The General Hospital Corporation

Aalborg University

Harvard College

Naar, Anders M.

Rajurkar, Mihir Shivadatta

Anders M Naar

Andreas Petri

Sakari Kauppinen

Seyed Hani Najafi-Shoushtari

Daniel Arie Haber

Shyamala Maheswaran

David T Ting

Raul Mostoslavsky

Sita Kugel

Francesca Bersani

Mihir Shivadatta Rajurkar

Gerhard Wagner

Haribabu Arthanari

Joy Luz Nishikawa

Methods for treating cancer, e.g., cancer of epithelial origin, by specifically targeting human satellite II (HSATII) using sequence specific agents such as oligonucleotides.

Targeting human satellite II (HSATII)

It has been discovered that NAD-dependent histone deacetylase SIRT6 is critical for suppression of PDAC by controlling the expression of Lin28b, which is a negative regulator of let-7 microRNA. Specifically, SIRT6 loss results in histone hyperacetylation at the Lin28b promoter, Myc recruitment, and pronounced induction of Lin28b and downstream let-7 target genes, HMGA2, IGF2BP1, and IGF2BP3. This invention relates generally to agents and methods of reducing expression or activity of Lin28b to treat (aggressive) PDAC in a subject.

Agents and methods for treating pancreatic ductal adenocarcinomas

Methods of treating Duchenne muscular dystrophy (DMD) and Becker muscular dystrophy (BMD), comprising administering an inhibitory nucleic acid that targets miR-128.

Therapeutic targeting of a microRNA to treat Duchenne muscular dystrophy

It has been discovered that NAD+-dependent histone deacetylase SIRT6 is critical for suppression of PDAC by controlling the expression of Lin28b, which is a negative regulator of let-7 microRNA. Specifically, SIRT6 loss results in histone hyperacetylation at the Lin28b promoter, Myc recruitment, and pronounced induction of Lin28b and downstream let-7 target genes, HMGA2, IGF2BP1, and IGF2BP3. This invention relates generally to agents and methods of reducing expression or activity of Lin28b to treat (aggressive) PDAC in a subject.

Methods for treating cancer, e.g., cancer of epithelial origin, by specifically targeting human satellite II (HSATII) using sequence specific agents such as oligonucleotides. As shown herein, the hetero chromatic HSATII satellite repeat is silenced in normal cells, but massively over expressed in epithelial cancers and in cancer cell lines when grown as xenografts or in 3D culture. Induction of HSATII RNA, either in xenografts or using in vitro reconstitution models, suggests the appearance of complementary DNA intermediates.

Methods for targeting microRNA 128 (miR-128) for regulating cholesterol/lipid metabolism and insulin sensitivity.

Methods targeting miR-128 for regulating cholesterol/lipid metabolism

Compositions comprising nucleic acid sequences that target MiR-33a/b microRNAs are described, together with uses of the same in the treatment of certain disorders related to elevated serum triglyceride levels and obesity.

Methods targeting miR-33 microRNAs for regulating lipid metabolism

The present invention relates to the identification of molecular mechanisms associated with multidrug resistance (MDR) in fungal infections. More specifically, fungi harbor a nuclear receptor-like pathway controlling MDR, which represents a novel therapeutic target for the treatment of MDR in pathogenic fungi such as

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Arlington, MA, United States of America

Anders M Naar