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  1. Article ; Online: Molecular analysis directs the prognosis, management and treatment of patients with xeroderma pigmentosum.

    Lehmann, Alan R / Fassihi, Hiva

    DNA repair

    2020  Volume 93, Page(s) 102907

    Abstract: Xeroderma pigmentosum (XP) is a well-studied disorder of (in most cases) nucleotide excision repair. The establishment in 2010 of a multidisciplinary XP clinic in the UK has enabled us to make a detailed analysis of genotype-phenotype relationships in XP ...

    Abstract Xeroderma pigmentosum (XP) is a well-studied disorder of (in most cases) nucleotide excision repair. The establishment in 2010 of a multidisciplinary XP clinic in the UK has enabled us to make a detailed analysis of genotype-phenotype relationships in XP patients and in several instances to make confident prognostic predictions. Splicing mutations in XPA and XPD and a specific amino acid change in XPD are associated with mild phenotypes, and individuals assigned to the XP-F group appear to have reduced pigmentation changes and a lower susceptibility to skin cancer than XPs in other groups. In an XP-C patient with advanced metastatic cancer arising from an angiosarcoma, molecular analysis of the tumour DNA suggested that immunotherapy, not normally recommended for angiosarcomas, might in this case be successful, and indeed the patient showed a dramatic recovery following immunotherapy treatment. These studies show that molecular analyses can improve the management, prognoses and therapy for individuals with XP.
    MeSH term(s) DNA Repair ; Disease Management ; Humans ; Immunotherapy ; Mutation ; Neoplasms/etiology ; Neoplasms/therapy ; Prognosis ; Skin Neoplasms ; Xeroderma Pigmentosum/complications ; Xeroderma Pigmentosum/diagnosis ; Xeroderma Pigmentosum/genetics
    Language English
    Publishing date 2020-07-07
    Publishing country Netherlands
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2071608-4
    ISSN 1568-7856 ; 1568-7864
    ISSN (online) 1568-7856
    ISSN 1568-7864
    DOI 10.1016/j.dnarep.2020.102907
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  2. Article ; Online: Xeroderma pigmentosum in the United kingdom.

    Lehmann, Alan R

    Photochemistry and photobiology

    2015  Volume 91, Issue 2, Page(s) 484–485

    Abstract: The seminal discovery by James Cleaver of defective DNA repair in xeroderma pigmentosum (XP) opened up an ever-expanding field of DNA repair-related disorders. In addition, it put XP on the map and has led to improved diagnosis, care and management of ... ...

    Abstract The seminal discovery by James Cleaver of defective DNA repair in xeroderma pigmentosum (XP) opened up an ever-expanding field of DNA repair-related disorders. In addition, it put XP on the map and has led to improved diagnosis, care and management of affected patients. In the United Kingdom, we recently established a multidisciplinary specialist clinic for XP patients. All XP patients in the United Kingdom are able to visit the clinic where they are examined and advised by a team of specialists with detailed knowledge of the different aspects of XP.
    MeSH term(s) Age of Onset ; DNA Damage ; DNA Repair ; DNA, Neoplasm/genetics ; DNA, Neoplasm/metabolism ; Humans ; Melanoma/diagnosis ; Melanoma/epidemiology ; Melanoma/etiology ; Melanoma/genetics ; Skin/metabolism ; Skin/pathology ; Skin/radiation effects ; Skin Neoplasms/diagnosis ; Skin Neoplasms/epidemiology ; Skin Neoplasms/etiology ; Skin Neoplasms/genetics ; Skin Pigmentation/radiation effects ; Ultraviolet Rays/adverse effects ; United Kingdom/epidemiology ; Xeroderma Pigmentosum/complications ; Xeroderma Pigmentosum/diagnosis ; Xeroderma Pigmentosum/epidemiology ; Xeroderma Pigmentosum/genetics
    Chemical Substances DNA, Neoplasm
    Language English
    Publishing date 2015-03
    Publishing country United States
    Document type Journal Article
    ZDB-ID 123540-0
    ISSN 1751-1097 ; 0031-8655
    ISSN (online) 1751-1097
    ISSN 0031-8655
    DOI 10.1111/php.12301
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: DNA repair, DNA replication and human disorders: a personal journey.

