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Article: Exploring pharmacokinetics of talazoparib in ABCB1/ABCG2-deficient mice using a novel UHPLC-MS/MS method.

Talebi, Zahra / Garrison, Dominique A / Eisenmann, Eric D / Parmar, Kalindi / Shapiro, Geoffrey I / Rudek, Michelle A / Sparreboom, Alex / Jin, Yan

Heliyon

2023 Volume 9, Issue 11, Page(s) e20972

Abstract: A rapid, sensitive, and simple UHPLC-MS/MS method for the determination of the PARP inhibitor talazoparib in mouse plasma was developed and validated using [ ...

Abstract	A rapid, sensitive, and simple UHPLC-MS/MS method for the determination of the PARP inhibitor talazoparib in mouse plasma was developed and validated using [
Language	English
Publishing date	2023-10-13
Publishing country	England
Document type	Journal Article
ZDB-ID	2835763-2
ISSN	2405-8440
ISSN	2405-8440
DOI	10.1016/j.heliyon.2023.e20972
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Aldehydes Pose a Threat to BRCA2 Mutation Carriers.

Parmar, Kalindi / D'Andrea, Alan D

Cell

2017 Volume 169, Issue 6, Page(s) 979–981

Abstract: Humans with inherited heterozygous BRCA2 mutations have an increased risk of developing cancer; however, what triggers carcinogenesis in these individuals is unclear. Tan et al. find that environmental and metabolic aldehydes pose a threat to these ... ...

Abstract	Humans with inherited heterozygous BRCA2 mutations have an increased risk of developing cancer; however, what triggers carcinogenesis in these individuals is unclear. Tan et al. find that environmental and metabolic aldehydes pose a threat to these individuals by promoting degradation of wild-type BRCA2 protein, thereby predisposing them to genomic instability and perhaps to cancer.
MeSH term(s)	Aldehydes ; BRCA2 Protein/genetics ; Breast Neoplasms/genetics ; Genes, BRCA1 ; Genomic Instability ; Germ-Line Mutation ; Heterozygote ; Humans ; Mutation
Chemical Substances	Aldehydes ; BRCA2 Protein
Language	English
Publishing date	2017--01
Publishing country	United States
Document type	Journal Article ; Comment
ZDB-ID	187009-9
ISSN	1097-4172 ; 0092-8674
ISSN (online)	1097-4172
ISSN	0092-8674
DOI	10.1016/j.cell.2017.05.021
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Article ; Online: Isolation of human and murine hematopoietic stem cells for DNA damage and DNA repair assays.

Rodríguez, Alfredo / Filiatrault, Jessica / Flores-Guzmán, Patricia / Mayani, Héctor / Parmar, Kalindi / D'Andrea, Alan D

STAR protocols

2021 Volume 2, Issue 4, Page(s) 100846

Abstract: Hematopoietic stem and progenitor cells (HSPCs) reside in the bone marrow and supply blood cells. Efficient methods for isolation of HSPCs are required. Here, we present protocols for the isolation of human and murine HSPCs using manual and FACS-assisted ...

Abstract	Hematopoietic stem and progenitor cells (HSPCs) reside in the bone marrow and supply blood cells. Efficient methods for isolation of HSPCs are required. Here, we present protocols for the isolation of human and murine HSPCs using manual and FACS-assisted techniques. Isolated HSPCs can be used for downstream applications, including colony forming unit assays and DNA damage and repair assays. For complete details on the use and execution of this protocol, please refer to Rodríguez et al. (2021a) and (2021b).
MeSH term(s)	Animals ; Bone Marrow ; Colony-Forming Units Assay ; DNA Damage/genetics ; DNA Repair ; Hematopoietic Stem Cells ; Humans ; Mice
Language	English
Publishing date	2021-09-27
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	2666-1667
ISSN (online)	2666-1667
DOI	10.1016/j.xpro.2021.100846
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Article: Aldehydes Pose a Threat to BRCA2 Mutation Carriers

Parmar, Kalindi / Alan D. D’Andrea

Cell. 2017 June 01, v. 169

2017

Abstract	Humans with inherited heterozygous BRCA2 mutations have an increased risk of developing cancer; however, what triggers carcinogenesis in these individuals is unclear. Tan et al. find that environmental and metabolic aldehydes pose a threat to these individuals by promoting degradation of wild-type BRCA2 protein, thereby predisposing them to genomic instability and perhaps to cancer.
Keywords	aldehydes ; carcinogenesis ; genomics ; heterozygosity ; humans ; mutation ; neoplasms ; risk ; tumor suppressor proteins
Language	English
Dates of publication	2017-0601
Size	p. 979-981.
Publishing place	Elsevier Inc.
Document type	Article
ZDB-ID	187009-9
ISSN	1097-4172 ; 0092-8674
ISSN (online)	1097-4172
ISSN	0092-8674
DOI	10.1016/j.cell.2017.05.021
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Article ; Online: Isolation of human and murine hematopoietic stem cells for DNA damage and DNA repair assays

