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Article: MTBP and MYC: A Dynamic Duo in Proliferation, Cancer, and Aging.

Grieb, Brian C / Eischen, Christine M

2022 Volume 11, Issue 6

Abstract: The oncogenic transcription factor c-MYC (MYC) is highly conserved across species and is frequently overexpressed or dysregulated in human cancers. MYC regulates a wide range of critical cellular and oncogenic activities including proliferation, ... ...

Abstract	The oncogenic transcription factor c-MYC (MYC) is highly conserved across species and is frequently overexpressed or dysregulated in human cancers. MYC regulates a wide range of critical cellular and oncogenic activities including proliferation, metabolism, metastasis, apoptosis, and differentiation by transcriptionally activating or repressing the expression of a large number of genes. This activity of MYC is not carried out in isolation, instead relying on its association with a myriad of protein cofactors. We determined that MDM Two Binding Protein (MTBP) indirectly binds MYC and is a novel MYC transcriptional cofactor. MTBP promotes MYC-mediated transcriptional activity, proliferation, and cellular transformation by binding in a protein complex with MYC at MYC-bound promoters. This discovery provided critical context for data linking MTBP to aging as well as a rapidly expanding body of evidence demonstrating MTBP is overexpressed in many human malignancies, is often linked to poor patient outcomes, and is necessary for cancer cell survival. As such, MTBP represents a novel and potentially broad reaching oncologic drug target, particularly when MYC is dysregulated. Here we have reviewed the discovery of MTBP and the initial controversy with its function as well as its associations with proliferation, MYC, DNA replication, aging, and human cancer.
Language	English
Publishing date	2022-06-08
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2661517-4
ISSN	2079-7737
ISSN	2079-7737
DOI	10.3390/biology11060881
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Decoding the lncRNAome Across Diverse Cellular Stresses Reveals Core p53-effector Pan-cancer Suppressive lncRNAs.

Mitra, Ramkrishna / Adams, Clare M / Eischen, Christine M

Cancer research communications

2023 Volume 3, Issue 5, Page(s) 842–859

Abstract: Despite long non-coding RNAs (lncRNAs) emerging as key contributors to malignancies, their transcriptional regulation, tissue-type expression under different conditions, and functions remain largely unknown. Developing a combined computational and ... ...

Abstract	Despite long non-coding RNAs (lncRNAs) emerging as key contributors to malignancies, their transcriptional regulation, tissue-type expression under different conditions, and functions remain largely unknown. Developing a combined computational and experimental framework, which integrates pan-cancer RNAi/CRISPR screens, and genomic, epigenetic, and expression profiles (including single-cell RNA sequencing), we report across multiple cancers, core p53-transcriptionally regulated lncRNAs, which were thought to be primarily cell/tissue-specific. These lncRNAs were consistently directly transactivated by p53 with different cellular stresses in multiple cell types and associated with pan-cancer cell survival/growth suppression and patient survival. Our prediction results were verified through independent validation datasets, our own patient cohort, and cancer cell experiments. Moreover, a top predicted p53-effector tumor-suppressive lncRNA (we termed Significance: Identification of pan-cancer suppressive lncRNAs transcriptionally regulated by p53 across different cellular stresses by integrating multilayered high-throughput molecular profiles. This study provides critical new insights into the p53 tumor suppressor by revealing the lncRNAs in the p53 cell-cycle regulatory network and their impact on cancer cell growth and patient survival.
MeSH term(s)	Humans ; RNA, Long Noncoding/genetics ; Tumor Suppressor Protein p53/genetics ; Gene Expression Regulation, Neoplastic/genetics ; Neoplasms/genetics ; Carcinogenesis/genetics ; Cell Transformation, Neoplastic/genetics
Chemical Substances	RNA, Long Noncoding ; Tumor Suppressor Protein p53
Language	English
Publishing date	2023-05-11
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ISSN	2767-9764
ISSN (online)	2767-9764
DOI	10.1158/2767-9764.CRC-22-0473
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Systematic lncRNA mapping to genome-wide co-essential modules uncovers cancer dependency on uncharacterized lncRNAs.

Mitra, Ramkrishna / Adams, Clare M / Eischen, Christine M

eLife

2022 Volume 11

Abstract: Quantification of gene dependency across hundreds of cell lines using genome-scale CRISPR screens has revealed co-essential pathways/modules and critical functions of uncharacterized genes. In contrast to protein-coding genes, robust CRISPR-based loss-of- ...