    Lehmann, Alan R

    DNA repair

    2012  Volume 11, Issue 4, Page(s) 328–334

    MeSH term(s) Academies and Institutes ; Biochemistry/history ; Cell Cycle Proteins/genetics ; Cell Cycle Proteins/metabolism ; Chromosomal Proteins, Non-Histone/genetics ; Chromosomal Proteins, Non-Histone/metabolism ; Cockayne Syndrome/genetics ; DNA Repair ; DNA Replication ; Disease/genetics ; Genomics ; History, 20th Century ; History, 21st Century ; Humans ; Schizosaccharomyces/genetics ; Schizosaccharomyces/metabolism ; Schizosaccharomyces pombe Proteins/genetics ; Schizosaccharomyces pombe Proteins/metabolism ; Xeroderma Pigmentosum/genetics
    Chemical Substances Cell Cycle Proteins ; Chromosomal Proteins, Non-Histone ; Schizosaccharomyces pombe Proteins ; Smc5 protein, S pombe ; smc6 protein, S pombe
    Language English
    Publishing date 2012-05-03
    Publishing country Netherlands
    Document type Autobiography ; Biography ; Historical Article ; Journal Article
    ZDB-ID 2071608-4
    ISSN 1568-7856 ; 1568-7864
    ISSN (online) 1568-7856
    ISSN 1568-7864
    DOI 10.1016/j.dnarep.2011.05.008
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  4. Article ; Online: DNA polymerases and repair synthesis in NER in human cells.

    Lehmann, Alan R

    DNA repair

    2011  Volume 10, Issue 7, Page(s) 730–733

    Abstract: The late steps of nucleotide excision repair, following incisions to remove the damaged section of DNA, comprise repair synthesis and ligation. In vitro and in vivo studies have shown the size of the repaired patch to be about 30 nucleotides. In vitro ... ...

    Abstract The late steps of nucleotide excision repair, following incisions to remove the damaged section of DNA, comprise repair synthesis and ligation. In vitro and in vivo studies have shown the size of the repaired patch to be about 30 nucleotides. In vitro studies implicated the replicative polymerases in repair synthesis, but recent in vivo data have shown that several DNA polymerases and ligases are involved in these steps in human cells.
    MeSH term(s) DNA/genetics ; DNA/metabolism ; DNA/radiation effects ; DNA Damage ; DNA Ligases/metabolism ; DNA Repair ; DNA Replication ; DNA-Directed DNA Polymerase/metabolism ; Humans ; Proliferating Cell Nuclear Antigen/genetics ; Proliferating Cell Nuclear Antigen/metabolism ; Ultraviolet Rays
    Chemical Substances Proliferating Cell Nuclear Antigen ; DNA (9007-49-2) ; DNA-Directed DNA Polymerase (EC 2.7.7.7) ; DNA Ligases (EC 6.5.1.-)
    Language English
    Publishing date 2011-07-15
    Publishing country Netherlands
    Document type Journal Article ; Review
    ZDB-ID 2071608-4
    ISSN 1568-7856 ; 1568-7864
    ISSN (online) 1568-7856
    ISSN 1568-7864
    DOI 10.1016/j.dnarep.2011.04.023
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Ubiquitin-family modifications in the replication of DNA damage.

    Lehmann, Alan R

    FEBS letters

    2011  Volume 585, Issue 18, Page(s) 2772–2779

    Abstract: The cell uses specialised Y-family DNA polymerases or damage avoidance mechanisms to replicate past damaged sites in DNA. These processes are under complex regulatory systems, which employ different types of post-translational modification. All the Y- ... ...