Alfredo Rodríguez / Jessica Filiatrault / Patricia Flores-Guzmán / Héctor Mayani / Kalindi Parmar / Alan D. D’Andrea

STAR Protocols, Vol 2, Iss 4, Pp 100846- (2021)

2021

Abstract: Summary: Hematopoietic stem and progenitor cells (HSPCs) reside in the bone marrow and supply blood cells. Efficient methods for isolation of HSPCs are required. Here, we present protocols for the isolation of human and murine HSPCs using manual and FACS- ...

Abstract	Summary: Hematopoietic stem and progenitor cells (HSPCs) reside in the bone marrow and supply blood cells. Efficient methods for isolation of HSPCs are required. Here, we present protocols for the isolation of human and murine HSPCs using manual and FACS-assisted techniques. Isolated HSPCs can be used for downstream applications, including colony forming unit assays and DNA damage and repair assays.For complete details on the use and execution of this protocol, please refer to Rodríguez et al. (2021a) and (2021b).
Keywords	Cell Biology ; Cell isolation ; Flow Cytometry/Mass Cytometry ; Cell-based Assays ; Genetics ; Microscopy ; Science (General) ; Q1-390
Language	English
Publishing date	2021-12-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Targeting DNA Repair with Combined Inhibition of NHEJ and MMEJ Induces Synthetic Lethality in TP53-Mutant Cancers.

Patterson-Fortin, Jeffrey / Bose, Arindam / Tsai, Wei-Chih / Grochala, Carter / Nguyen, Huy / Zhou, Jia / Parmar, Kalindi / Lazaro, Jean-Bernard / Liu, Joyce / McQueen, Kelsey / Shapiro, Geoffrey I / Kozono, David / D'Andrea, Alan D

Cancer research

2022 Volume 82, Issue 20, Page(s) 3815–3829

Abstract: DNA repair pathway inhibitors are a new class of anticancer drugs that are advancing in clinical trials. Peposertib is an inhibitor of DNA-dependent protein kinase (DNA-PK), which is a key driver of nonhomologous end-joining (NHEJ). To identify ... ...

Abstract	DNA repair pathway inhibitors are a new class of anticancer drugs that are advancing in clinical trials. Peposertib is an inhibitor of DNA-dependent protein kinase (DNA-PK), which is a key driver of nonhomologous end-joining (NHEJ). To identify regulators of response to peposertib, we performed a genome-wide CRISPR knockout screen and found that loss of POLQ (polymerase theta, POLθ) and other genes in the microhomology-mediated end-joining (MMEJ) pathway are key predictors of sensitivity to DNA-PK inhibition. Simultaneous disruption of two DNA repair pathways via combined treatment with peposertib plus a POLθ inhibitor novobiocin exhibited synergistic synthetic lethality resulting from accumulation of toxic levels of DNA double-strand break end resection. TP53-mutant tumor cells were resistant to peposertib but maintained elevated expression of POLQ and increased sensitivity to novobiocin. Consequently, the combination of peposertib plus novobiocin resulted in synthetic lethality in TP53-deficient tumor cell lines, organoid cultures, and patient-derived xenograft models. Thus, the combination of a targeted DNA-PK/NHEJ inhibitor with a targeted POLθ/MMEJ inhibitor may provide a rational treatment strategy for TP53-mutant solid tumors. Significance: Combined inhibition of NHEJ and MMEJ using two nontoxic, targeted DNA repair inhibitors can effectively induce toxic DNA damage to treat TP53-deficient cancers.
MeSH term(s)	DNA/metabolism ; DNA End-Joining Repair ; DNA Repair ; DNA-Activated Protein Kinase/genetics ; DNA-Activated Protein Kinase/metabolism ; DNA-Directed DNA Polymerase/metabolism ; Humans ; Neoplasms/drug therapy ; Neoplasms/genetics ; Novobiocin ; Pyridazines ; Quinazolines ; Synthetic Lethal Mutations ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism
Chemical Substances	Pyridazines ; Quinazolines ; TP53 protein, human ; Tumor Suppressor Protein p53 ; Novobiocin (17EC19951N) ; DNA (9007-49-2) ; DNA-Activated Protein Kinase (EC 2.7.11.1) ; DNA-Directed DNA Polymerase (EC 2.7.7.7) ; peposertib (GN429E725A)
Language	English
Publishing date	2022-08-16
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	1432-1
ISSN	1538-7445 ; 0008-5472
ISSN (online)	1538-7445
ISSN	0008-5472
DOI	10.1158/0008-5472.CAN-22-1124
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Article ; Online: TGFβ pathway is required for viable gestation of Fanconi anemia embryos.

