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Abstracts from the 8th International Congress of the Asia Pacific Society of Infection Control (APSIC) : Bangkok, Thailand. 12-15 February 2017

Sutthiruk, Nantanit ; Botti, Mari ; Considine, Julie ; [et al.]

Springer Science and Business Media LLC ; 2017

In: Antimicrobial Resistance & Infection Control Vol. 6, No. S2 ( 2017-2)

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In: Antimicrobial Resistance & Infection Control, Springer Science and Business Media LLC, Vol. 6, No. S2 ( 2017-2)

Type of Medium: Online Resource

ISSN: 2047-2994

URL: Article

DOI: 10.1186/s13756-017-0176-1

Language: English

Publisher: Springer Science and Business Media LLC

Publication Date: 2017

detail.hit.zdb_id: 2666706-X

SSG: 15,3

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5th International Symposium on Focused Ultrasound : North Bethesda, MD, USA. 28 August- 1 September 2016

Zaaroor, Menashe ; Sinai, Alon ; Goldsher, Dorit ; [et al.]

Springer Science and Business Media LLC ; 2016

In: Journal of Therapeutic Ultrasound Vol. 4, No. S1 ( 2016-11)

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In: Journal of Therapeutic Ultrasound, Springer Science and Business Media LLC, Vol. 4, No. S1 ( 2016-11)

Type of Medium: Online Resource

ISSN: 2050-5736

URL: Article

DOI: 10.1186/s40349-016-0076-5

Language: English

Publisher: Springer Science and Business Media LLC

Publication Date: 2016

detail.hit.zdb_id: 2714301-6

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Differences in Expression of Key DNA Damage Repair Genes after Epigenetic-Induced BRCAness Dictate Synthetic Lethality with PARP1 Inhibition

Wiegmans, Adrian P. ; Yap, Pei-Yi ; Ward, Ambber ; [et al.]

American Association for Cancer Research (AACR) ; 2015

In: Molecular Cancer Therapeutics Vol. 14, No. 10 ( 2015-10-01), p. 2321-2331

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In: Molecular Cancer Therapeutics, American Association for Cancer Research (AACR), Vol. 14, No. 10 ( 2015-10-01), p. 2321-2331

Abstract: The triple-negative breast cancer (TNBC) subtype represents a cancer that is highly aggressive with poor patient outcome. Current preclinical success has been gained through synthetic lethality, targeting genome instability with PARP inhibition in breast cancer cells that harbor silencing of the homologous recombination (HR) pathway. Histone deacetylase inhibitors (HDACi) are a class of drugs that mediate epigenetic changes in expression of HR pathway genes. Here, we compare the activity of the pan-HDAC inhibitor suberoylanilide hydroxamic acid (SAHA), the class I/IIa HDAC inhibitor valproic acid (VPA), and the HDAC1/2–specific inhibitor romidepsin (ROMI) for their capability to regulate DNA damage repair gene expression and in sensitizing TNBC to PARPi. We found that two of the HDACis tested, SAHA and ROMI, but not VPA, indeed inhibit HR repair and that RAD51, BARD1, and FANCD2 represent key proteins whose inhibition is required for HDACi-mediated therapy with PARP inhibition in TNBC. We also observed that restoration of BRCA1 function stabilizes the genome compared with mutant BRCA1 that results in enhanced polyploid population after combination treatment with HDACi and PARPi. Furthermore, we found that overexpression of the key HR protein RAD51 represents a mechanism for this resistance, promoting aberrant repair and the enhanced polyploidy observed. These findings highlight the key components of HR in guiding synthetic lethality with PARP inhibition and support the rationale for utilizing the novel combination of HDACi and PARPi against TNBC in the clinical setting. Mol Cancer Ther; 14(10); 2321–31. ©2015 AACR.

Type of Medium: Online Resource

ISSN: 1535-7163 , 1538-8514

URL: Article

DOI: 10.1158/1535-7163.MCT-15-0374

Language: English

Publisher: American Association for Cancer Research (AACR)

Publication Date: 2015

detail.hit.zdb_id: 2062135-8

SSG: 12

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SMG1 heterozygosity exacerbates haematopoietic cancer development in Atm null mice by increasing persistent DNA damage and oxidative stress

Ho, Uda ; Luff, John ; James, Alexander ; [et al.]

