflicting results, many studies have been conducted to better define the role of autophagy in cancer cells in response to chemotherapy. In this review, we describe the main alkylating agents used in clinical oncology as well as the cellular response they evoke with emphasis on autophagy. © 2013 Elsevier B.V. All rights reserved.

  • Calvo JA, Meira LB, Lee CY, Moroski-Erkul CA, Abolhassani N, Taghizadeh K, Eichinger LW, Muthupalani S, Nordstrand LM, Klungland A, Samson LD. (2012) 'DNA repair is indispensable for survival after acute inflammation.'. American Society for Clinical Investigation J Clin Invest., 122 (7), pp. 2680-2689.

    Abstract

    More than 15% of cancer deaths worldwide are associated with underlying infections or inflammatory conditions, therefore understanding how inflammation contributes to cancer etiology is important for both cancer prevention and treatment. Inflamed tissues are known to harbor elevated etheno-base (ε-base) DNA lesions induced by the lipid peroxidation that is stimulated by reactive oxygen and nitrogen species (RONS) released from activated neutrophils and macrophages. Inflammation contributes to carcinogenesis in part via RONS-induced cytotoxic and mutagenic DNA lesions, including ε-base lesions. The mouse alkyl adenine DNA glycosylase (AAG, also known as MPG) recognizes such base lesions, thus protecting against inflammation-associated colon cancer. Two other DNA repair enzymes are known to repair ε-base lesions, namely ALKBH2 and ALKBH3; thus, we sought to determine whether these DNA dioxygenase enzymes could protect against chronic inflammation-mediated colon carcinogenesis. Using established chemically induced colitis and colon cancer models in mice, we show here that ALKBH2 and ALKBH3 provide cancer protection similar to that of the DNA glycosylase AAG. Moreover, Alkbh2 and Alkbh3 each display apparent epistasis with Aag. Surprisingly, deficiency in all 3 DNA repair enzymes confers a massively synergistic phenotype, such that animals lacking all 3 DNA repair enzymes cannot survive even a single bout of chemically induced colitis.

  • Villela I, Heidenreich B, Cheema M, di Martino T, Samson LD, Meira LB. (2011) 'Dissecting the mechanism of DNA damage induced photoreceptor cell death'. TOXICOLOGY, 290 (2-3), pp. 143-143.
  • Kisby GE, Fry RC, Lasarev MR, Bammler TK, Beyer RP, Churchwell M, Doerge DR, Meira LB, Palmer VS, Ramos-Crawford A-L, Ren X, Sullivan RC, Kavanagh TJ, Samson LD, Zarbl H, Spencer PS. (2011) 'The Cycad Genotoxin MAM Modulates Brain Cellular Pathways Involved in Neurodegenerative Disease and Cancer in a DNA Damage-Linked Manner'. PUBLIC LIBRARY SCIENCE PLOS ONE, 6 (6) Article number ARTN e20911
  • Unnikrishnan A, Raffoul JJ, Patel HV, Prychitko TM, Anyangwe N, Meira LB, Friedberg EC, Cabelof DC, Heydari AR. (2009) 'Oxidative stress alters base excision repair pathway and increases apoptotic response in apurinic/apyrimidinic endonuclease 1/redox factor-1 haploinsufficient mice'. ELSEVIER SCIENCE INC FREE RADICAL BIOLOGY AND MEDICINE, 46 (11), pp. 1488-1499.
  • Bugni JM, Meira LB, Samson LD. (2009) 'Alkylation-induced colon tumorigenesis in mice deficient in the Mgmt and Msh6 proteins'. NATURE PUBLISHING GROUP ONCOGENE, 28 (5), pp. 734-741.
  • Meira LB, Moroski-Erkul CA, Green SL, Calvo JA, Bronson RT, Shah D, Samson LD. (2009) 'Aag-initiated base excision repair drives alkylation-induced retinal degeneration in mice.'. Proc Natl Acad Sci U S A, United States: 106 (3), pp. 888-893.

