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Article: Adding to the CASeload: unwarranted p53 signaling induced by Cas9.

Rendo, Veronica / Enache, Oana M / Ben-David, Uri

Molecular & cellular oncology

2020 Volume 7, Issue 5, Page(s) 1789419

Abstract: We investigated the genetic and transcriptional changes associated with Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR) associated protein 9 (Cas9) expression in human cancer cell lines. For a subset of cell lines with a wild-type ... ...

Abstract	We investigated the genetic and transcriptional changes associated with Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR) associated protein 9 (Cas9) expression in human cancer cell lines. For a subset of cell lines with a wild-type tumor protein TP53 (best known as p53), we detected p53 pathway activation, DNA damage accumulation and emerging p53-inactivating mutations following Cas9 introduction. We discuss the potential implications of our findings in basic and translational research.
Language	English
Publishing date	2020-07-14
Publishing country	United States
Document type	Journal Article
ISSN	2372-3556
ISSN	2372-3556
DOI	10.1080/23723556.2020.1789419
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Article: Targeting tumor vulnerabilities associated with loss of heterozygosity.

Rendo, Veronica / Stoimenov, Ivaylo / Sjöblom, Tobias

Molecular & cellular oncology

2020 Volume 7, Issue 4, Page(s) 1759390

Abstract: We show that N-acetyltransferase 2 ( ...

Abstract	We show that N-acetyltransferase 2 (
Language	English
Publishing date	2020-05-13
Publishing country	United States
Document type	Journal Article
ISSN	2372-3556
ISSN	2372-3556
DOI	10.1080/23723556.2020.1759390
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Article ; Online: Comparison of high-throughput single-cell RNA-seq methods for ex vivo drug screening.

Gezelius, Henrik / Enblad, Anna Pia / Lundmark, Anders / Åberg, Martin / Blom, Kristin / Rudfeldt, Jakob / Raine, Amanda / Harila, Arja / Rendo, Verónica / Heinäniemi, Merja / Andersson, Claes / Nordlund, Jessica

NAR genomics and bioinformatics

2024 Volume 6, Issue 1, Page(s) lqae001

Abstract: Functional precision medicine (FPM) aims to optimize patient-specific drug selection based on the unique characteristics of their cancer cells. Recent advancements in high ... ...

Abstract	Functional precision medicine (FPM) aims to optimize patient-specific drug selection based on the unique characteristics of their cancer cells. Recent advancements in high throughput
Language	English
Publishing date	2024-01-29
Publishing country	England
Document type	Journal Article
ISSN	2631-9268
ISSN (online)	2631-9268
DOI	10.1093/nargab/lqae001
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Article ; Online: Women in cancer research and oncology.

Joyce, Johanna / Wakelee, Heather / Davis, Melissa B / Teo, Soo-Hwang / Bell, Sigourney / Rendo, Veronica

Cancer cell

2021 Volume 39, Issue 3, Page(s) 285–287

Abstract: March 8 is International Women's Day. Women, particularly women of color, are still underrepresented in science and medical careers and face severe health disparities. To commemorate this day, we asked female cancer researchers and oncologists to talk ... ...

Abstract	March 8 is International Women's Day. Women, particularly women of color, are still underrepresented in science and medical careers and face severe health disparities. To commemorate this day, we asked female cancer researchers and oncologists to talk about their work experiences and their efforts to improve equity, representation, and leadership.
MeSH term(s)	Biomedical Research/methods ; Female ; Humans ; Leadership ; Medical Oncology/methods
Language	English
Publishing date	2021-03-05
Publishing country	United States
Document type	Journal Article
ZDB-ID	2078448-X
ISSN	1878-3686 ; 1535-6108
ISSN (online)	1878-3686
ISSN	1535-6108
DOI	10.1016/j.ccell.2021.02.008
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Article ; Online: Unexpected Acetylation of Endogenous Aliphatic Amines by Arylamine N-Acetyltransferase NAT2.

Conway, Louis P / Rendo, Veronica / Correia, Mário S P / Bergdahl, Ingvar A / Sjöblom, Tobias / Globisch, Daniel

Angewandte Chemie (International ed. in English)

2020 Volume 59, Issue 34, Page(s) 14342–14346

Abstract: N-Acetyltransferases play critical roles in the deactivation and clearance of xenobiotics, including clinical drugs. NAT2 has been classified as an arylamine N-acetyltransferase that mainly converts aromatic amines, hydroxylamines, and hydrazines. Herein, ...

