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  1. Article ; Online: The GR-PDK4 Axis of Evil: Hijacking a Stress SOS to Drive Metastasis.

    Chakraborty, Abhishek A / Keri, Ruth A

    Endocrinology

    2023  Volume 164, Issue 8

    MeSH term(s) Humans ; Female ; Receptors, Glucocorticoid/metabolism ; Breast Neoplasms/genetics ; Cell Line, Tumor ; Signal Transduction ; Cell Movement
    Chemical Substances Receptors, Glucocorticoid
    Language English
    Publishing date 2023-07-17
    Publishing country United States
    Document type Editorial ; Comment
    ZDB-ID 427856-2
    ISSN 1945-7170 ; 0013-7227
    ISSN (online) 1945-7170
    ISSN 0013-7227
    DOI 10.1210/endocr/bqad112
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Chromatin Organization and Transcriptional Programming of Breast Cancer Cell Identity.

    Bobbitt, Jessica R / Seachrist, Darcie D / Keri, Ruth A

    Endocrinology

    2023  Volume 164, Issue 8

    Abstract: The advent of sequencing technologies for assessing chromosome conformations has provided a wealth of information on the organization of the 3-dimensional genome and its role in cancer progression. It is now known that changes in chromatin folding and ... ...

    Abstract The advent of sequencing technologies for assessing chromosome conformations has provided a wealth of information on the organization of the 3-dimensional genome and its role in cancer progression. It is now known that changes in chromatin folding and accessibility can promote aberrant activation or repression of transcriptional programs that can drive tumorigenesis and progression in diverse cancers. This includes breast cancer, which comprises several distinct subtypes defined by their unique transcriptomes that dictate treatment response and patient outcomes. Of these, basal-like breast cancer is an aggressive subtype controlled by a pluripotency-enforcing transcriptome. Meanwhile, the more differentiated luminal subtype of breast cancer is driven by an estrogen receptor-dominated transcriptome that underlies its responsiveness to antihormone therapies and conveys improved patient outcomes. Despite the clear differences in molecular signatures, the genesis of each subtype from normal mammary epithelial cells remains unclear. Recent technical advances have revealed key distinctions in chromatin folding and organization between subtypes that could underlie their transcriptomic and, hence, phenotypic differences. These studies also suggest that proteins controlling particular chromatin states may be useful targets for treating aggressive disease. In this review, we explore the current state of understanding of chromatin architecture in breast cancer subtypes and its potential role in defining their phenotypic characteristics.
    MeSH term(s) Humans ; Female ; Breast Neoplasms/genetics ; Breast Neoplasms/metabolism ; Cell Line, Tumor ; Breast/metabolism ; Chromatin/genetics ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic
    Chemical Substances Chromatin
    Language English
    Publishing date 2023-07-11
    Publishing country United States
    Document type Review ; Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 427856-2
    ISSN 1945-7170 ; 0013-7227
    ISSN (online) 1945-7170
    ISSN 0013-7227
    DOI 10.1210/endocr/bqad100
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Up to your NEK2 in CIN.

    Seachrist, Darcie D / Anstine, Lindsey J / Keri, Ruth A

    Oncotarget

    2021  Volume 12, Issue 8, Page(s) 723–725

    Language English
    Publishing date 2021-04-13
    Publishing country United States
    Document type Editorial
    ZDB-ID 2560162-3
    ISSN 1949-2553 ; 1949-2553
    ISSN (online) 1949-2553
    ISSN 1949-2553
    DOI 10.18632/oncotarget.27918
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  4. Article: FOXA1: A Pioneer of Nuclear Receptor Action in Breast Cancer.

    Seachrist, Darcie D / Anstine, Lindsey J / Keri, Ruth A

    Cancers

    2021  Volume 13, Issue 20

    Abstract: The pioneering function of FOXA1 establishes estrogen-responsive transcriptomes in luminal breast cancer. Dysregulated FOXA1 chromatin occupancy through focal amplification, mutation, or cofactor recruitment modulates estrogen receptor (ER) ... ...