    Abstract The cell uses specialised Y-family DNA polymerases or damage avoidance mechanisms to replicate past damaged sites in DNA. These processes are under complex regulatory systems, which employ different types of post-translational modification. All the Y-family polymerases have ubiquitin binding domains that bind to mono-ubiquitinated PCNA to effect the switching from replicative to Y-family polymerase. Ubiquitination and de-ubiquitination of PCNA are tightly regulated. There is also evidence for another as yet unidentified ubiquitinated protein being involved in recruitment of Y-family polymerases to chromatin. Poly-ubiquitination of PCNA stimulates damage avoidance, and, at least in yeast, PCNA is SUMOylated to prevent unwanted recombination events at the replication fork. The Y-family polymerases themselves can be ubiquitinated and, in the case of DNA polymerase η, this results in the polymerase being excluded from chromatin.
    MeSH term(s) Animals ; DNA/genetics ; DNA/metabolism ; DNA Damage ; DNA Replication ; DNA-Directed DNA Polymerase/metabolism ; Humans ; Models, Genetic ; Proliferating Cell Nuclear Antigen/metabolism ; Protein Processing, Post-Translational ; Ubiquitin/metabolism
    Chemical Substances Proliferating Cell Nuclear Antigen ; Ubiquitin ; DNA (9007-49-2) ; DNA-Directed DNA Polymerase (EC 2.7.7.7) ; Rad30 protein (EC 2.7.7.7)
    Language English
    Publishing date 2011-06-23
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 212746-5
    ISSN 1873-3468 ; 0014-5793
    ISSN (online) 1873-3468
    ISSN 0014-5793
    DOI 10.1016/j.febslet.2011.06.005
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  6. Article: XPD structure reveals its secrets.

    Lehmann, Alan R

    DNA repair

    2008  Volume 7, Issue 11, Page(s) 1912–1915

    Abstract: The XPD protein is central to our understanding of the relationship between NER deficiencies and human disorders. Three recent papers report the crystal structures of XPD from archaea. Apart from anticipated helicase domains the structures reveal a 4FeS ... ...

    Abstract The XPD protein is central to our understanding of the relationship between NER deficiencies and human disorders. Three recent papers report the crystal structures of XPD from archaea. Apart from anticipated helicase domains the structures reveal a 4FeS cluster and novel "Arch" domain. The structures help our understanding of genotype-phenotype relationships in the XPD gene.
    MeSH term(s) Binding Sites ; Crystallography, X-Ray ; Genotype ; Humans ; Models, Biological ; Models, Genetic ; Models, Molecular ; Molecular Conformation ; Mutation ; Phenotype ; Protein Binding ; Protein Conformation ; Protein Structure, Tertiary ; Sulfolobus acidocaldarius/metabolism ; Xeroderma Pigmentosum Group D Protein/genetics ; Xeroderma Pigmentosum Group D Protein/physiology
    Chemical Substances Xeroderma Pigmentosum Group D Protein (EC 3.6.4.12) ; ERCC2 protein, human (EC 5.99.-)
    Language English
    Publishing date 2008-11-01
    Publishing country Netherlands
    Document type Journal Article ; Review
    ZDB-ID 2071608-4
    ISSN 1568-7856 ; 1568-7864
    ISSN (online) 1568-7856
    ISSN 1568-7864
    DOI 10.1016/j.dnarep.2008.07.008
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  7. Article ; Online: Metronidazole-Induced Hepatitis in a Teenager With Xeroderma Pigmentosum and Trichothiodystrophy Overlap.

    Abiona, Adesoji / Cordeiro, Nuno / Fawcett, Heather / Tamura, Deborah / Khan, Sikandar G / DiGiovanna, John J / Lehmann, Alan R / Fassihi, Hiva

    Pediatrics

    2021  Volume 148, Issue 4

    Abstract: A teenage girl had the rare combined phenotype of xeroderma pigmentosum and trichothiodystrophy, resulting from mutations in the XPD (ERCC2) gene involved in nucleotide excision repair (NER). After treatment with antibiotics, including metronidazole for ... ...