Abstract	N-Acetyltransferases play critical roles in the deactivation and clearance of xenobiotics, including clinical drugs. NAT2 has been classified as an arylamine N-acetyltransferase that mainly converts aromatic amines, hydroxylamines, and hydrazines. Herein, we demonstrate that the human arylamine N-acetyltransferase NAT2 also acetylates aliphatic endogenous amines. Metabolomic analysis and chemical synthesis revealed increased intracellular concentrations of mono- and diacetylated spermidine in human cell lines expressing the rapid compared to the slow acetylator NAT2 phenotype. The regioselective N
MeSH term(s)	Acetylation ; Amines/metabolism ; Arylamine N-Acetyltransferase/genetics ; Arylamine N-Acetyltransferase/metabolism ; Cell Line, Tumor ; Chromatography, Liquid/methods ; Genotype ; Humans ; Kinetics ; Mass Spectrometry/methods
Chemical Substances	Amines ; Arylamine N-Acetyltransferase (EC 2.3.1.5) ; NAT2 protein, human (EC 2.3.1.5)
Language	English
Publishing date	2020-07-08
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2011836-3
ISSN	1521-3773 ; 1433-7851
ISSN (online)	1521-3773
ISSN	1433-7851
DOI	10.1002/anie.202005915
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Article ; Online: Common and mutation specific phenotypes of KRAS and BRAF mutations in colorectal cancer cells revealed by integrative -omics analysis.

Kundu, Snehangshu / Ali, Muhammad Akhtar / Handin, Niklas / Conway, Louis P / Rendo, Veronica / Artursson, Per / He, Liqun / Globisch, Daniel / Sjöblom, Tobias

Journal of experimental & clinical cancer research : CR

2021 Volume 40, Issue 1, Page(s) 225

Abstract: Background: Genes in the Ras pathway have somatic mutations in at least 60 % of colorectal cancers. Despite activating the same pathway, the BRAF V600E mutation and the prevalent mutations in codon 12 and 13 of KRAS have all been linked to different ... ...

Abstract	Background: Genes in the Ras pathway have somatic mutations in at least 60 % of colorectal cancers. Despite activating the same pathway, the BRAF V600E mutation and the prevalent mutations in codon 12 and 13 of KRAS have all been linked to different clinical outcomes, but the molecular mechanisms behind these differences largely remain to be clarified. Methods: To characterize the similarities and differences between common activating KRAS mutations and between KRAS and BRAF mutations, we used genome editing to engineer KRAS G12C/D/V and G13D mutations in colorectal cancer cells that had their mutant BRAF V600E allele removed and subjected them to transcriptome sequencing, global proteomics and metabolomics analyses. Results: By intersecting differentially expressed genes, proteins and metabolites, we uncovered (i) two-fold more regulated genes and proteins when comparing KRAS to BRAF mutant cells to those lacking Ras pathway mutation, (ii) five differentially expressed proteins in KRAS mutants compared to cells lacking Ras pathway mutation (IFI16, S100A10, CD44, GLRX and AHNAK2) and 6 (CRABP2, FLNA, NXN, LCP1, S100A10 and S100A2) compared to BRAF mutant cells, (iii) 19 proteins expressed differentially in a KRAS mutation specific manner versus BRAF V600E cells, (iv) regulation of the Integrin Linked Kinase pathway by KRAS but not BRAF mutation, (v) regulation of amino acid metabolism, particularly of the tyrosine, histidine, arginine and proline pathways, the urea cycle and purine metabolism by Ras pathway mutations, (vi) increased free carnitine in KRAS and BRAF mutant RKO cells. Conclusions: This comprehensive integrative -omics analysis confirms known and adds novel genes, proteins and metabolic pathways regulated by mutant KRAS and BRAF signaling in colorectal cancer. The results from the new model systems presented here can inform future development of diagnostic and therapeutic approaches targeting tumors with KRAS and BRAF mutations.
MeSH term(s)	Colorectal Neoplasms/genetics ; Colorectal Neoplasms/metabolism ; Colorectal Neoplasms/pathology ; Humans ; Mutation ; Phenotype ; Proto-Oncogene Proteins B-raf/genetics ; Proto-Oncogene Proteins B-raf/metabolism ; Proto-Oncogene Proteins p21(ras)/genetics ; Proto-Oncogene Proteins p21(ras)/metabolism
Chemical Substances	KRAS protein, human ; BRAF protein, human (EC 2.7.11.1) ; Proto-Oncogene Proteins B-raf (EC 2.7.11.1) ; Proto-Oncogene Proteins p21(ras) (EC 3.6.5.2)
Language	English
Publishing date	2021-07-07
Publishing country	England
Document type	Journal Article
ZDB-ID	803138-1
ISSN	1756-9966 ; 0392-9078
ISSN (online)	1756-9966
ISSN	0392-9078
DOI	10.1186/s13046-021-02025-2
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Article: TIRR inhibits the 53BP1-p53 complex to alter cell-fate programs