Abstract	Quantification of gene dependency across hundreds of cell lines using genome-scale CRISPR screens has revealed co-essential pathways/modules and critical functions of uncharacterized genes. In contrast to protein-coding genes, robust CRISPR-based loss-of-function screens are lacking for long noncoding RNAs (lncRNAs), which are key regulators of many cellular processes, leaving many essential lncRNAs unidentified and uninvestigated. Integrating copy number, epigenetic, and transcriptomic data of >800 cancer cell lines with CRISPR-derived co-essential pathways, our method recapitulates known essential lncRNAs and predicts proliferation/growth dependency of 289 poorly characterized lncRNAs. Analyzing lncRNA dependencies across 10 cancer types and their expression alteration by diverse growth inhibitors across cell types, we prioritize 30 high-confidence pan-cancer proliferation/growth-regulating lncRNAs. Further evaluating two previously uncharacterized top
MeSH term(s)	Gene Regulatory Networks ; Humans ; Neoplasms/genetics ; RNA, Long Noncoding/genetics ; Transcriptome
Chemical Substances	RNA, Long Noncoding
Language	English
Publishing date	2022-06-13
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2687154-3
ISSN	2050-084X ; 2050-084X
ISSN (online)	2050-084X
ISSN	2050-084X
DOI	10.7554/eLife.77357
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Article ; Online: Role of Mdm2 and Mdmx in DNA repair.

Eischen, Christine M

Journal of molecular cell biology

2017 Volume 9, Issue 1, Page(s) 69–73

Abstract: Mdm2 and Mdmx are critical regulators of the p53 tumour suppressor and are overexpressed in many human malignancies. However, in recent years, their impact on genome instability was shown to be at least, in part, independent of p53. Both Mdm2 and Mdmx ... ...

Abstract	Mdm2 and Mdmx are critical regulators of the p53 tumour suppressor and are overexpressed in many human malignancies. However, in recent years, their impact on genome instability was shown to be at least, in part, independent of p53. Both Mdm2 and Mdmx inhibit DNA break repair through their association with the Mre11/Rad50/Nbs1 DNA repair complex. Recent evidence indicates that harnessing Mdm2 and/or Mdmx-mediated inhibition of DNA break repair in cancer cells could provide a therapeutic opportunity, particularly for those malignancies that have lost functional p53.
MeSH term(s)	Animals ; DNA Repair ; Genomic Instability ; Humans ; Models, Biological ; Neoplasms/metabolism ; Neoplasms/therapy ; Proto-Oncogene Proteins c-mdm2/metabolism ; Tumor Suppressor Protein p53/metabolism
Chemical Substances	Tumor Suppressor Protein p53 ; Proto-Oncogene Proteins c-mdm2 (EC 2.3.2.27)
Language	English
Publishing date	2017-02-01
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2500949-7
ISSN	1759-4685 ; 1674-2788
ISSN (online)	1759-4685
ISSN	1674-2788
DOI	10.1093/jmcb/mjw052
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Article ; Online: Genome Stability Requires p53.

Eischen, Christine M

Cold Spring Harbor perspectives in medicine

2016 Volume 6, Issue 6

Abstract: It is now clear that functional p53 is critical to protect the genome from alterations that lead to tumorigenesis. However, with the myriad of cellular stresses and pathways linked to p53 activation, much remains unknown about how p53 maintains genome ... ...

Abstract	It is now clear that functional p53 is critical to protect the genome from alterations that lead to tumorigenesis. However, with the myriad of cellular stresses and pathways linked to p53 activation, much remains unknown about how p53 maintains genome stability and the proteins involved. The current understanding of the multiple ways p53 contributes to genome stability and how two of its negative regulators, Mdm2 and Mdmx, induce genome instability will be described.
MeSH term(s)	Animals ; Cell Transformation, Neoplastic ; DNA Damage ; Gene Amplification ; Genomic Instability ; Humans ; Mice ; MicroRNAs/genetics ; Mutation ; Nuclear Proteins/genetics ; Nuclear Proteins/metabolism ; Proto-Oncogene Proteins/genetics ; Proto-Oncogene Proteins/metabolism ; Proto-Oncogene Proteins c-mdm2/genetics ; Proto-Oncogene Proteins c-mdm2/metabolism ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism
Chemical Substances	MDM4 protein, human ; MicroRNAs ; Nuclear Proteins ; Proto-Oncogene Proteins ; TP53 protein, human ; Tumor Suppressor Protein p53 ; MDM2 protein, human (EC 2.3.2.27) ; Proto-Oncogene Proteins c-mdm2 (EC 2.3.2.27)
Language	English
Publishing date	2016-06-01
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural
ISSN	2157-1422
ISSN (online)	2157-1422
DOI	10.1101/cshperspect.a026096
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Article ; Online: Systematic lncRNA mapping to genome-wide co-essential modules uncovers cancer dependency on uncharacterized lncRNAs