Wiley ; 2019

In: Journal of Cellular and Molecular Medicine Vol. 23, No. 12 ( 2019-12), p. 8151-8160

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In: Journal of Cellular and Molecular Medicine, Wiley, Vol. 23, No. 12 ( 2019-12), p. 8151-8160

Abstract: Suppressor of morphogenesis in genitalia 1 (SMG1) and ataxia telangiectasia mutated (ATM) are members of the PI3‐kinase like–kinase (PIKK) family of proteins. ATM is a well‐established tumour suppressor. Loss of one or both alleles of ATM results in an increased risk of cancer development, particularly haematopoietic cancer and breast cancer in both humans and mouse models. In mice, total loss of SMG1 is embryonic lethal and loss of a single allele results in an increased rate of cancer development, particularly haematopoietic cancers and lung cancer. In this study, we generated mice deficient in Atm and lacking one allele of Smg1 , Atm −/− Smg1 gt/+ mice. These mice developed cancers more rapidly than either of the parental genotypes, and all cancers were haematopoietic in origin. The combined loss of Smg1 and Atm resulted in a higher level of basal DNA damage and oxidative stress in tissues than loss of either gene alone. Furthermore, Atm −/− Smg1 gt/+ mice displayed increased cytokine levels in haematopoietic tissues compared with wild‐type animals indicating the development of low‐level inflammation and a pro‐tumour microenvironment. Overall, our data demonstrated that combined loss of Atm expression and decreased Smg1 expression increases haematopoietic cancer development.

Type of Medium: Online Resource

ISSN: 1582-1838 , 1582-4934

URL: Issue

URL: Article

DOI: 10.1111/jcmm.v23.12

DOI: 10.1111/jcmm.14685

Language: English

Publisher: Wiley

Publication Date: 2019

detail.hit.zdb_id: 2076114-4

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PDTB-19. EphA RECEPTOR TYROSINE KINASES AS TARGETS FOR THERAPY IN PAEDIATRIC MEDULLOBLASTOMA

Carrington, Benjamin ; Al-Ejeh, Fares ; Lim, Yi Chieh ; [et al.]

Oxford University Press (OUP) ; 2016

In: Neuro-Oncology Vol. 18, No. suppl_6 ( 2016-11-01), p. vi153-vi154

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In: Neuro-Oncology, Oxford University Press (OUP), Vol. 18, No. suppl_6 ( 2016-11-01), p. vi153-vi154

Type of Medium: Online Resource

ISSN: 1522-8517 , 1523-5866

URL: Article

DOI: 10.1093/neuonc/now212.638

Language: English

Publisher: Oxford University Press (OUP)

Publication Date: 2016

detail.hit.zdb_id: 2094060-9

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Simultaneous targeting of DNA replication and homologous recombination in glioblastoma with a polyether ionophore

Lim, Yi Chieh ; Ensbey, Kathleen S ; Offenhäuser, Carolin ; [et al.]

Oxford University Press (OUP) ; 2019

In: Neuro-Oncology ( 2019-08-30)

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In: Neuro-Oncology, Oxford University Press (OUP), ( 2019-08-30)

