LIVIVO - Search results -

Search results

Result 1 - 10 of total 94

Search options

Article: CXCR4 Mediates Enhanced Cell Migration in

Fertal, Shelby A / Zaidi, Sayyed K / Stein, Janet L / Stein, Gary S / Heath, Jessica L

2022 Volume 11, Page(s) 708915

Abstract: Leukemia transformed by ... ...

Abstract	Leukemia transformed by the
Language	English
Publishing date	2022-01-05
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2649216-7
ISSN	2234-943X
ISSN	2234-943X
DOI	10.3389/fonc.2021.708915
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

Article ; Online: The role of cell adhesion in hematopoiesis and leukemogenesis.

Heath, Jessica L / Cohn, Gabriel M / Zaidi, Sayyed K / Stein, Gary S

Journal of cellular physiology

2019 Volume 234, Issue 11, Page(s) 19189–19198

Abstract: The cells of the bone marrow microenvironment are emerging as important contributors and regulators of normal hematopoiesis. This microenvironment is perturbed during leukemogenesis, and evidence points toward a bidirectional communication between ... ...

Abstract	The cells of the bone marrow microenvironment are emerging as important contributors and regulators of normal hematopoiesis. This microenvironment is perturbed during leukemogenesis, and evidence points toward a bidirectional communication between leukemia cells and the normal cells of the bone marrow, mediated by direct cell-cell contact as well as soluble factors. These interactions are increasingly appreciated to play a role in leukemogenesis and possibly in resistance to chemotherapy. In fact, several compounds that specifically target the bone marrow microenvironment, including inhibitors of cell adhesion, are being tested as adjuncts to leukemia therapy.
MeSH term(s)	Bone Marrow/metabolism ; Carcinogenesis/genetics ; Cell Adhesion/genetics ; Hematopoiesis/genetics ; Humans ; Leukemia/genetics ; Leukemia/pathology ; Stem Cell Niche/genetics ; Tumor Microenvironment/genetics
Language	English
Publishing date	2019-04-13
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	3116-1
ISSN	1097-4652 ; 0021-9541
ISSN (online)	1097-4652
ISSN	0021-9541
DOI	10.1002/jcp.28636
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Uc I Zs.212: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾

Article ; Online: Epigenetic and transcriptome responsiveness to ER modulation by tissue selective estrogen complexes in breast epithelial and breast cancer cells.

Messier, Terri L / Boyd, Joseph R / Gordon, Jonathan A R / Tye, Coralee E / Page, Natalie A / Toor, Rabail H / Zaidi, Sayyed K / Komm, Barry S / Frietze, Seth / Stein, Janet L / Lian, Jane B / Stein, Gary S

PloS one

2022 Volume 17, Issue 7, Page(s) e0271725

Abstract: Selective estrogen receptor modulators (SERMs), including the SERM/SERD bazedoxifene (BZA), are used to treat postmenopausal osteoporosis and may reduce breast cancer (BCa) risk. One of the most persistent unresolved questions regarding menopausal ... ...

Abstract	Selective estrogen receptor modulators (SERMs), including the SERM/SERD bazedoxifene (BZA), are used to treat postmenopausal osteoporosis and may reduce breast cancer (BCa) risk. One of the most persistent unresolved questions regarding menopausal hormone therapy is compromised control of proliferation and phenotype because of short- or long-term administration of mixed-function estrogen receptor (ER) ligands. To gain insight into epigenetic effectors of the transcriptomes of hormone and BZA-treated BCa cells, we evaluated a panel of histone modifications. The impact of short-term hormone treatment and BZA on gene expression and genome-wide epigenetic profiles was examined in ERαneg mammary epithelial cells (MCF10A) and ERα+ luminal breast cancer cells (MCF7). We tested individual components and combinations of 17β-estradiol (E2), estrogen compounds (EC10) and BZA. RNA-seq for gene expression and ChIP-seq for active (H3K4me3, H3K4ac, H3K27ac) and repressive (H3K27me3) histone modifications were performed. Our results show that the combination of BZA with E2 or EC10 reduces estrogen-mediated patterns of histone modifications and gene expression in MCF-7ERα+ cells. In contrast, BZA has minimal effects on these parameters in MCF10A mammary epithelial cells. BZA-induced changes in histone modifications in MCF7 cells are characterized by altered H3K4ac patterns, with changes at distal enhancers of ERα-target genes and at promoters of non-ERα bound proliferation-related genes. Notably, the ERα target gene GREB1 is the most sensitive to BZA treatment. Our findings provide direct mechanistic-based evidence that BZA induces epigenetic changes in E2 and EC10 mediated control of ERα regulatory programs to target distinctive proliferation gene pathways that restrain the potential for breast cancer development.
MeSH term(s)	Breast Neoplasms/drug therapy ; Breast Neoplasms/genetics ; Breast Neoplasms/metabolism ; Epigenesis, Genetic ; Estrogen Receptor alpha/genetics ; Estrogen Receptor alpha/metabolism ; Estrogens/pharmacology ; Estrogens, Conjugated (USP)/pharmacology ; Female ; Humans ; Receptors, Estrogen/genetics ; Receptors, Estrogen/metabolism ; Selective Estrogen Receptor Modulators/pharmacology ; Transcriptome
Chemical Substances	Estrogen Receptor alpha ; Estrogens ; Estrogens, Conjugated (USP) ; Receptors, Estrogen ; Selective Estrogen Receptor Modulators
Language	English
Publishing date	2022-07-21
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2267670-3
ISSN	1932-6203 ; 1932-6203
ISSN (online)	1932-6203
ISSN	1932-6203
DOI	10.1371/journal.pone.0271725
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article: Mitotic Gene Bookmarking: An Epigenetic Mechanism for Coordination of Lineage Commitment, Cell Identity and Cell Growth.