    Abstract The pioneering function of FOXA1 establishes estrogen-responsive transcriptomes in luminal breast cancer. Dysregulated FOXA1 chromatin occupancy through focal amplification, mutation, or cofactor recruitment modulates estrogen receptor (ER) transcriptional programs and drives endocrine-resistant disease. However, ER is not the sole nuclear receptor (NR) expressed in breast cancers, nor is it the only NR for which FOXA1 serves as a licensing factor. Receptors for androgens, glucocorticoids, and progesterone are also found in the majority of breast cancers, and their functions are also impacted by FOXA1. These NRs interface with ER transcriptional programs and, depending on their activation level, can reprogram FOXA1-ER cistromes. Thus, NR interplay contributes to endocrine therapy response and resistance and may provide a vulnerability for future therapeutic benefit in patients. Herein, we review what is known regarding FOXA1 regulation of NR function in breast cancer in the context of cell identity, endocrine resistance, and NR crosstalk in breast cancer progression and treatment.
    Language English
    Publishing date 2021-10-17
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2527080-1
    ISSN 2072-6694
    ISSN 2072-6694
    DOI 10.3390/cancers13205205
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  5. Article ; Online: Centrosome Aberrations as Drivers of Chromosomal Instability in Breast Cancer.

    Piemonte, Katrina M / Anstine, Lindsey J / Keri, Ruth A

    Endocrinology

    2021  Volume 162, Issue 12

    Abstract: Chromosomal instability (CIN), or the dynamic change in chromosome number and composition, has been observed in cancer for decades. Recently, this phenomenon has been implicated as facilitating the acquisition of cancer hallmarks and enabling the ... ...

    Abstract Chromosomal instability (CIN), or the dynamic change in chromosome number and composition, has been observed in cancer for decades. Recently, this phenomenon has been implicated as facilitating the acquisition of cancer hallmarks and enabling the formation of aggressive disease. Hence, CIN has the potential to serve as a therapeutic target for a wide range of cancers. CIN in cancer often occurs as a result of disrupting key regulators of mitotic fidelity and faithful chromosome segregation. As a consequence of their essential roles in mitosis, dysfunctional centrosomes can induce and maintain CIN. Centrosome defects are common in breast cancer, a heterogeneous disease characterized by high CIN. These defects include amplification, structural defects, and loss of primary cilium nucleation. Recent studies have begun to illuminate the ability of centrosome aberrations to instigate genomic flux in breast cancer cells and the tumor evolution associated with aggressive disease and poor patient outcomes. Here, we review the role of CIN in breast cancer, the processes by which centrosome defects contribute to CIN in this disease, and the emerging therapeutic approaches that are being developed to capitalize upon such aberrations.
    MeSH term(s) Animals ; Breast Neoplasms/genetics ; Breast Neoplasms/pathology ; Centrosome/metabolism ; Centrosome/pathology ; Centrosome/physiology ; Chromosomal Instability/genetics ; Female ; Genomic Instability/genetics ; Humans
    Language English
    Publishing date 2021-10-04
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
    ZDB-ID 427856-2
    ISSN 1945-7170 ; 0013-7227
    ISSN (online) 1945-7170
    ISSN 0013-7227
    DOI 10.1210/endocr/bqab208
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: The Activin Social Network: Activin, Inhibin, and Follistatin in Breast Development and Cancer.

    Seachrist, Darcie D / Keri, Ruth A

    Endocrinology

    2019  Volume 160, Issue 5, Page(s) 1097–1110

    Abstract: Activins and inhibins are closely related protein heterodimers with a similar tissue distribution; however, these two complexes have opposing functions in development and disease. Both are secreted cytokine hormones, with activin the primary inducer of ... ...