    Abstract A teenage girl had the rare combined phenotype of xeroderma pigmentosum and trichothiodystrophy, resulting from mutations in the XPD (ERCC2) gene involved in nucleotide excision repair (NER). After treatment with antibiotics, including metronidazole for recurrent infections, she showed signs of acute and severe hepatotoxicity, which gradually resolved after withdrawal of the treatment. Cultured skin fibroblasts from the patient revealed cellular sensitivity to killing by metronidazole compared with cells from a range of other donors. This reveals that the metronidazole sensitivity was an intrinsic property of her cells. It is well recognized that patients with Cockayne syndrome, another NER disorder, are at high risk of metronidazole-induced hepatotoxicity, but this had not been reported in individuals with other NER disorders. We would urge extreme caution in the use of metronidazole in the management of individuals with the xeroderma pigmentosum and trichothiodystrophy overlap or trichothiodystrophy phenotypes.
    MeSH term(s) Adolescent ; Anti-Bacterial Agents/adverse effects ; Chemical and Drug Induced Liver Injury/etiology ; Female ; Fibroblasts/drug effects ; Humans ; Metronidazole/adverse effects ; Mutation ; Trichothiodystrophy Syndromes/complications ; Trichothiodystrophy Syndromes/genetics ; Xeroderma Pigmentosum/complications ; Xeroderma Pigmentosum/genetics ; Xeroderma Pigmentosum Group D Protein/genetics
    Chemical Substances Anti-Bacterial Agents ; Metronidazole (140QMO216E) ; Xeroderma Pigmentosum Group D Protein (EC 3.6.4.12) ; ERCC2 protein, human (EC 5.99.-)
    Language English
    Publishing date 2021-09-30
    Publishing country United States
    Document type Case Reports ; Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 207677-9
    ISSN 1098-4275 ; 0031-4005
    ISSN (online) 1098-4275
    ISSN 0031-4005
    DOI 10.1542/peds.2021-050360
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  8. Article ; Online: Neurological disease in xeroderma pigmentosum: prospective cohort study of its features and progression.

    Garcia-Moreno, Hector / Langbehn, Douglas R / Abiona, Adesoji / Garrood, Isabel / Fleszar, Zofia / Manes, Marta Antonia / Morley, Ana M Susana / Craythorne, Emma / Mohammed, Shehla / Henshaw, Tanya / Turner, Sally / Naik, Harsha / Bodi, Istvan / Sarkany, Robert P E / Fassihi, Hiva / Lehmann, Alan R / Giunti, Paola

    Brain : a journal of neurology

    2023  Volume 146, Issue 12, Page(s) 5044–5059

    Abstract: Xeroderma pigmentosum (XP) results from biallelic mutations in any of eight genes involved in DNA repair systems, thus defining eight different genotypes (XPA, XPB, XPC, XPD, XPE, XPF, XPG and XP variant or XPV). In addition to cutaneous and ... ...

    Abstract Xeroderma pigmentosum (XP) results from biallelic mutations in any of eight genes involved in DNA repair systems, thus defining eight different genotypes (XPA, XPB, XPC, XPD, XPE, XPF, XPG and XP variant or XPV). In addition to cutaneous and ophthalmological features, some patients present with XP neurological disease. It is unknown whether the different neurological signs and their progression differ among groups. Therefore, we aim to characterize the XP neurological disease and its evolution in the heterogeneous UK XP cohort. Patients with XP were followed in the UK National XP Service, from 2009 to 2021. Age of onset for different events was recorded. Cerebellar ataxia and additional neurological signs and symptoms were rated with the Scale for the Assessment and Rating of Ataxia (SARA), the Inventory of Non-Ataxia Signs (INAS) and the Activities of Daily Living questionnaire (ADL). Patients' mutations received scores based on their predicted effects. Data from available ancillary tests were collected. Ninety-three XP patients were recruited. Thirty-six (38.7%) reported neurological symptoms, especially in the XPA, XPD and XPG groups, with early-onset and late-onset forms, and typically appearing after cutaneous and ophthalmological symptoms. XPA, XPD and XPG patients showed higher SARA scores compared to XPC, XPE and XPV. SARA total scores significantly increased over time in XPD (0.91 points/year, 95% confidence interval: 0.61, 1.21) and XPA (0.63 points/year, 95% confidence interval: 0.38, 0.89). Hyporeflexia, hypopallesthaesia, upper motor neuron signs, chorea, dystonia, oculomotor signs and cognitive impairment were frequent findings in XPA, XPD and XPG. Cerebellar and global brain atrophy, axonal sensory and sensorimotor neuropathies, and sensorineural hearing loss were common findings in patients. Some XPC, XPE and XPV cases presented with abnormalities on examination and/or ancillary tests, suggesting underlying neurological involvement. More severe mutations were associated with a faster progression in SARA total score in XPA (0.40 points/year per 1-unit increase in severity score) and XPD (0.60 points/year per 1-unit increase), and in ADL total score in XPA (0.35 points/year per 1-unit increase). Symptomatic and asymptomatic forms of neurological disease are frequent in XP patients, and neurological symptoms can be an important cause of disability. Typically, the neurological disease will be preceded by cutaneous and ophthalmological features, and these should be actively searched in patients with idiopathic late-onset neurological syndromes. Scales assessing cerebellar function, especially walking and speech, and disability can show progression in some of the groups. Mutation severity can be used as a prognostic biomarker for stratification purposes in clinical trials.
    MeSH term(s) Humans ; Xeroderma Pigmentosum/complications ; Xeroderma Pigmentosum/genetics ; Xeroderma Pigmentosum/diagnosis ; Activities of Daily Living ; Prospective Studies ; DNA Repair ; Mutation/genetics ; Central Nervous System Diseases
    Language English
    Publishing date 2023-12-01
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 80072-7
    ISSN 1460-2156 ; 0006-8950
    ISSN (online) 1460-2156
    ISSN 0006-8950
    DOI 10.1093/brain/awad266
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  9. Article: New functions for Y family polymerases.