    Abstract

    Vision loss affects >3 million Americans and many more people worldwide. Although predisposing genes have been identified their link to known environmental factors is unclear. In wild-type animals DNA alkylating agents induce photoreceptor apoptosis and severe retinal degeneration. Alkylation-induced retinal degeneration is totally suppressed in the absence of the DNA repair protein alkyladenine DNA glycosylase (Aag) in both differentiating and postmitotic retinas. Moreover, transgenic expression of Aag activity restores the alkylation sensitivity of photoreceptors in Aag null animals. Aag heterozygotes display an intermediate level of retinal degeneration, demonstrating haploinsufficiency and underscoring that Aag expression confers a dominant retinal degeneration phenotype.

  • Klapacz J, Meira LB, Luchetti DG, Calvo JA, Bronson RT, Edelmann W, Samson LD. (2009) 'O-6-methylguanine-induced cell death involves exonuclease 1 as well as DNA mismatch recognition in vivo'. NATL ACAD SCIENCES PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 106 (2), pp. 576-581.
  • Maor-Shoshani A, Meira LB, Yang X, Samson LD. (2008) '3-methyladenine DNA glycosylase ill important for cellular resistance to psoralen interstrand cross-links'. ELSEVIER SCIENCE BV DNA REPAIR, 7 (8), pp. 1399-1406.
  • Meira LB, Bugni JM, Green SL, Lee C-W, Pang B, Borenshtein D, Rickman BH, Rogers AB, Moroski-Erkul CA, McFaline JL, Schauer DB, Dedon PC, Fox JG, Samson LD. (2008) 'DNA damage induced by chronic inflammation contributes to colon carcinogenesis in mice'. AMER SOC CLINICAL INVESTIGATION INC JOURNAL OF CLINICAL INVESTIGATION, 118 (7), pp. 2516-2525.
  • Lingaraju GM, Kartalou M, Meira LB, Samson LD. (2008) 'Substrate specificity and sequence-dependent activity of the Saccharomyces cerevisiae 3-methyladenine DNA glycosylase (Mag)'. ELSEVIER SCIENCE BV DNA REPAIR, 7 (6), pp. 970-982.
  • Ringvoll J, Moen MN, Nordstrand LM, Meira LB, Pang B, Bekkelund A, Dedon PC, Bjelland S, Samson LD, Falnes PO, Klungland A. (2008) 'AlkB homologue 2-mediated repair of ethenoadenine lesions in mammalian DNA'. AMER ASSOC CANCER RESEARCH CANCER RESEARCH, 68 (11), pp. 4142-4149.
  • Dong L, Meira LB, Hazra TK, Samson LD, Cao W. (2008) 'Oxanine DNA glycosylase activities in mammalian systems'. ELSEVIER SCIENCE BV DNA REPAIR, 7 (1), pp. 128-134.
  • Longerich S, Meira L, Shah D, Samson LD, Storb U. (2007) 'Alkyladenine DNA glycosylase (Aag) in somatic hypermutation and class switch recombination'. ELSEVIER SCIENCE BV DNA REPAIR, 6 (12), pp. 1764-1773.
  • Beyer RP, Fry RC, Lasarev MR, McConnachie LA, Meira LB, Palmer VS, Powell CL, Ross PK, Bammler TK, Bradford BU, Cranson AB, Cunningham ML, Fannin RD, Higgins GM, Hurban P, Kayton RJ, Kerr KF, Kosyk O, Lobenhofer EK, Sieber SO, Vliet PA, Weis BK, Wolfinger R, Woods CG, Freedman JH, Linney E, Kaufmann WK, Kavanagh TJ, Paules RS, Rusyn I, Samson LD, Spencer PS, Suk W, Tennant RJ, Zarbl H. (2007) 'Multicenter study of acetaminophen hepatotoxicity reveals the importance of biological endpoints in genomic analyses'. OXFORD UNIV PRESS TOXICOLOGICAL SCIENCES, 99 (1), pp. 326-337.