    Abstract Activins and inhibins are closely related protein heterodimers with a similar tissue distribution; however, these two complexes have opposing functions in development and disease. Both are secreted cytokine hormones, with activin the primary inducer of downstream signaling cascades and inhibin acting as a rheostat that exquisitely governs activin function. Adding to the complexity of activin signaling, follistatin, a highly glycosylated monomeric protein, binds activin with high affinity and restrains downstream pathway activation but through a mechanism distinct from that of inhibin. These three proteins were first identified as key ovarian hormones in the pituitary-gonadal axis that direct the synthesis and secretion of FSH from the pituitary, hence controlling folliculogenesis. Research during the past 30 years has expanded the roles of these proteins, first by discovering the ubiquitous expression of the trio and then by implicating them in a wide array of biological functions. In concert, these three hormones govern tissue development, homeostasis, and disease in multiple organ systems through diverse autocrine and paracrine mechanisms. In the present study, we have reviewed the actions of activin and its biological inhibitors, inhibin, and follistatin, in mammary gland morphogenesis and cancer.
    MeSH term(s) Activins/genetics ; Activins/metabolism ; Animals ; Breast Neoplasms/genetics ; Breast Neoplasms/metabolism ; Breast Neoplasms/pathology ; Female ; Follistatin/genetics ; Follistatin/metabolism ; Gene Expression Regulation, Neoplastic ; Humans ; Inhibins/genetics ; Inhibins/metabolism ; Mammary Glands, Human/metabolism ; Signal Transduction
    Chemical Substances Follistatin ; Activins (104625-48-1) ; Inhibins (57285-09-3)
    Language English
    Publishing date 2019-03-14
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 427856-2
    ISSN 1945-7170 ; 0013-7227
    ISSN (online) 1945-7170
    ISSN 0013-7227
    DOI 10.1210/en.2019-00015
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  7. Article ; Online: The PML1-WDR5 axis regulates H3K4me3 marks and promotes stemness of estrogen receptor-positive breast cancer.

    Pai, Chun-Peng / Wang, Han / Seachrist, Darcie D / Agarwal, Neel / Adams, Joshua A / Liu, Zhenghao / Keri, Ruth A / Cao, Kaixiang / Schiemann, William P / Kao, Hung-Ying

    Cell death and differentiation

    2024  

    Abstract: The alternative splicing of PML precursor mRNA gives rise to various PML isoforms, yet their expression profile in breast cancer cells remains uncharted. We discovered that PML1 is the most abundant isoform in all breast cancer subtypes, and its ... ...

    Abstract The alternative splicing of PML precursor mRNA gives rise to various PML isoforms, yet their expression profile in breast cancer cells remains uncharted. We discovered that PML1 is the most abundant isoform in all breast cancer subtypes, and its expression is associated with unfavorable prognosis in estrogen receptor-positive (ER+) breast cancers. PML depletion reduces cell proliferation, invasion, and stemness, while heterologous PML1 expression augments these processes and fuels tumor growth and resistance to fulvestrant, an FDA-approved drug for ER+ breast cancer, in a mouse model. Moreover, PML1, rather than the well-known tumor suppressor isoform PML4, rescues the proliferation of PML knockdown cells. ChIP-seq analysis reveals significant overlap between PML-, ER-, and Myc-bound promoters, suggesting their coordinated regulation of target gene expression, including genes involved in breast cancer stem cells (BCSCs), such as JAG1, KLF4, YAP1, SNAI1, and MYC. Loss of PML reduces BCSC-related gene expression, and exogenous PML1 expression elevates their expression. Consistently, PML1 restores the association of PML with these promoters in PML-depleted cells. We identified a novel association between PML1 and WDR5, a key component of H3K4 methyltransferase (HMTs) complexes that catalyze H3K4me1 and H3K4me3. ChIP-seq analyses showed that the loss of PML1 reduces H3K4me3 in numerous loci, including BCSC-associated gene promoters. Additionally, PML1, not PML4, re-establishes the H3K4me3 mark on these promoters in PML-depleted cells. Significantly, PML1 is essential for recruiting WDR5, MLL1, and MLL2 to these gene promoters. Inactivating WDR5 by knockdown or inhibitors phenocopies the effects of PML1 loss, reducing BCSC-related gene expression and tumorsphere formation and enhancing fulvestrant's anticancer activity. Our findings challenge the conventional understanding of PML as a tumor suppressor, redefine its role as a promoter of tumor growth in breast cancer, and offer new insights into the unique roles of PML isoforms in breast cancer.
    Language English
    Publishing date 2024-04-16
    Publishing country England
    Document type Journal Article
    ZDB-ID 1225672-9
    ISSN 1476-5403 ; 1350-9047
    ISSN (online) 1476-5403
    ISSN 1350-9047
    DOI 10.1038/s41418-024-01294-6
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  8. Article ; Online: Targeting bromodomain and extraterminal proteins in breast cancer.