Abstract: Despite significant endeavor having been applied to identify effective therapies to treat glioblastoma (GBM), survival outcomes remain intractable. The greatest nonsurgical benefit arises from radiotherapy, though tumors typically recur due to robust DNA repair. Patients could therefore benefit from therapies with the potential to prevent DNA repair and synergize with radiotherapy. In this work, we investigated the potential of salinomycin to enhance radiotherapy and further uncover novel dual functions of this ionophore to induce DNA damage and prevent repair. Methods In vitro primary GBM models and ex vivo GBM patient explants were used to determine the mechanism of action of salinomycin by immunoblot, flow cytometry, immunofluorescence, immunohistochemistry, and mass spectrometry. In vivo efficacy studies were performed using orthotopic GBM animal xenograft models. Salinomycin derivatives were synthesized to increase drug efficacy and explore structure-activity relationships. Results Here we report novel dual functions of salinomycin. Salinomycin induces toxic DNA lesions and prevents subsequent recovery by targeting homologous recombination (HR) repair. Salinomycin appears to target the more radioresistant GBM stem cell–like population and synergizes with radiotherapy to significantly delay tumor formation in vivo. We further developed salinomycin derivatives which display greater efficacy in vivo while retaining the same beneficial mechanisms of action. Conclusion Our findings highlight the potential of salinomycin to induce DNA lesions and inhibit HR to greatly enhance the effect of radiotherapy. Importantly, first-generation salinomycin derivatives display greater efficacy and may pave the way for clinical testing of these agents.

Type of Medium: Online Resource

ISSN: 1522-8517 , 1523-5866

URL: Article

DOI: 10.1093/neuonc/noz159

Language: English

Publisher: Oxford University Press (OUP)

Publication Date: 2019

detail.hit.zdb_id: 2094060-9

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Rats with a missense mutation in Atm display neuroinflammation and neurodegeneration subsequent to accumulation of cytosolic DNA following unrepaired DNA damage

Quek, Hazel ; Luff, John ; Cheung, KaGeen ; [et al.]

Oxford University Press (OUP) ; 2017

In: Journal of Leukocyte Biology Vol. 101, No. 4 ( 2017-04-01), p. 927-947

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In: Journal of Leukocyte Biology, Oxford University Press (OUP), Vol. 101, No. 4 ( 2017-04-01), p. 927-947

Abstract: Mutations in the ataxia-telangiectasia (A-T)-mutated (ATM) gene give rise to the human genetic disorder A-T, characterized by immunodeficiency, cancer predisposition, and neurodegeneration. Whereas a series of animal models recapitulate much of the A-T phenotype, they fail to present with ataxia or neurodegeneration. We describe here the generation of an Atm missense mutant [amino acid change of leucine (L) to proline (P) at position 2262 (L2262P)] rat by intracytoplasmic injection (ICSI) of mutant sperm into oocytes. Atm-mutant rats (AtmL2262P/L2262P) expressed low levels of ATM protein, suggesting a destabilizing effect of the mutation, and had a significantly reduced lifespan compared with Atm+/+. Whereas these rats did not show cerebellar atrophy, they succumbed to hind-limb paralysis (45%), and the remainder developed tumors. Closer examination revealed the presence of both dsDNA and ssDNA in the cytoplasm of cells in the hippocampus, cerebellum, and spinal cord of AtmL2262P/L2262P rats. Significantly increased levels of IFN-β and IL-1β in all 3 tissues were indicative of DNA damage induction of the type 1 IFN response. This was further supported by NF-κB activation, as evidenced by p65 phosphorylation (P65) and translocation to the nucleus in the spinal cord and parahippocampus. Other evidence of neuroinflammation in the brain and spinal cord was the loss of motor neurons and the presence of increased activation of microglia. These data provide support for a proinflammatory phenotype that is manifested in the Atm mutant rat as hind-limb paralysis. This mutant represents a useful model to investigate the importance of neuroinflammation in A-T.

Type of Medium: Online Resource

ISSN: 0741-5400 , 1938-3673

URL: Article

DOI: 10.1189/jlb.4VMA0716-316R

RVK:

XA 10000

Language: English

Publisher: Oxford University Press (OUP)

Publication Date: 2017

detail.hit.zdb_id: 2026833-6

SSG: 12

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SPT6-driven error-free DNA repair safeguards genomic stability of glioblastoma cancer stem-like cells

Obara, Elisabeth Anne Adanma ; Aguilar-Morante, Diana ; Rasmussen, Rikke Darling ; [et al.]