Zaidi, Sayyed K / Lian, Jane B / van Wijnen, Andre / Stein, Janet L / Stein, Gary S

Advances in experimental medicine and biology

2017 Volume 962, Page(s) 95–102

Abstract: Epigenetic control of gene expression contributes to dynamic responsiveness of cellular processes that include cell cycle, cell growth and differentiation. Mitotic gene bookmarking, retention of sequence-specific transcription factors at target gene loci, ...

Abstract	Epigenetic control of gene expression contributes to dynamic responsiveness of cellular processes that include cell cycle, cell growth and differentiation. Mitotic gene bookmarking, retention of sequence-specific transcription factors at target gene loci, including the RUNX regulatory proteins, provide a novel dimension to epigenetic regulation that sustains cellular identity in progeny cells following cell division. Runx transcription factor retention during mitosis coordinates physiological control of cell growth and differentiation in a broad spectrum of biological conditions, and is associated with compromised gene expression in pathologies that include cancer.
MeSH term(s)	Animals ; Cell Cycle/genetics ; Cell Differentiation/genetics ; Cell Lineage/genetics ; Cell Proliferation/genetics ; Epigenesis, Genetic/genetics ; Gene Expression/genetics ; Humans ; Mitosis/genetics
Language	English
Publishing date	2017-07-20
Publishing country	United States
Document type	Journal Article ; Review
ISSN	2214-8019 ; 0065-2598
ISSN (online)	2214-8019
ISSN	0065-2598
DOI	10.1007/978-981-10-3233-2_7
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: Inhibition of the RUNX1-CBFβ transcription factor complex compromises mammary epithelial cell identity: a phenotype potentially stabilized by mitotic gene bookmarking.

Rose, Joshua T / Moskovitz, Eliana / Boyd, Joseph R / Gordon, Jonathan A / Bouffard, Nicole A / Fritz, Andrew J / Illendula, Anuradha / Bushweller, John H / Lian, Jane B / Stein, Janet L / Zaidi, Sayyed K / Stein, Gary S

Oncotarget

2020 Volume 11, Issue 26, Page(s) 2512–2530

Abstract: RUNX1 has recently been shown to play an important role in determination of mammary epithelial cell identity. However, mechanisms by which loss of the RUNX1 transcription factor in mammary epithelial cells leads to epithelial-to-mesenchymal transition ( ... ...

