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Invasive phenotype in triple negative breast cancer is inhibited by blocking SIN3A–PF1 interaction through KLF9 mediated repression of ITGA6 and ITGB1

Translational oncology, 2022-02, Vol.16, p.101320-101320, Article 101320

2022

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The Sin3A/MAD1 Complex, through Its PAH2 Domain, Acts as a Second Repressor of Retinoic Acid Receptor Beta Expression in Breast Cancer Cells

Cells (Basel, Switzerland), 2022-03, Vol.11 (7), p.1179

2022

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Selective Inhibition of SIN3 Corepressor with Avermectins as a Novel Therapeutic Strategy in Triple-Negative Breast Cancer

Molecular cancer therapeutics, 2015-08, Vol.14 (8), p.1824-1836

2015

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Heterochromatic Silencing and HP1 Localization in Drosophila Are Dependent on the RNAi Machinery

Science (American Association for the Advancement of Science), 2004-01, Vol.303 (5658), p.669-672

2004

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The MMSET protein is a histone methyltransferase with characteristics of a transcriptional corepressor

Blood, 2008-03, Vol.111 (6), p.3145-3154

2008

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Targeted interference of SIN3A-TGIF1 function by SID decoy treatment inhibits Wnt signaling and invasion in triple negative breast cancer cells

Oncotarget, 2017-10, Vol.8 (51), p.88421-88436

2017

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Interference with Sin3 function induces epigenetic reprogramming and differentiation in breast cancer cells

Proceedings of the National Academy of Sciences - PNAS, 2010-06, Vol.107 (26), p.11811-11816

2010

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Targeting the SIN3A-PF1 interaction inhibits epithelial to mesenchymal transition and maintenance of a stem cell phenotype in triple negative breast cancer

Oncotarget, 2015-10, Vol.6 (33), p.34087-34105

2015

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Chromatin organization and transcriptional control of gene expression in Drosophila

Gene, 2000-08, Vol.253 (2), p.117-136

2000

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GAGA Factor and the TFIID Complex Collaborate in Generating an Open Chromatin Structure at the Drosophila melanogaster hsp26 Promoter

Molecular and Cellular Biology, 2002-09, Vol.22 (17), p.6148-6157

2002

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Abstract 31: Targeted dissociation of PF1 from SIN3A chromatin regulator complex inhibits tumor growth and metastasis in triple-negative breast cancer

Cancer research (Chicago, Ill.), 2018-07, Vol.78 (13_Supplement), p.31-31

2018

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Abstract 3511: Targeted epigenetic reprogramming reverts tumor progression in triple-negative breast cancer models by the activation of retinoic acid receptor alpha

Cancer research (Chicago, Ill.), 2015-08, Vol.75 (15_Supplement), p.3511-3511

2015

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Abstract 4115: Inhibition of triple negative breast cancer cell invasion by the targeted interference of Sin3A function affecting Wnt and TGFβ signaling

Cancer research (Chicago, Ill.), 2016-07, Vol.76 (14_Supplement), p.4115-4115

2016

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Abstract 1989: Targeting Sin3-Pf1 complex: Novel site-specific epigenetic therapy for triple negative breast cancer

Cancer research (Chicago, Ill.), 2015-08, Vol.75 (15_Supplement), p.1989-1989

2015

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Blocking the PAH2 domain of Sin3A inhibits tumorigenesis and confers retinoid sensitivity in triple negative breast cancer

Oncotarget, 2016-07, Vol.7 (28), p.43689-43702

2016

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Abstract 411: Targeted PF1, JARID1B inhibition induces epigenetic reprogramming in triple negative breast cancer

Cancer research (Chicago, Ill.), 2014-10, Vol.74 (19_Supplement), p.411-411

2014

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Abstract 807: Selamectin and ivermectin are small molecule inhibitors that interfere with Sin3A-PAH2 function and exert anti-tumor activity in triple-negative breast cancer

Cancer research (Chicago, Ill.), 2014-10, Vol.74 (19_Supplement), p.807-807

2014

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Abstract 1826: Anti-tumorigenic effects by targeted functional disruption of the Sin3 PAH-2 domain

Cancer research (Chicago, Ill.), 2012-04, Vol.72 (8_Supplement), p.1826-1826

2012

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Abstract 2826: Reversal of the basal phenotype in triple negative (TN) breast cancer using a SID decoy

Cancer research (Chicago, Ill.), 2011-04, Vol.71 (8_Supplement), p.2826-2826

2011

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Adipocyte derived paracrine mediators of mammary ductal morphogenesis controlled by retinoic acid receptors