Parnandi, Nishita / Rendo, Veronica / Cui, Gaofeng / Botuyan, Maria Victoria / Remisova, Michaela / Nguyen, Huy / Drané, Pascal / Beroukhim, Rameen / Altmeyer, Matthias / Mer, Georges / Chowdhury, Dipanjan

Molecular cell. 2021 June 17, v. 81, no. 12

2021

Abstract: 53BP1 influences genome stability via two independent mechanisms: (1) regulating DNA double-strand break (DSB) repair and (2) enhancing p53 activity. We discovered a protein, Tudor-interacting repair regulator (TIRR), that associates with the 53BP1 Tudor ...

Abstract	53BP1 influences genome stability via two independent mechanisms: (1) regulating DNA double-strand break (DSB) repair and (2) enhancing p53 activity. We discovered a protein, Tudor-interacting repair regulator (TIRR), that associates with the 53BP1 Tudor domain and prevents its recruitment to DSBs. Here, we elucidate how TIRR affects 53BP1 function beyond its recruitment to DSBs and biochemically links the two distinct roles of 53BP1. Loss of TIRR causes an aberrant increase in the gene transactivation function of p53, affecting several p53-mediated cell-fate programs. TIRR inhibits the complex formation between the Tudor domain of 53BP1 and a dimethylated form of p53 (K382me2) that is poised for transcriptional activation of its target genes. TIRR mRNA expression levels negatively correlate with the expression of key p53 target genes in breast and prostate cancers. Further, TIRR loss is selectively not tolerated in p53-proficient tumors. Therefore, we establish that TIRR is an important inhibitor of the 53BP1-p53 complex.
Keywords	DNA ; breasts ; gene expression ; genes ; transcriptional activation
Language	English
Dates of publication	2021-0617
Size	p. 2583-2595.e6.
Publishing place	Elsevier Inc.
Document type	Article
ZDB-ID	1415236-8
ISSN	1097-4164 ; 1097-2765
ISSN (online)	1097-4164
ISSN	1097-2765
DOI	10.1016/j.molcel.2021.03.039
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Article ; Online: Cancer aneuploidies are shaped primarily by effects on tumour fitness.

Shih, Juliann / Sarmashghi, Shahab / Zhakula-Kostadinova, Nadja / Zhang, Shu / Georgis, Yohanna / Hoyt, Stephanie H / Cuoco, Michael S / Gao, Galen F / Spurr, Liam F / Berger, Ashton C / Ha, Gavin / Rendo, Veronica / Shen, Hui / Meyerson, Matthew / Cherniack, Andrew D / Taylor, Alison M / Beroukhim, Rameen

Nature

2023 Volume 619, Issue 7971, Page(s) 793–800

Abstract: Aneuploidies-whole-chromosome or whole-arm imbalances-are the most prevalent alteration in cancer ... ...

Abstract	Aneuploidies-whole-chromosome or whole-arm imbalances-are the most prevalent alteration in cancer genomes
MeSH term(s)	Humans ; Aneuploidy ; Cell Transformation, Neoplastic/genetics ; DNA Copy Number Variations/genetics ; Neoplasms/genetics ; Neoplasms/pathology ; Oncogenes/genetics ; Telomere/genetics ; Centromere/genetics ; Cell Lineage ; Chromosomes, Human, Pair 8/genetics ; Genes, Tumor Suppressor
Chemical Substances	WRN protein, human (EC 3.6.4.12)
Language	English
Publishing date	2023-06-28
Publishing country	England
Document type	Journal Article
ZDB-ID	120714-3
ISSN	1476-4687 ; 0028-0836
ISSN (online)	1476-4687
ISSN	0028-0836
DOI	10.1038/s41586-023-06266-3
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Article ; Online: Enhanced cytotoxicity of a novel family of ATPase inhibitors in colorectal cancer cells with high NAT2 activity.

Zhang, Xiaonan / Akcan, Ece / Correia, Mario / Rameika, Natallia / Kundu, Snehangshu / Stoimenov, Ivaylo / Rendo, Veronica / Eriksson, Anna U / Haraldsson, Martin / Globisch, Daniel / Sjöblom, Tobias

Biochemical pharmacology

2022 Volume 203, Page(s) 115184

Abstract: Loss of heterozygosity (LOH) is a hallmark feature of cancer genomes that reduces allelic variation, thereby creating tumor specific vulnerabilities which could be exploited for therapeutic purposes. We previously reported that loss of drug metabolic ... ...