Springer Science and Business Media LLC ; 2020

In: Nature Communications Vol. 11, No. 1 ( 2020-09-18)

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In: Nature Communications, Springer Science and Business Media LLC, Vol. 11, No. 1 ( 2020-09-18)

Abstract: Glioblastoma cancer-stem like cells (GSCs) display marked resistance to ionizing radiation (IR), a standard of care for glioblastoma patients. Mechanisms underpinning radio-resistance of GSCs remain largely unknown. Chromatin state and the accessibility of DNA lesions to DNA repair machineries are crucial for the maintenance of genomic stability. Understanding the functional impact of chromatin remodeling on DNA repair in GSCs may lay the foundation for advancing the efficacy of radio-sensitizing therapies. Here, we present the results of a high-content siRNA microscopy screen, revealing the transcriptional elongation factor SPT6 to be critical for the genomic stability and self-renewal of GSCs. Mechanistically, SPT6 transcriptionally up-regulates BRCA1 and thereby drives an error-free DNA repair in GSCs. SPT6 loss impairs the self-renewal, genomic stability and tumor initiating capacity of GSCs. Collectively, our results provide mechanistic insights into how SPT6 regulates DNA repair and identify SPT6 as a putative therapeutic target in glioblastoma.

Type of Medium: Online Resource

ISSN: 2041-1723

URL: Article

DOI: 10.1038/s41467-020-18549-8

Language: English

Publisher: Springer Science and Business Media LLC

Publication Date: 2020

detail.hit.zdb_id: 2553671-0

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ATM-dependent phosphorylation of MRE11 controls extent of resection during homology directed repair by signalling through Exonuclease 1

Kijas, Amanda W. ; Lim, Yi Chieh ; Bolderson, Emma ; [et al.]

Oxford University Press (OUP) ; 2015

In: Nucleic Acids Research Vol. 43, No. 17 ( 2015-09-30), p. 8352-8367

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In: Nucleic Acids Research, Oxford University Press (OUP), Vol. 43, No. 17 ( 2015-09-30), p. 8352-8367

Type of Medium: Online Resource

ISSN: 0305-1048 , 1362-4962

URL: Article

DOI: 10.1093/nar/gkv754

RVK:

WA 15000

Language: English

Publisher: Oxford University Press (OUP)

Publication Date: 2015

detail.hit.zdb_id: 1472175-2

SSG: 12

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AarF Domain Containing Kinase 3 (ADCK3) Mutant Cells Display Signs of Oxidative Stress, Defects in Mitochondrial Homeostasis and Lysosomal Accumulation

Cullen, Jason K. ; Abdul Murad, Norazian ; Yeo, Abrey ; [et al.]

Public Library of Science (PLoS) ; 2016

In: PLOS ONE Vol. 11, No. 2 ( 2016-2-11), p. e0148213-

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In: PLOS ONE, Public Library of Science (PLoS), Vol. 11, No. 2 ( 2016-2-11), p. e0148213-

Type of Medium: Online Resource

ISSN: 1932-6203

URL: Article

DOI: 10.1371/journal.pone.0148213

DOI: 10.1371/journal.pone.0148213.g001

DOI: 10.1371/journal.pone.0148213.g002

DOI: 10.1371/journal.pone.0148213.g003

DOI: 10.1371/journal.pone.0148213.g004

DOI: 10.1371/journal.pone.0148213.g005

DOI: 10.1371/journal.pone.0148213.g006

DOI: 10.1371/journal.pone.0148213.g007

DOI: 10.1371/journal.pone.0148213.t001

DOI: 10.1371/journal.pone.0148213.s001

DOI: 10.1371/journal.pone.0148213.s002

DOI: 10.1371/journal.pone.0148213.s003

DOI: 10.1371/journal.pone.0148213.s004

DOI: 10.1371/journal.pone.0148213.s005

DOI: 10.1371/journal.pone.0148213.s006

DOI: 10.1371/journal.pone.0148213.s007

DOI: 10.1371/journal.pone.0148213.s008

DOI: 10.1371/journal.pone.0148213.s009

DOI: 10.1371/journal.pone.0148213.s010

DOI: 10.1371/journal.pone.0148213.s011

DOI: 10.1371/journal.pone.0148213.s012

Language: English

Publisher: Public Library of Science (PLoS)

Publication Date: 2016

detail.hit.zdb_id: 2267670-3

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