  • Lee CW, Rickman B, Meira LB, Samson L, Fox JG. (2007) 'Base excision repair genes alkyl adenine DNA glycosylase (Aag) and O6-methylguanine DNA methyltransferase (Mgmt) suppresses Helicobacter pylori-associated inflammation and progression to cancer'. W B SAUNDERS CO-ELSEVIER INC GASTROENTEROLOGY, 132 (4), pp. A319-A319.
  • Friedberg EC, Meira LB. (2006) 'Database of mouse strains carrying targeted mutations in genes affecting biological responses to DNA damage Version 7'. ELSEVIER SCIENCE BV DNA REPAIR, 5 (2), pp. 189-209.
  • Friedberg EC, Meira LB. (2004) 'Database of mouse strains carrying targeted mutations in genes affecting biological responses to DNA damage (Version 6)'. ELSEVIER SCIENCE BV DNA REPAIR, 3 (12), pp. 1617-1638.
  • Hitchcock TM, Dong L, Connor EE, Meira LB, Samson LD, Wyatt MD, Cao WG. (2004) 'Oxanine DNA glycosylase activity from mammalian alkyladenine glycosylase'. AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC JOURNAL OF BIOLOGICAL CHEMISTRY, 279 (37), pp. 38177-38183.
  • Raffoul JJ, Cabelof DC, Nakamura J, Meira LB, Friedberg EC, Heydari AR. (2004) 'Apurinic/apyrimidinic endonuclease (APE/REF-1) haploinsufficient mice display tissue-specific differences in DNA polymerase beta-dependent base excision repair'. AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC JOURNAL OF BIOLOGICAL CHEMISTRY, 279 (18), pp. 18425-18433.
  • Ham AJL, Engelward BP, Koc H, Sangaiah R, Meira LB, Samson LD, Swenberg JA. (2004) 'New immunoaffinity-LC-MS/MS methodology reveals that Aag null mice are deficient in their ability to clear 1,N-6-etheno-deoxyadenosine DNA lesions from lung and liver in vivo'. ELSEVIER SCIENCE BV DNA REPAIR, 3 (3), pp. 257-265.
  • Friedberg EC, Meira LB. (2003) 'Database of mouse strains carrying targeted mutations in genes affecting biological responses to DNA damage Version 5'. ELSEVIER SCIENCE BV DNA REPAIR, 2 (5), pp. 501-530.
  • Meira LB, Cheo DL, Reis AM, Chaij N, Burns DK, te Riele H, Friedberg EC. (2002) 'Mice defective in the mismatch repair gene Msh2 show increased predisposition to UVB radiation-induced skin cancer (vol 1, pg 929, 2002)'. ELSEVIER SCIENCE BV DNA REPAIR, 1 (12) Article number PII S1568-7864(02)00200-8 , pp. 1063-1063.
  • Meira LB, Cheo DL, Reis AM, Claij N, Burns DK, Riele HT, Friedberg EC. (2002) 'Mice defective in the mismatch repair gene Msh2 show increased predisposition to UVB radiation-induced skin cancer'. ELSEVIER SCIENCE BV DNA REPAIR, 1 (11) Article number PII S1568-7864(02)00143-X , pp. 929-934.
  • Meira LB, Devaraj S, Kisby GE, Burns DK, Daniel RL, Hammer RE, Grundy S, Jialal I, Friedberg EC. (2001) 'Heterozygosity for the mouse Apex gene results in phenotypes associated with oxidative stress'. AMER ASSOC CANCER RESEARCH CANCER RESEARCH, 61 (14), pp. 5552-5557.