Ramkrishna Mitra / Clare M Adams / Christine M Eischen

eLife, Vol

2022 Volume 11

Abstract	Quantification of gene dependency across hundreds of cell lines using genome-scale CRISPR screens has revealed co-essential pathways/modules and critical functions of uncharacterized genes. In contrast to protein-coding genes, robust CRISPR-based loss-of-function screens are lacking for long noncoding RNAs (lncRNAs), which are key regulators of many cellular processes, leaving many essential lncRNAs unidentified and uninvestigated. Integrating copy number, epigenetic, and transcriptomic data of >800 cancer cell lines with CRISPR-derived co-essential pathways, our method recapitulates known essential lncRNAs and predicts proliferation/growth dependency of 289 poorly characterized lncRNAs. Analyzing lncRNA dependencies across 10 cancer types and their expression alteration by diverse growth inhibitors across cell types, we prioritize 30 high-confidence pan-cancer proliferation/growth-regulating lncRNAs. Further evaluating two previously uncharacterized top proliferation-suppressive lncRNAs (PSLR-1, PSLR-2) showed they are transcriptionally regulated by p53, induced by multiple cancer treatments, and significantly correlate to increased cancer patient survival. These lncRNAs modulate G2 cell cycle-regulating genes within the FOXM1 transcriptional network, inducing a G2 arrest and inhibiting proliferation and colony formation. Collectively, our results serve as a powerful resource for exploring lncRNA-mediated regulation of cellular fitness in cancer, circumventing current limitations in lncRNA research.
Keywords	cancer dependency ; co-essential networks ; long non-coding RNA ; proliferation ; cell cycle ; Medicine ; R ; Science ; Q ; Biology (General) ; QH301-705.5
Subject code	610
Language	English
Publishing date	2022-06-01T00:00:00Z
Publisher	eLife Sciences Publications Ltd
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: MTBP and MYC

Brian C. Grieb / Christine M. Eischen

Biology, Vol 11, Iss 881, p

A Dynamic Duo in Proliferation, Cancer, and Aging

2022 Volume 881

Abstract	The oncogenic transcription factor c-MYC (MYC) is highly conserved across species and is frequently overexpressed or dysregulated in human cancers. MYC regulates a wide range of critical cellular and oncogenic activities including proliferation, metabolism, metastasis, apoptosis, and differentiation by transcriptionally activating or repressing the expression of a large number of genes. This activity of MYC is not carried out in isolation, instead relying on its association with a myriad of protein cofactors. We determined that MDM Two Binding Protein (MTBP) indirectly binds MYC and is a novel MYC transcriptional cofactor. MTBP promotes MYC-mediated transcriptional activity, proliferation, and cellular transformation by binding in a protein complex with MYC at MYC-bound promoters. This discovery provided critical context for data linking MTBP to aging as well as a rapidly expanding body of evidence demonstrating MTBP is overexpressed in many human malignancies, is often linked to poor patient outcomes, and is necessary for cancer cell survival. As such, MTBP represents a novel and potentially broad reaching oncologic drug target, particularly when MYC is dysregulated. Here we have reviewed the discovery of MTBP and the initial controversy with its function as well as its associations with proliferation, MYC, DNA replication, aging, and human cancer.
Keywords	MTBP ; MYC ; proliferation ; cancer ; transcription ; aging ; Biology (General) ; QH301-705.5
Subject code	500
Language	English
Publishing date	2022-06-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article: MTBP and MYC: A Dynamic Duo in Proliferation, Cancer, and Aging

Grieb, Brian C. / Eischen, Christine M.

