The Brigham and Women's Hospital, Inc.

Dana-farber-cancer Institute Inc.

The General Hospital Corporation

The Broad Institute, Inc.

University of Miami

The General Hospital Corporation D/b/a Massachusetts General Hospital

Jon C Aster

James Elliott Bradner

James Bradner

Bradley Bernstein

Tan A Ince

Adolfo A Ferrando

David Root

A Thomas Look

Stephen C Blacklow

Christopher J Ott

Birgit Knoechel

Andrew P Weng

Christopher French

Matthias Hofer

Andrew Lane

James E Bradner

Bradley E Bernstein

The present invention is based in part on the identification of DPH1 and other members of the diphthamide synthesis pathway as biomarkers of resistance to an ADP-ribosylating toxin in a cell, and methods for identification, assessment, and treatment of a condition that is resistant to an ADP-ribosylating toxin.

Methods determining and treating cellular resistance to ADP-rtbosylating toxin

The invention relates to methods of treatment and diagnosis of subjects with cancer. In some aspects, the invention relates to methods of treatment and diagnosis of subjects with cancer, wherein the cancer is characterized by a Notch pathway activation mutation or by resistance to a Notch pathway inhibitor.

Diagnostic and treatment methods in subjects having or at risk of developing resistance to cancer therapy

We describe cell culture media for in vitro culture of a human cancer cell of the lymphocyte lineage (e.g., leukemia, lymphoma, or other blasts) or a precursor thereof, especially T-cell acute lymphoblastic leukemia lymphoma (T-ALL), as well as methods for at least maintenance, propagation, or both of the human cancer cell or its precursor.

In vitro culture conditions for T-cell acute lymphoblastic leukemia/lymphoma

The present invention is based upon the identification of regions within the NOTCH-1 receptor that, when mutated, lead to increase receptor signaling. The mutations are associated with uncontrolled cellular growth and this growth may be arrested using agents that interfere with NOTCH-1 activity, such as inhibitors of gamma-secretase. Assays for the NOTCH-1 mutations may be used diagnostically or as part of a treatment regimen for cancer patients.

NOTCH mutations leading to increased receptor signaling

The present invention is directed, inter alia, to methods of treating NUT midline carcinoma (NMC) by administering compounds that promote increased histone acetylation. The invention also includes assay methods for determining the responsiveness of NMC to specific histone deacetylases and other compounds.

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Lexington, MA, United States of America

Jon C Aster