    Lehmann, Alan R

    Molecular cell

    2006  Volume 24, Issue 4, Page(s) 493–495

    Abstract: The Y family of DNA polymerases plays crucial roles in carrying out translesion synthesis past damaged bases in DNA. Several recent papers suggest that they might have other roles as well in gene conversion, in nucleotide excision repair (NER), and in ... ...

    Abstract The Y family of DNA polymerases plays crucial roles in carrying out translesion synthesis past damaged bases in DNA. Several recent papers suggest that they might have other roles as well in gene conversion, in nucleotide excision repair (NER), and in DNA replication under stressed conditions.
    MeSH term(s) Animals ; Cell Cycle ; DNA Repair ; DNA Replication/physiology ; DNA-Directed DNA Polymerase/physiology ; Humans ; Nuclear Proteins ; Nucleotidyltransferases/physiology ; Recombination, Genetic
    Chemical Substances Nuclear Proteins ; Nucleotidyltransferases (EC 2.7.7.-) ; REV1 protein, human (EC 2.7.7.-) ; DNA-Directed DNA Polymerase (EC 2.7.7.7)
    Language English
    Publishing date 2006-12-21
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 1415236-8
    ISSN 1097-4164 ; 1097-2765
    ISSN (online) 1097-4164
    ISSN 1097-2765
    DOI 10.1016/j.molcel.2006.10.021
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  10. Article: Clubbing together on clamps: The key to translesion synthesis.

    Lehmann, Alan R

    DNA repair

    2006  Volume 5, Issue 3, Page(s) 404–407

    Abstract: Translesion synthesis is an important mechanism by which cells replicate past DNA damage. The sliding clamp DNA polymerase processivity factors play a central role in this process. The clamps are dimeric in bacteria and trimeric in eukaryotes and archaea, ...

    Abstract Translesion synthesis is an important mechanism by which cells replicate past DNA damage. The sliding clamp DNA polymerase processivity factors play a central role in this process. The clamps are dimeric in bacteria and trimeric in eukaryotes and archaea, raising the question of whether more than one polymerase can interact with the clamp simultaneously. Recently published data suggest that this is indeed the case.
    MeSH term(s) DNA Replication ; DNA-Binding Proteins/chemistry ; DNA-Binding Proteins/metabolism ; DNA-Directed DNA Polymerase/chemistry ; DNA-Directed DNA Polymerase/metabolism ; Eukaryotic Cells/metabolism ; Humans ; Models, Molecular ; Trans-Activators
    Chemical Substances DNA-Binding Proteins ; Trans-Activators ; DNA-Directed DNA Polymerase (EC 2.7.7.7)
    Language English
    Publishing date 2006-01-19
    Publishing country Netherlands
    Document type Journal Article ; Review
    ZDB-ID 2071608-4
    ISSN 1568-7856 ; 1568-7864
    ISSN (online) 1568-7856
    ISSN 1568-7864
    DOI 10.1016/j.dnarep.2005.12.005
    Database MEDical Literature Analysis and Retrieval System OnLINE

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