Biology. 2022 June 08, v. 11, no. 6

2022

Abstract	The oncogenic transcription factor c-MYC (MYC) is highly conserved across species and is frequently overexpressed or dysregulated in human cancers. MYC regulates a wide range of critical cellular and oncogenic activities including proliferation, metabolism, metastasis, apoptosis, and differentiation by transcriptionally activating or repressing the expression of a large number of genes. This activity of MYC is not carried out in isolation, instead relying on its association with a myriad of protein cofactors. We determined that MDM Two Binding Protein (MTBP) indirectly binds MYC and is a novel MYC transcriptional cofactor. MTBP promotes MYC-mediated transcriptional activity, proliferation, and cellular transformation by binding in a protein complex with MYC at MYC-bound promoters. This discovery provided critical context for data linking MTBP to aging as well as a rapidly expanding body of evidence demonstrating MTBP is overexpressed in many human malignancies, is often linked to poor patient outcomes, and is necessary for cancer cell survival. As such, MTBP represents a novel and potentially broad reaching oncologic drug target, particularly when MYC is dysregulated. Here we have reviewed the discovery of MTBP and the initial controversy with its function as well as its associations with proliferation, MYC, DNA replication, aging, and human cancer.
Keywords	DNA replication ; apoptosis ; cell viability ; drugs ; humans ; metabolism ; metastasis ; neoplasm cells ; patients ; transcription (genetics) ; transcription factors
Language	English
Dates of publication	2022-0608
Publishing place	Multidisciplinary Digital Publishing Institute
Document type	Article
ZDB-ID	2661517-4
ISSN	2079-7737
ISSN	2079-7737
DOI	10.3390/biology11060881
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Engaging community members in cancer research: an assessment of an NCI-designated cancer center.

Leader, Amy E / Melillo, Rebecca J / Greene, Quincy / Blanding-Godbolt, Joshua / Shimada, Ayako / Eischen, Christine M / Aplin, Andrew E

Cancer causes & control : CCC

2023 Volume 34, Issue 4, Page(s) 307–319

Abstract: ... in research will help the SKCC address cancer disparities in the catchment area" (M 4.2, SD 0.9) and less ... in my research" (M 2.5, SD 1.3). Investigators mentioned challenges in communicating complex science to a lay ...

Abstract	Purpose: Despite the importance of engaging community members in research, multiple barriers exist. We conducted a mixed-methods evaluation to understand the opportunities and challenges of engaging community members in basic, clinical, translational, and population science research. Methods: We designed a survey and an interview guide based on the constructs of the Consolidated Framework for Implementation Research. Surveys were distributed electronically to all cancer center investigators and interviews were conducted virtually with a select group of basic, clinical, and population science investigators. Survey data (n = 77) were analyzed across all respondents using frequency counts and mean scores; bivariate analyses examined differences in responses by research program affiliation, gender, race, and faculty rank. Interviews (n = 16) were audio recorded, transcribed verbatim, and analyzed using a reflective thematic approach. Results: There was strong agreement among investigators that "Community engagement in research will help the SKCC address cancer disparities in the catchment area" (M 4.2, SD 0.9) and less agreement with items such as "I know how to find and connect with community members who I can engage in my research" (M 2.5, SD 1.3). Investigators mentioned challenges in communicating complex science to a lay audience but were open to training and workshops to acquire skills needed to integrate community members into their research. Conclusion: Cancer centers should develop and promote training and collaborative opportunities for investigators and community members. Overcoming challenges will lead to more patient- and community-centered cancer research in the future.
MeSH term(s)	Humans ; Research Design ; Neoplasms/therapy
Language	English
Publishing date	2023-01-04
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	1064022-8
ISSN	1573-7225 ; 0957-5243
ISSN (online)	1573-7225
ISSN	0957-5243
DOI	10.1007/s10552-022-01666-8
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Article ; Online: Molecular underpinnings of HDAC inhibition revealed.

Adams, Clare M / Eischen, Christine M

Cell cycle (Georgetown, Tex.)

2016 Volume 15, Issue 15, Page(s) 1943–1944

MeSH term(s)	Apoptosis ; Histone Deacetylase Inhibitors/pharmacology ; Proto-Oncogene Proteins c-bcl-2 ; bcl-X Protein
Chemical Substances	Histone Deacetylase Inhibitors ; Proto-Oncogene Proteins c-bcl-2 ; bcl-X Protein
Language	English
Publishing date	2016-05-06
Publishing country	United States
Document type	Editorial
ZDB-ID	2146183-1
ISSN	1551-4005 ; 1538-4101 ; 1554-8627
ISSN (online)	1551-4005
ISSN	1538-4101 ; 1554-8627
DOI	10.1080/15384101.2016.1184513
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