Abstract	RUNX1 has recently been shown to play an important role in determination of mammary epithelial cell identity. However, mechanisms by which loss of the RUNX1 transcription factor in mammary epithelial cells leads to epithelial-to-mesenchymal transition (EMT) are not known. Here, we report that interaction between RUNX1 and its heterodimeric partner CBFβ is essential for sustaining mammary epithelial cell identity. Disruption of RUNX1-CBFβ interaction, DNA binding, and association with mitotic chromosomes alters cell morphology, global protein synthesis, and phenotype-related gene expression. During interphase, RUNX1 is organized as punctate, predominantly nuclear, foci that are dynamically redistributed during mitosis, with a subset localized to mitotic chromosomes. Genome-wide RUNX1 occupancy profiles for asynchronous, mitotically enriched, and early G1 breast epithelial cells reveal RUNX1 associates with RNA Pol II-transcribed protein coding and long non-coding RNA genes and RNA Pol I-transcribed ribosomal genes critical for mammary epithelial proliferation, growth, and phenotype maintenance. A subset of these genes remains occupied by the protein during the mitosis to G1 transition. Together, these findings establish that the RUNX1-CBFβ complex is required for maintenance of the normal mammary epithelial phenotype and its disruption leads to EMT. Importantly, our results suggest, for the first time, that RUNX1 mitotic bookmarking of a subset of epithelial-related genes may be an important epigenetic mechanism that contributes to stabilization of the mammary epithelial cell identity.
Language	English
Publishing date	2020-06-30
Publishing country	United States
Document type	Journal Article
ZDB-ID	2560162-3
ISSN	1949-2553 ; 1949-2553
ISSN (online)	1949-2553
ISSN	1949-2553
DOI	10.18632/oncotarget.27637
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: Mitotic Gene Bookmarking: An Epigenetic Program to Maintain Normal and Cancer Phenotypes.

Zaidi, Sayyed K / Nickerson, Jeffrey A / Imbalzano, Anthony N / Lian, Jane B / Stein, Janet L / Stein, Gary S

Molecular cancer research : MCR

2018 Volume 16, Issue 11, Page(s) 1617–1624

Abstract: Reconfiguration of nuclear structure and function during mitosis presents a significant challenge to resume the next cell cycle in the progeny cells without compromising structural and functional identity of the cells. Equally important is the ... ...

Abstract	Reconfiguration of nuclear structure and function during mitosis presents a significant challenge to resume the next cell cycle in the progeny cells without compromising structural and functional identity of the cells. Equally important is the requirement for cancer cells to retain the transformed phenotype, that is, unrestricted proliferative potential, suppression of cell phenotype, and activation of oncogenic pathways. Mitotic gene bookmarking retention of key regulatory proteins that include sequence-specific transcription factors, chromatin-modifying factors, and components of RNA Pol (RNAP) I and II regulatory machineries at gene loci on mitotic chromosomes plays key roles in coordinate control of cell phenotype, growth, and proliferation postmitotically. There is growing recognition that three distinct protein types, mechanistically, play obligatory roles in mitotic gene bookmarking: (i) Retention of phenotypic transcription factors on mitotic chromosomes is essential to sustain lineage commitment; (ii) Select chromatin modifiers and posttranslational histone modifications/variants retain competency of mitotic chromatin for gene reactivation as cells exit mitosis; and (iii) Functional components of RNAP I and II transcription complexes (e.g., UBF and TBP, respectively) are retained on genes poised for reactivation immediately following mitosis. Importantly, recent findings have identified oncogenes that are associated with target genes on mitotic chromosomes in cancer cells. The current review proposes that mitotic gene bookmarking is an extensively utilized epigenetic mechanism for stringent control of proliferation and identity in normal cells and hypothesizes that bookmarking plays a pivotal role in maintenance of tumor phenotypes, that is, unrestricted proliferation and compromised control of differentiation.
MeSH term(s)	Cell Differentiation ; Epigenesis, Genetic ; Humans ; Mitosis/genetics ; Neoplasms/genetics ; Neoplasms/pathology ; Phenotype
Language	English
Publishing date	2018-07-12
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2098788-2
ISSN	1557-3125 ; 1541-7786
ISSN (online)	1557-3125
ISSN	1541-7786
DOI	10.1158/1541-7786.MCR-18-0415
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Zs.A 5744: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (2.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾

Article ; Online: Unique Regulatory Mechanisms for the Human Embryonic Stem Cell Cycle.

VanOudenhove, Jennifer J / Grandy, Rodrigo A / Ghule, Prachi N / Lian, Jane B / Stein, Janet L / Zaidi, Sayyed K / Stein, Gary S

Journal of cellular physiology

2017 Volume 232, Issue 6, Page(s) 1254–1257

Abstract: The cell cycle in pluripotent human embryonic stem cells is governed by unique mechanisms that support unrestricted proliferation and competency for endodermal, mesodermal, and ectodermal differentiation. The abbreviated G1 period with retention of ... ...