Rodríguez, Alfredo / Epperly, Michael / Filiatrault, Jessica / Velázquez, Martha / Yang, Chunyu / McQueen, Kelsey / Sambel, Larissa A / Nguyen, Huy / Iyer, Divya Ramalingam / Juárez, Ulises / Ayala-Zambrano, Cecilia / Martignetti, David B / Frías, Sara / Fisher, Renee / Parmar, Kalindi / Greenberger, Joel S / D'Andrea, Alan D

PLoS genetics

2022 Volume 18, Issue 11, Page(s) e1010459

Abstract: Overexpression of the TGFβ pathway impairs the proliferation of the hematopoietic stem and progenitor cells (HSPCs) pool in Fanconi anemia (FA). TGFβ promotes the expression of NHEJ genes, known to function in a low-fidelity DNA repair pathway, and ... ...

Abstract	Overexpression of the TGFβ pathway impairs the proliferation of the hematopoietic stem and progenitor cells (HSPCs) pool in Fanconi anemia (FA). TGFβ promotes the expression of NHEJ genes, known to function in a low-fidelity DNA repair pathway, and pharmacological inhibition of TGFβ signaling rescues FA HSPCs. Here, we demonstrate that genetic disruption of Smad3, a transducer of the canonical TGFβ pathway, modifies the phenotype of FA mouse models deficient for Fancd2. We observed that the TGFβ and NHEJ pathway genes are overexpressed during the embryogenesis of Fancd2-/- mice and that the Fancd2-/-Smad3-/- double knockout (DKO) mice undergo high levels of embryonic lethality due to loss of the TGFβ-NHEJ axis. Fancd2-deficient embryos acquire extensive genomic instability during gestation which is not reversed by Smad3 inactivation. Strikingly, the few DKO survivors have activated the non-canonical TGFβ-ERK pathway, ensuring expression of NHEJ genes during embryogenesis and improved survival. Activation of the TGFβ-NHEJ axis was critical for the survival of the few Fancd2-/-Smad3-/- DKO newborn mice but had detrimental consequences for these surviving mice, such as enhanced genomic instability and ineffective hematopoiesis.
MeSH term(s)	Mice ; Animals ; Fanconi Anemia/genetics ; Transforming Growth Factor beta/genetics
Chemical Substances	Transforming Growth Factor beta
Language	English
Publishing date	2022-11-28
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, Non-U.S. Gov't
ZDB-ID	2186725-2
ISSN	1553-7404 ; 1553-7390
ISSN (online)	1553-7404
ISSN	1553-7390
DOI	10.1371/journal.pgen.1010459
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Article ; Online: Phase 1 Combination Study of the CHK1 Inhibitor Prexasertib and the PARP Inhibitor Olaparib in High-grade Serous Ovarian Cancer and Other Solid Tumors.

Do, Khanh T / Kochupurakkal, Bose / Kelland, Sarah / de Jonge, Adrienne / Hedglin, Jennifer / Powers, Allison / Quinn, Nicholas / Gannon, Courtney / Vuong, Loan / Parmar, Kalindi / Lazaro, Jean-Bernard / D'Andrea, Alan D / Shapiro, Geoffrey I

Clinical cancer research : an official journal of the American Association for Cancer Research

2021 Volume 27, Issue 17, Page(s) 4710–4716

Abstract: Purpose: Checkpoint kinase 1 (CHK1) plays a central role in the response to replication stress through modulation of cell-cycle checkpoints and homologous recombination (HR) repair. In BRCA-deficient cancers with : Patients and methods: This study ... ...