    Sahni, Jennifer M / Keri, Ruth A

    Pharmacological research

    2017  Volume 129, Page(s) 156–176

    Abstract: Breast cancer is a collection of distinct tumor subtypes that are driven by unique gene expression profiles. These transcriptomes are controlled by various epigenetic marks that dictate which genes are expressed and suppressed. During carcinogenesis, ... ...

    Abstract Breast cancer is a collection of distinct tumor subtypes that are driven by unique gene expression profiles. These transcriptomes are controlled by various epigenetic marks that dictate which genes are expressed and suppressed. During carcinogenesis, extensive restructuring of the epigenome occurs, including aberrant acetylation, alteration of methylation patterns, and accumulation of epigenetic readers at oncogenes. As epigenetic alterations are reversible, epigenome-modulating drugs could provide a mechanism to silence numerous oncogenes simultaneously. Here, we review the impact of inhibitors of the Bromodomain and Extraterminal (BET) family of epigenetic readers in breast cancer. These agents, including the prototypical BET inhibitor JQ1, have been shown to suppress a variety of oncogenic pathways while inducing minimal, if any, toxicity in models of several subtypes of breast cancer. BET inhibitors also synergize with multiple approved anti-cancer drugs, providing a greater response in breast cancer cell lines and mouse models than either single agent. The combined findings of the studies discussed here provide an excellent rationale for the continued investigation of the utility of BET inhibitors in breast cancer.
    MeSH term(s) Animals ; Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Breast Neoplasms/drug therapy ; Breast Neoplasms/metabolism ; Female ; Humans ; Molecular Targeted Therapy ; Proteins/antagonists & inhibitors ; Proteins/chemistry ; Proteins/metabolism
    Chemical Substances Antineoplastic Agents ; Proteins ; bromodomain and extra-terminal domain protein, human
    Language English
    Publishing date 2017-11-16
    Publishing country Netherlands
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 1003347-6
    ISSN 1096-1186 ; 0031-6989 ; 1043-6618
    ISSN (online) 1096-1186
    ISSN 0031-6989 ; 1043-6618
    DOI 10.1016/j.phrs.2017.11.015
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article: Alterations in the preneoplastic breast microenvironment of

    Caputo, Anthony / Vipparthi, Kavya / Bazeley, Peter / Downs-Kelly, Erinn / McIntire, Patrick / Ni, Ying / Hu, Bo / Keri, Ruth A / Karaayvaz, Mihriban

    bioRxiv : the preprint server for biology

    2023  

    Abstract: Breast cancer is the most common cancer in females, affecting one in every eight women and accounting for the majority of cancer-related deaths in women worldwide. Germline mutations in ... ...

    Abstract Breast cancer is the most common cancer in females, affecting one in every eight women and accounting for the majority of cancer-related deaths in women worldwide. Germline mutations in the
    Language English
    Publishing date 2023-05-25
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2023.05.24.542078
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  10. Article: BETi induction of mitotic catastrophe: towing the LIN9.

    Gayle, Sylvia S / Sahni, Jennifer M / Keri, Ruth A

    Oncoscience

    2017  Volume 4, Issue 9-10, Page(s) 128–130

    Language English
    Publishing date 2017-10-23
    Publishing country United States
    Document type Editorial
    ISSN 2331-4737
    ISSN 2331-4737
    DOI 10.18632/oncoscience.372
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