  • Meira LB, Reis AMC, Cheo DL, Nahari D, Burns DK, Friedberg EC. (2001) 'Cancer predisposition in mutant mice defective in multiple genetic pathways: uncovering important genetic interactions'. ELSEVIER SCIENCE BV MUTATION RESEARCH-FUNDAMENTAL AND MOLECULAR MECHANISMS OF MUTAGENESIS, 477 (1-2), pp. 51-58.
  • Friedberg EC, Meira LB. (2000) 'Database of mouse strains carrying targeted mutations in genes affecting cellular responses to DNA damage. Version 4'. ELSEVIER SCIENCE BV MUTATION RESEARCH-DNA REPAIR, 459 (4), pp. 243-274.
  • Graham JM, Meira LB, Greenberg CR, Busch DB, Doughty ATB, Ziffer DW, Coleman DM, Savre-Train I, Friedberg EC. (2000) 'Original COFS syndrome Manitoba Aboriginal kindred has a mutation in the Cockayne syndrome group B (CSB) gene'. INT PEDIATRIC RESEARCH FOUNDATION, INC PEDIATRIC RESEARCH, 47 (4), pp. 81A-81A.
  • Meira LB, Graham JM, Greenberg CR, Busch DB, Doughty ATB, Ziffer DW, Coleman DM, Savre-Train I, Friedberg EC. (2000) 'Manitoba aboriginal kindred with original cerebro-oculo-facio-skeletal syndrome has a mutation in the Cockayne syndrome group B (CSB) gene'. UNIV CHICAGO PRESS AMERICAN JOURNAL OF HUMAN GENETICS, 66 (4), pp. 1221-1228.
  • Friedberg EC, Bond JP, Burns DK, Cheo DL, Greenblatt MS, Meira LB, Nahari D, Reis AM. (2000) 'Defective nucleotide excision repair in Xpc mutant mice and its association with cancer predisposition'. ELSEVIER SCIENCE BV MUTATION RESEARCH-DNA REPAIR, 459 (2), pp. 99-108.
  • Cheo DL, Meira LB, Burns DK, Reis AM, Issac T, Friedberg EC. (2000) 'Ultraviolet B radiation-induced skin cancer in mice defective in the Xpc, Trp53, and Apex (HAP1) genes: Genotype-specific effects on cancer predisposition and pathology of tumors'. AMER ASSOC CANCER RESEARCH CANCER RESEARCH, 60 (6), pp. 1580-1584.
  • Reis AM, Cheo DL, Meira LB, Greenblatt MS, Bond JP, Nahari D, Friedberg EC. (2000) 'Genotype-specific Trp53 mutational analysis in ultraviolet B radiation-induced skin cancers in Xpc and Xpc Trp53 mutant mice'. AMER ASSOC CANCER RESEARCH CANCER RESEARCH, 60 (6), pp. 1571-1579.
  • Graham JM, Meira LB, Greenberg CR, Busch D, Friedberg EC. (2000) 'Original COFS syndrome kindred from Manitoba has a mutation in the cockayne syndrome group B (CSB) gene.'. LIPPINCOTT WILLIAMS & WILKINS JOURNAL OF INVESTIGATIVE MEDICINE, 48 (1), pp. 48A-48A.
  • Graham JM, Meira LB, Greenberg CR, Jaspers NGJ, Busch D, Coleman DM, Ziffer DW, Friedberg EC. (1999) 'Original COFS syndrome Manitoba Aboriginal kindred has a mutation in the Cockayne syndrome group B (CSB) gene.'. UNIV CHICAGO PRESS AMERICAN JOURNAL OF HUMAN GENETICS, 65 (4), pp. A299-A299.
  • Friedberg EC, Meira LB. (1999) 'Database of mouse strains carrying targeted mutations in genes affecting cellular responses to DNA damage: version 3'. ELSEVIER SCIENCE BV MUTATION RESEARCH-DNA REPAIR, 433 (2), pp. 69-87.