Abstract	Purpose: Checkpoint kinase 1 (CHK1) plays a central role in the response to replication stress through modulation of cell-cycle checkpoints and homologous recombination (HR) repair. In BRCA-deficient cancers with Patients and methods: This study followed a 3+3 design with a 7-day lead-in of olaparib alone, followed by 28-day cycles with prexasertib administered on days 1 and 15 in combination with an attenuated dose of olaparib on days 1-5 and 15-19. Pharmacokinetic blood samples were collected after olaparib alone and following combination therapy. Patients enrolled to the expansion phase of the study underwent paired tumor biopsies for pharmacodynamic (PD) assessments. Results: Twenty-nine patients were treated. DLTs included grade 3 neutropenia and grade 3 febrile neutropenia. The MTD/recommended phase 2 dose (RP2D) was prexasertib at 70 mg/m Conclusions: Prexasertib combined with olaparib has preliminary clinical activity in
MeSH term(s)	Adult ; Aged ; Aged, 80 and over ; Cystadenocarcinoma, Serous/drug therapy ; Cystadenocarcinoma, Serous/pathology ; Drug Combinations ; Female ; Humans ; Male ; Middle Aged ; Neoplasm Grading ; Neoplasms/drug therapy ; Neoplasms/pathology ; Ovarian Neoplasms/drug therapy ; Ovarian Neoplasms/pathology ; Phthalazines/administration & dosage ; Piperazines/administration & dosage ; Poly(ADP-ribose) Polymerase Inhibitors/administration & dosage ; Protein Kinase Inhibitors/administration & dosage ; Pyrazines/administration & dosage ; Pyrazoles/administration & dosage
Chemical Substances	Drug Combinations ; Phthalazines ; Piperazines ; Poly(ADP-ribose) Polymerase Inhibitors ; Protein Kinase Inhibitors ; Pyrazines ; Pyrazoles ; prexasertib ; olaparib (WOH1JD9AR8)
Language	English
Publishing date	2021-06-15
Publishing country	United States
Document type	Clinical Trial, Phase I ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1225457-5
ISSN	1557-3265 ; 1078-0432
ISSN (online)	1557-3265
ISSN	1078-0432
DOI	10.1158/1078-0432.CCR-21-1279
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Article ; Online: Stressed out: endogenous aldehydes damage hematopoietic stem cells.

Parmar, Kalindi / D'Andrea, Alan D

Cell stem cell

2012 Volume 11, Issue 5, Page(s) 583–584

Abstract: Despite a well-defined role for the Fanconi anemia (FA) pathway in mediating DNA repair, the mechanisms underlying the bone marrow failure in FA patients are poorly defined. Recently in Nature, Garaycoechea et al. (2012), identify aldehyde-mediated ... ...

Abstract	Despite a well-defined role for the Fanconi anemia (FA) pathway in mediating DNA repair, the mechanisms underlying the bone marrow failure in FA patients are poorly defined. Recently in Nature, Garaycoechea et al. (2012), identify aldehyde-mediated genotoxicity of hematopoietic stem cells as a cause for bone marrow failure.
Language	English
Publishing date	2012-11-05
Publishing country	United States
Document type	Comment ; Journal Article
ZDB-ID	2375354-7
ISSN	1875-9777 ; 1934-5909
ISSN (online)	1875-9777
ISSN	1934-5909
DOI	10.1016/j.stem.2012.10.007
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Article ; Online: Cooperation of the ATM and Fanconi Anemia/BRCA Pathways in Double-Strand Break End Resection.

Cai, Mu-Yan / Dunn, Connor E / Chen, Wenxu / Kochupurakkal, Bose S / Nguyen, Huy / Moreau, Lisa A / Shapiro, Geoffrey I / Parmar, Kalindi / Kozono, David / D'Andrea, Alan D

Cell reports

2020 Volume 30, Issue 7, Page(s) 2402–2415.e5

Abstract: Cells deficient in ataxia telangiectasia mutated (ATM) are hypersensitive to ionizing radiation and other anti-cancer agents that induce double-strand DNA breaks. ATM inhibitors may therefore sensitize cancer cells to these agents. Some cancers may also ... ...

Abstract	Cells deficient in ataxia telangiectasia mutated (ATM) are hypersensitive to ionizing radiation and other anti-cancer agents that induce double-strand DNA breaks. ATM inhibitors may therefore sensitize cancer cells to these agents. Some cancers may also have underlying genetic defects predisposing them to an ATM inhibitor monotherapy response. We have conducted a genome-wide CRISPR screen to identify genetic vulnerabilities that sensitize lung cancer cells to ATM inhibitors. Knockout of genes in the Fanconi anemia (FA)/BRCA pathway results in hypersensitivity to the ATM inhibitor M3541. Knockdown of either an FA gene or of ATM results in reduced double-strand break end resection, enhanced non-homologous end joining (NHEJ) repair, and decreased homologous recombination repair. Knockout of both the FA/BRCA pathway and ATM strongly inhibits end resection and generates toxic levels of NHEJ, thereby elucidating a mechanism of cellular death by synthetic lethality. ATM inhibitors may therefore be useful for the treatment of tumors with a defective FA/BRCA pathway.
MeSH term(s)	Ataxia Telangiectasia/genetics ; Clustered Regularly Interspaced Short Palindromic Repeats/genetics ; DNA Breaks, Double-Stranded ; DNA-Binding Proteins/metabolism ; Fanconi Anemia/genetics ; Humans
Chemical Substances	DNA-Binding Proteins
Language	English
Publishing date	2020-02-07
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2020.01.052
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