Abstract	The cell cycle in pluripotent human embryonic stem cells is governed by unique mechanisms that support unrestricted proliferation and competency for endodermal, mesodermal, and ectodermal differentiation. The abbreviated G1 period with retention of uncompromised fidelity for genetic and epigenetic mechanisms operative in control of proliferation support competency for expansion of the pluripotent cell population that is fundamental for initial stages of development. Regulatory events during the G1 period of the pluripotent cell cycle are decisive for the transition from pluripotency to lineage commitment. Recent findings indicate that a G2 cell cycle pause is present in both endodermal and mesodermal lineage cells, and is obligatory for differentiation to endoderm. J. Cell. Physiol. 232: 1254-1257, 2017. © 2016 Wiley Periodicals, Inc.
MeSH term(s)	Cell Cycle ; Cell Differentiation ; Cell Lineage ; Human Embryonic Stem Cells/cytology ; Humans ; Models, Biological
Language	English
Publishing date	2017-06
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	3116-1
ISSN	1097-4652 ; 0021-9541
ISSN (online)	1097-4652
ISSN	0021-9541
DOI	10.1002/jcp.25567
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Uc I Zs.212: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾

Article ; Online: Precocious Phenotypic Transcription-Factor Expression During Early Development.

VanOudenhove, Jennifer J / Medina, Ricardo / Ghule, Prachi N / Lian, Jane B / Stein, Janet L / Zaidi, Sayyed K / Stein, Gary S

Journal of cellular biochemistry

2017 Volume 118, Issue 5, Page(s) 953–958

Abstract: A novel role for phenotypic transcription factors in very early differentiation was recently observed and merits further study to elucidate what role this precocious expression may have in development. The RUNX1 transcription factor exhibits selective ... ...

Abstract	A novel role for phenotypic transcription factors in very early differentiation was recently observed and merits further study to elucidate what role this precocious expression may have in development. The RUNX1 transcription factor exhibits selective and transient upregulation during early mesenchymal differentiation. In contrast to phenotype-associated transcriptional control of gene expression to establish and sustain hematopoietic/myeloid lineage identity, precocious expression of RUNX1 is functionally linked to control of an epithelial to mesenchymal transition that is obligatory for development. This early RUNX1 expression spike provides a paradigm for precocious expression of a phenotypic transcription factor that invites detailed mechanistic study to fully understand its biological importance. J. Cell. Biochem. 118: 953-958, 2017. © 2016 Wiley Periodicals, Inc.
Language	English
Publishing date	2017-05
Publishing country	United States
Document type	Journal Article
ZDB-ID	392402-6
ISSN	1097-4644 ; 0730-2312
ISSN (online)	1097-4644
ISSN	0730-2312
DOI	10.1002/jcb.25723
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Zs.A 1114: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾

Article ; Online: RUNX1 and RUNX2 transcription factors function in opposing roles to regulate breast cancer stem cells.

Fritz, Andrew J / Hong, Deli / Boyd, Joseph / Kost, Jason / Finstaad, Kristiaan H / Fitzgerald, Mark P / Hanna, Sebastian / Abuarqoub, Alqassem H / Malik, Miles / Bushweller, John / Tye, Coralee / Ghule, Prachi / Gordon, Jonathan / Frietze, Seth / Zaidi, Sayyed K / Lian, Jane B / Stein, Janet L / Stein, Gary S

Journal of cellular physiology

2020 Volume 235, Issue 10, Page(s) 7261–7272

Abstract: Breast cancer stem cells (BCSCs) are competent to initiate tumor formation and growth and refractory to conventional therapies. Consequently BCSCs are implicated in tumor recurrence. Many signaling cascades associated with BCSCs are critical for ... ...

Abstract	Breast cancer stem cells (BCSCs) are competent to initiate tumor formation and growth and refractory to conventional therapies. Consequently BCSCs are implicated in tumor recurrence. Many signaling cascades associated with BCSCs are critical for epithelial-to-mesenchymal transition (EMT). We developed a model system to mechanistically examine BCSCs in basal-like breast cancer using MCF10AT1 FACS sorted for CD24 (negative/low in BCSCs) and CD44 (positive/high in BCSCs). Ingenuity Pathway Analysis comparing RNA-seq on the CD24
MeSH term(s)	Animals ; Biomarkers, Tumor/genetics ; Biomarkers, Tumor/metabolism ; Breast Neoplasms/genetics ; Breast Neoplasms/metabolism ; Breast Neoplasms/pathology ; Cell Line, Tumor ; Core Binding Factor Alpha 1 Subunit/antagonists & inhibitors ; Core Binding Factor Alpha 1 Subunit/genetics ; Core Binding Factor Alpha 1 Subunit/metabolism ; Core Binding Factor Alpha 2 Subunit/antagonists & inhibitors ; Core Binding Factor Alpha 2 Subunit/genetics ; Core Binding Factor Alpha 2 Subunit/metabolism ; Epithelial-Mesenchymal Transition/genetics ; Female ; Gene Expression Regulation, Neoplastic ; Heterografts ; Humans ; Mice ; Mice, SCID ; Neoplastic Stem Cells/metabolism ; Neoplastic Stem Cells/pathology ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Signal Transduction ; Tumor Microenvironment/genetics
Chemical Substances	Biomarkers, Tumor ; Core Binding Factor Alpha 1 Subunit ; Core Binding Factor Alpha 2 Subunit ; RNA, Messenger ; RUNX1 protein, human ; RUNX2 protein, human
Language	English
Publishing date	2020-03-17
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	3116-1
ISSN	1097-4652 ; 0021-9541
ISSN (online)	1097-4652
ISSN	0021-9541
DOI	10.1002/jcp.29625
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Uc I Zs.212: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾

Article ; Online: An AML1-ETO/miR-29b-1 regulatory circuit modulates phenotypic properties of acute myeloid leukemia cells.

Zaidi, Sayyed K / Perez, Andrew W / White, Elizabeth S / Lian, Jane B / Stein, Janet L / Stein, Gary S

Oncotarget

2017 Volume 8, Issue 25, Page(s) 39994–40005

Abstract: Acute myeloid leukemia (AML) is characterized by an aggressive clinical course and frequent cytogenetic abnormalities that include specific chromosomal translocations. The 8;21 chromosomal rearrangement disrupts the key hematopoietic RUNX1 transcription ... ...

Abstract	Acute myeloid leukemia (AML) is characterized by an aggressive clinical course and frequent cytogenetic abnormalities that include specific chromosomal translocations. The 8;21 chromosomal rearrangement disrupts the key hematopoietic RUNX1 transcription factor, and contributes to leukemia through recruitment of co-repressor complexes to RUNX1 target genes, altered subnuclear localization, and deregulation of the myeloid gene regulatory program. However, a role of non-coding microRNAs (miRs) in t(8;21)-mediated leukemogenesis is minimally understood. We present evidence of an interplay between the tumor suppressor miR-29b-1 and the AML1-ETO (also designated RUNX1-RUNX1T1) oncogene that is encoded by the t(8;21). We find that AML1-ETO and corepressor NCoR co-occupy the miR-29a/b-1 locus and downregulate its expression in leukemia cells. Conversely, re-introduction of miR-29b-1 in leukemia cells expressing AML1-ETO causes significant downregulation at the protein level through direct targeting of the 3' untranslated region of the chimeric transcript. Restoration of miR-29b-1 expression in leukemia cells results in decreased cell growth and increased apoptosis. The AML1-ETO-dependent differentiation block and transcriptional program are partially reversed by miR-29b-1. Our findings establish a novel regulatory circuit between the tumor-suppressive miR-29b-1 and the oncogenic AML1-ETO that controls the leukemic phenotype in t(8;21)-carrying acute myeloid leukemia.
MeSH term(s)	Acute Disease ; Apoptosis/genetics ; Cell Differentiation/genetics ; Cell Line, Tumor ; Cell Proliferation/genetics ; Chromosomes, Human, Pair 21/genetics ; Chromosomes, Human, Pair 8/genetics ; Co-Repressor Proteins/genetics ; Co-Repressor Proteins/metabolism ; Core Binding Factor Alpha 2 Subunit/genetics ; Core Binding Factor Alpha 2 Subunit/metabolism ; Gene Expression Regulation, Leukemic ; Humans ; Leukemia, Myeloid/genetics ; Leukemia, Myeloid/metabolism ; Leukemia, Myeloid/pathology ; MicroRNAs/genetics ; Oncogene Proteins, Fusion/genetics ; Oncogene Proteins, Fusion/metabolism ; Phenotype ; RUNX1 Translocation Partner 1 Protein/genetics ; RUNX1 Translocation Partner 1 Protein/metabolism ; Translocation, Genetic
Chemical Substances	AML1-ETO fusion protein, human ; Co-Repressor Proteins ; Core Binding Factor Alpha 2 Subunit ; MIRN29a microRNA, human ; MicroRNAs ; Oncogene Proteins, Fusion ; RUNX1 Translocation Partner 1 Protein
Language	English
Publishing date	2017-03-28
Publishing country	United States
Document type	Journal Article
ZDB-ID	2560162-3
ISSN	1949-2553 ; 1949-2553
ISSN (online)	1949-2553
ISSN	1949-2553
DOI	10.18632/oncotarget.18127
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

To top

More links

Kategorien

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito