Janssen Biotech, Inc.

The Salk Institute for Biological Studies

Janssen Pharmaceuticals, Inc.

Jason DeHart

Manuel Sepulveda

Kurt Iver Kamrud

Ricardo Attar

Selina Khan

Clodagh O'Shea

Nathaniel Stephen Wang

Parinaz Aliahmad

Vinod Krishna

Vipul Bhargava

Christian Maine

Patrick Wilkinson

Jenifer Lum

Roland Zahn

Barbara Sanders

Disclosed herein are self-replicating RNA molecules encoding prostate neoantigens, vaccines, and methods of treating and preventing prostate cancer.

Prostate neoantigens and their uses

Provided are vaccines, polypeptides and polynucleotides based on mutant CALR and JAK2 sequences, vectors, host cells, viruses, and methods of making and using them. The disclosure also provides methods of inducing an immune response and methods of treating, preventing, reducing a risk of onset or delaying the onset of a clinical condition characterized by an expression of JAK2V617F or CALR exon 9 mutant, or both JAK2V617F and CALR exon 9 mutant, wherein the method comprises a plurality of administrations of any of the compositions comprising polynucleotides, polypeptides or vectors disclosed herein.

Vaccines based on mutant CALR and JAK2 and their uses

The present disclosure generally relates to the use of different self-amplifying RNA molecules to enhance immune responses, for example immune responses following prophylactic vaccination or therapeutic administration. Some embodiments relate to compositions and methods for inducing an immune response in a subject using prime-boost immunization regimens.

Induce and enhance immune responses using recombinant replicon systems

Recombinant herpes simplex virus (HSV)-1 capable of selectively replicating in alternative lengthening of telomeres (ALT)-dependent tumor cells are described. The recombinant HSV-1 are ICP0-deficient, such as by complete deletion of the ICP0 gene, or mutation of the ICP0 gene sufficient to diminish or eliminate E3 ubiquitin ligase activity of ICP0. In some cases, the recombinant HSV-1 further include additional gene deletions or mutations, such as those that render the virus glycoprotein C (gC) deficient, or include a heterologous gene, such as a gene encoding an immunostimulatory molecule. Methods of treating ALT-dependent cancer, and methods of selectively killing ALT-dependent tumor cells are also described.

HSV-1 oncolytic virus therapies that specifically kill ALT dependent cancers

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San Diego, CA, United States of America

Jason DeHart