Developmental biology, 2011-01, Vol.349 (2), p.125-136

2011

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Abstract 572: Interference with Sin3 PAH-2 domain function induces epigenetic reprogramming, differentiation and growth inhibition in breast cancer cells

Cancer research (Chicago, Ill.), 2010-04, Vol.70 (8_Supplement), p.572-572

2010

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The MMSET Protein Is Tightly Associated with Chromatin, Mediates Methylation of Specific Histone Residues and Forms a Complex with a Histone Demethylase

Blood, 2006-11, Vol.108 (11), p.730-730

2006

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The Multiple Myeloma SET Domain (MMSET) Protein Is a Histone H3 and H4 Methyltransferase with Properties of a Transcriptional Co-Repressor

Blood, 2005-11, Vol.106 (11), p.358-358

2005

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PD19-10 THE CHEMOABLATIVE EFFECT OF VESIGEL INSTILLATION IN PATIENTS WITH NMIBC – RESPONSE RATE AND 1-YEAR DURABILITY

The Journal of urology, 2017-04, Vol.197 (4), p.e368-e369

2017

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PD11-05 THE CHEMOABLATIVE EFFECT OF VESIGEL INSTILLATION IN PATIENTS WITH NMIBC – PRELIMINARY RESULTS

The Journal of urology, 2016-04, Vol.195 (4), p.e289-e290

2016

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Invasive phenotype in triple negative breast cancer is inhibited by blocking SIN3A–PF1 interaction through KLF9 mediated repression of ITGA6 and ITGB1

The Sin3A/MAD1 Complex, through Its PAH2 Domain, Acts as a Second Repressor of Retinoic Acid Receptor Beta Expression in Breast Cancer Cells

Selective Inhibition of SIN3 Corepressor with Avermectins as a Novel Therapeutic Strategy in Triple-Negative Breast Cancer

Heterochromatic Silencing and HP1 Localization in Drosophila Are Dependent on the RNAi Machinery

The MMSET protein is a histone methyltransferase with characteristics of a transcriptional corepressor

Targeted interference of SIN3A-TGIF1 function by SID decoy treatment inhibits Wnt signaling and invasion in triple negative breast cancer cells

Interference with Sin3 function induces epigenetic reprogramming and differentiation in breast cancer cells

Targeting the SIN3A-PF1 interaction inhibits epithelial to mesenchymal transition and maintenance of a stem cell phenotype in triple negative breast cancer

Chromatin organization and transcriptional control of gene expression in Drosophila

GAGA Factor and the TFIID Complex Collaborate in Generating an Open Chromatin Structure at the Drosophila melanogaster hsp26 Promoter

Abstract 31: Targeted dissociation of PF1 from SIN3A chromatin regulator complex inhibits tumor growth and metastasis in triple-negative breast cancer

Abstract 3511: Targeted epigenetic reprogramming reverts tumor progression in triple-negative breast cancer models by the activation of retinoic acid receptor alpha

Abstract 4115: Inhibition of triple negative breast cancer cell invasion by the targeted interference of Sin3A function affecting Wnt and TGFβ signaling

Abstract 1989: Targeting Sin3-Pf1 complex: Novel site-specific epigenetic therapy for triple negative breast cancer

Blocking the PAH2 domain of Sin3A inhibits tumorigenesis and confers retinoid sensitivity in triple negative breast cancer

Abstract 411: Targeted PF1, JARID1B inhibition induces epigenetic reprogramming in triple negative breast cancer

Abstract 807: Selamectin and ivermectin are small molecule inhibitors that interfere with Sin3A-PAH2 function and exert anti-tumor activity in triple-negative breast cancer

Abstract 1826: Anti-tumorigenic effects by targeted functional disruption of the Sin3 PAH-2 domain

Abstract 2826: Reversal of the basal phenotype in triple negative (TN) breast cancer using a SID decoy

Adipocyte derived paracrine mediators of mammary ductal morphogenesis controlled by retinoic acid receptors

Abstract 572: Interference with Sin3 PAH-2 domain function induces epigenetic reprogramming, differentiation and growth inhibition in breast cancer cells

The MMSET Protein Is Tightly Associated with Chromatin, Mediates Methylation of Specific Histone Residues and Forms a Complex with a Histone Demethylase

The Multiple Myeloma SET Domain (MMSET) Protein Is a Histone H3 and H4 Methyltransferase with Properties of a Transcriptional Co-Repressor

PD19-10 THE CHEMOABLATIVE EFFECT OF VESIGEL INSTILLATION IN PATIENTS WITH NMIBC – RESPONSE RATE AND 1-YEAR DURABILITY

PD11-05 THE CHEMOABLATIVE EFFECT OF VESIGEL INSTILLATION IN PATIENTS WITH NMIBC – PRELIMINARY RESULTS

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