Abstract	Loss of heterozygosity (LOH) is a hallmark feature of cancer genomes that reduces allelic variation, thereby creating tumor specific vulnerabilities which could be exploited for therapeutic purposes. We previously reported that loss of drug metabolic arylamine N-acetyltransferase 2 (NAT2) activity following LOH at 8p22 could be targeted for collateral lethality anticancer therapy in colorectal cancer (CRC). Here, we report a novel compound CBK034026C that exhibits specific toxicity towards CRC cells with high NAT2 activity. Connectivity Map analysis revealed that CBK034026C elicited a response pattern related to ATPase inhibitors. Similar to ouabain, a potent inhibitor of the Na
MeSH term(s)	Acetyltransferases/genetics ; Adenosine Triphosphatases ; Alleles ; Antineoplastic Agents/pharmacology ; Arylamine N-Acetyltransferase/genetics ; Arylamine N-Acetyltransferase/metabolism ; Colorectal Neoplasms/drug therapy ; Colorectal Neoplasms/genetics ; Humans
Chemical Substances	Antineoplastic Agents ; Acetyltransferases (EC 2.3.1.-) ; Arylamine N-Acetyltransferase (EC 2.3.1.5) ; NAT2 protein, human (EC 2.3.1.5) ; Adenosine Triphosphatases (EC 3.6.1.-)
Language	English
Publishing date	2022-07-22
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	208787-x
ISSN	1873-2968 ; 0006-2952
ISSN (online)	1873-2968
ISSN	0006-2952
DOI	10.1016/j.bcp.2022.115184
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Article ; Online: Defining eligible patients for allele-selective chemotherapies targeting NAT2 in colorectal cancer.

Rendo, Veronica / Kundu, Snehangshu / Rameika, Natallia / Ljungström, Viktor / Svensson, Richard / Palin, Kimmo / Aaltonen, Lauri / Stoimenov, Ivaylo / Sjöblom, Tobias

Scientific reports

2020 Volume 10, Issue 1, Page(s) 22436

Abstract: Therapies targeting somatic bystander genetic events represent a new avenue for cancer treatment. We recently identified a subset of colorectal cancer (CRC) patients who are heterozygous for a wild-type and a low activity allele (NAT2*6) but lack the ... ...

Abstract	Therapies targeting somatic bystander genetic events represent a new avenue for cancer treatment. We recently identified a subset of colorectal cancer (CRC) patients who are heterozygous for a wild-type and a low activity allele (NAT26) but lack the wild-type allele in their tumors due to loss of heterozygosity (LOH) at 8p22. These tumors were sensitive to treatment with a cytotoxic substrate of NAT2 (6-(4-aminophenyl)-N-(3,4,5-trimethoxyphenyl)pyrazin-2-amine, APA), and pointed to NAT2 loss being a therapeutically exploitable vulnerability of CRC tumors. To better estimate the total number of treatable CRC patients, we here determined whether tumor cells retaining also other NAT2 low activity variants after LOH respond to APA treatment. The prevalent low activity alleles NAT25 and NAT214, but not NAT27, were found to be low metabolizers with high sensitivity to APA. By analysis of two different CRC patient cohorts, we detected heterozygosity for NAT2 alleles targetable by APA, along with allelic imbalances pointing to LOH, in ~ 24% of tumors. Finally, to haplotype the NAT2 locus in tumor and patient-matched normal samples in a clinical setting, we develop and demonstrate a long-read sequencing based assay. In total, > 79.000 CRC patients per year fulfil genetic criteria for high sensitivity to a NAT2 LOH therapy and their eligibility can be assessed by clinical sequencing.
MeSH term(s)	Alleles ; Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Arylamine N-Acetyltransferase/antagonists & inhibitors ; Arylamine N-Acetyltransferase/genetics ; Cell Line, Tumor ; Cell Survival/drug effects ; Cell Survival/genetics ; Colorectal Neoplasms/drug therapy ; Colorectal Neoplasms/genetics ; Enzyme Inhibitors/pharmacology ; Enzyme Inhibitors/therapeutic use ; Gene Frequency ; Haplotypes ; High-Throughput Nucleotide Sequencing ; Humans ; Molecular Targeted Therapy ; Phenotype ; Single Molecule Imaging
Chemical Substances	Antineoplastic Agents ; Enzyme Inhibitors ; Arylamine N-Acetyltransferase (EC 2.3.1.5) ; NAT2 protein, human (EC 2.3.1.5)
Language	English
Publishing date	2020-12-31
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-020-80288-z
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