  • Cheo DL, Burns DK, Meira LB, Houle JF, Friedberg EC. (1999) 'Mutational inactivation of the xeroderma pigmentosum group C gene confers predisposition to 2-acetylaminofluorene-induced liver and lung cancer and to spontaneous testicular cancer in Trp53(-/-) mice'. AMER ASSOC CANCER RESEARCH CANCER RESEARCH, 59 (4), pp. 771-775.
  • Friedberg EC, Meira LB, Cheo DL. (1998) 'Database of mouse strains carrying targeted mutations in genes affecting cellular responses to DNA damage. Version 2'. ELSEVIER SCIENCE BV MUTATION RESEARCH-DNA REPAIR, 407 (3), pp. 217-226.
  • Meira LB, Cheo DL, Hammer RE, Burns DK, Reis A, Friedberg EC. (1997) 'Genetic interaction between HAP1/REF-1 and p53'. NATURE PUBLISHING CO NATURE GENETICS, 17 (2), pp. 145-145.
  • Friedberg EC, Meira LB, Cheo DL. (1997) 'Database of mouse strains carrying targeted mutations in genes affecting cellular responses to DNA damage'. ELSEVIER SCIENCE BV MUTATION RESEARCH-DNA REPAIR, 383 (2), pp. 183-188.
  • Cheo DL, Ruven HJT, Meira LB, Hammer RE, Burns DK, Tappe NJ, vanZeeland AA, Mullenders LHF, Friedberg EC. (1997) 'Characterization of defective nucleotide excision repair in XPC mutant mice'. ELSEVIER SCIENCE BV MUTATION RESEARCH-FUNDAMENTAL AND MOLECULAR MECHANISMS OF MUTAGENESIS, 374 (1), pp. 1-9.
  • Cheo DL, Meira LB, Hammer RE, Burns DK, Doughty ATB, Friedberg EC. (1996) 'Synergistic interactions between XPC and p53 mutations in double-mutant mice: Neural tube abnormalities and accelerated UV radiation-induced skin cancer'. CURRENT BIOLOGY LTD CURRENT BIOLOGY, 6 (12), pp. 1691-1694.
  • MEIRA LB, HENRIQUES JAP, MAGANASCHWENCKE N. (1995) '8-METHOXYPSORALEN PHOTOINDUCED PLASMID-CHROMOSOME RECOMBINATION IN SACCHAROMYCES-CEREVISIAE USING A CENTROMERIC VECTOR'. OXFORD UNIV PRESS NUCLEIC ACIDS RESEARCH, 23 (9), pp. 1614-1620.
  • MEIRA LB, MAGANASCHWENCKE N, AVERBECK D, HENRIQUES JAP. (1994) 'INVOLVEMENT OF THE PS03 GENE OF SACCHAROMYCES-CEREVISIAE IN INTRACHROMOSONAL MITOTIC RECOMBINATION AND GENE AMPLIFICATION'. SPRINGER VERLAG MOLECULAR & GENERAL GENETICS, 245 (6), pp. 750-759.
  • QUEROL CB, PAESITORESAN SO, MEIRA LB, BRENDEL M, HENRIQUES JAP. (1994) 'ISOLATION AND CHARACTERIZATION OF 3 MUTANTS WITH INCREASED SENSITIVITY TO PHOTOACTIVATED 3-CARBETHOXYPSORALEN IN SACCHAROMYCES-CEREVISIAE'. SPRINGER VERLAG CURRENT GENETICS, 25 (5), pp. 407-411.
  • MEIRA LB, FONSECA MB, AVERBECK D, SCHENBERG ACG, HENRIQUES JAP. (1992) 'THE PSO4-1 MUTATION REDUCES SPONTANEOUS MITOTIC GENE CONVERSION AND RECIPROCAL RECOMBINATION IN SACCHAROMYCES-CEREVISIAE'. SPRINGER VERLAG MOLECULAR & GENERAL GENETICS, 235 (2-3), pp. 311-316.
  • AVERBECK D, DARDALHON M, MAGANASCHWENCKE N, MEIRA LB, MENIEL V, BOITEUX S, SAGE E. (1992) 'NEW ASPECTS OF THE REPAIR AND GENOTOXICITY OF PSORALEN PHOTOINDUCED LESIONS IN DNA'. ELSEVIER SCIENCE SA LAUSANNE JOURNAL OF PHOTOCHEMISTRY AND PHOTOBIOLOGY B-BIOLOGY, 14 (1-2), pp. 47-63.

Conference papers

  • Alasmael N, Meira LB, Swales K, Plant N. (2013) 'FXR is implicated in matrix metalloproteinases regulation, tumor invasion and metastasis in breast cancer'. AMER ASSOC CANCER RESEARCH CANCER RESEARCH, Washington, DC: 104th Annual Meeting of the American-Association-for-Cancer-Research (AACR) 73 (8)
  • Calvo J, Meira L, Lee C-Y, Moroski-Erkul C, Abolhassani N, Taghizadeh K, Muthupalani S, Nordstrand L, Klungland A, Samson L. (2012) 'DNA Repair Is Indispensable for Survival after Acute Inflammation in Mice'. WILEY-BLACKWELL ENVIRONMENTAL AND MOLECULAR MUTAGENESIS, Bellevue, WA: 43rd Annual Meeting of the Environmental-Mutagen-Society (EMS) 53, pp. S14-S14.
  • Dong L, Glass RA, Meira LB, Samson LD, Cao W. (2007) 'Novel xanthine DNA glycosylase (XDG) activities in mammalian and yeast systems.'. WILEY-LISS ENVIRONMENTAL AND MOLECULAR MUTAGENESIS, Atlanta, GA: 38th Annual Meeting of the Environmental-Mutagen-Society 48 (7), pp. 569-569.
  • Shah D, Marinov G, Meira L, Samson L. (2006) 'Cellular responses to 3-methyladenine DNA lesions.'. WILEY-LISS ENVIRONMENTAL AND MOLECULAR MUTAGENESIS, Vancouver, CANADA: 37th Annual Meeting of the Environmental-Mutagen-Society 47 (6), pp. 467-467.
  • Dong L, Meira LB, Hazra TK, Samson LD, Cao W. (2006) 'Novel oxanine DNA glycosylase activities in mammalian systems.'. WILEY-LISS ENVIRONMENTAL AND MOLECULAR MUTAGENESIS, Vancouver, CANADA: 37th Annual Meeting of the Environmental-Mutagen-Society 47 (6), pp. 449-449.
  • Meira LB, Pease K, Kerrison F, Dong M, Fry R, Dedon P, Samson LD. (2004) 'Defective repair of alkylation DNA damage in mice'. WILEY-LISS ENVIRONMENTAL AND MOLECULAR MUTAGENESIS, Pittsburgh, PA: 35th Annual Meeting of the Environmental-Mutagen-Society 44 (3), pp. 215-215.
  • Klapacz J, Meira LB, Edelmann W, Samson LD. (2004) 'Investigating the role of exonuclease I in the O-6-methylguanine-induced apoptosis'. WILEY-LISS ENVIRONMENTAL AND MOLECULAR MUTAGENESIS, Pittsburgh, PA: 35th Annual Meeting of the Environmental-Mutagen-Society 44 (3), pp. 210-210.
  • Kobayashi K, Meira LB, Samson LD. (2003) 'Transcriptional responses of Aag knockout mouse embryonic stem cells upon exposure to Me-Lex.'. OXFORD UNIV PRESS TOXICOLOGICAL SCIENCES, SALT LAKE CITY, UTAH: 42nd Annual Meeting of the Society-of-Toxicology 72, pp. 256-256.
  • Meira LB, Samson L. (2003) 'Complex responses to damaging agents'. MARCEL DEKKER INC DRUG METABOLISM REVIEWS, PROVIDENCE, RHODE ISLAND: 12th North American ISSX Meeting 35, pp. 15-15.

Book chapters

  • Meira LB, Burgis NE, Samson LD. (2005) 'Base excision repair'. in Back N, Cohen IR, Kritchevsky D, Lajtha A, Paoletti R, Nigg EA (eds.) Genome Instability in Cancer Development SPRINGER 570, pp. 125-173.

Teaching

Undergraduate: BMS2036, BMS2048, BMS3063, BMS3065
MSc Toxicology: TOX M001, TOX M007, TOX M008 (module organiser)

Undergraduate lecture notes

PG lecture notes

Departmental Duties

Admissions Tutor for the MSc Toxicology Programme

Biosciences Library Representative

Faculty Coordinator for the Science without Borders Programme

Chair of the MSc Toxicology Board of Studies

Page Owner: lm0017
Page Created: Thursday 3 September 2009 14:52:41 by t00345
Last Modified: Wednesday 27 November 2013 14:41:51 by lm0017
Expiry Date: Friday 3 December 2010 14:51:41
Assembly date: Wed Sep 17 22:07:03 BST 2014
Content ID: 13762
Revision: 3
Community: 1204