Abstract: The present invention is based, in part, on cancer vaccine compositions that comprise PTEN- and p53-deficient cancer cells with activated TGF?-Smad/p63 signaling pathway, and methods for using same to prevent and/or treat cancer.

Abstract: The present invention is based, in part, on the identification of novel FI.3K-mTORCI-S6K 1 signaling pathway biomarkers predictive of responsiveness to anti-cancer therapies.

Abstract: The present invention relates to methods of treating brain metastases using synergistic combinations of anti-PI3K and anti-mTOR therapies. It has also been determined that blocking PI3K and mTOR provides therapeutic benefit for treating brain metastases.

Abstract: The present invention relates to use of pyrimido-diazepinone compounds that are able to modulate protein kinases such as PI3K-? and PI3K-?, which are members of the Class I Type IA and Class I Type IB family of phosphatidylinositol-4,5-bisphosphate 3-kinases, and the use of such compounds in the treatment of various diseases, disorders or conditions.

Abstract: The present invention provides methods for measuring translation rates of RNA associated with a ribosome (e.g., mRNA) in a rapid, cost-effective, and targeted manner.

Abstract: The present invention relates to methods for treating PTEN deficient epithelial cancers using a combination of anti-PI3Kbeta and anti-immune checkpoint agents.

Abstract: The present invention relates to methods for treating PTEN deficient epithelial cancers using a combination of anti-PI3Kbeta and anti-immune checkpoint agents.

Abstract: Provided herein are small molecule inhibitors of maternal embryonic leucine zipper kinase (MELK) having the structure of formula (I), wherein X and R1-R3 are defined in the specification. The compounds are useful for treating cancer and other conditions or diseases associated with aberrant MELK expression. Also provided herein are pharmaceutical compositions comprising a compound of formula (I) and a pharmaceutically acceptable carrier. The invention also provides methods of treating cancers associated with over-expression of MELK.

Abstract: Aspects of the disclosure provide fusion proteins that bind cells expressing one or more target molecules including, for example, one or more cell surface multisubunit signaling receptors (e.g.

Abstract: The present invention provides a cancer vaccine comprising DNA repair-deficient cancer cells, wherein the cancer cells are contacted with a PARP inhibitor to induce DNA breaks. In another aspect, a method of treating a subject afflicted with a cancer comprising administering to the subject a therapeutically effective amount of a cancer vaccine comprising DNA repair-deficient cancer cells, wherein the cancer cells are contacted with a PARP inhibitor to induce DNA breaks, is provided. The present invention also provides a kit comprising DNA repair-deficient cancer cells modified as described herein, PARP inhibitors, immune checkpoint inhibitors, and combinations thereof, packaged in a suitable container.

Abstract: The present invention is based, in part, on methods for modulating regulatory T cells and immune responses using CDK4/6 inhibitors.

Abstract: Provided herein are tricyclic small molecule inhibitors of maternal embryonic leucine zipper kinase (MELK). The compounds are useful for treating cancer and other conditions or diseases associated with aberrant MELK expression. Also provided herein are pharmaceutical compositions comprising a tricyclic compound of the invention and a pharmaceutically acceptable carrier. The invention also provides methods of treating cancers associated with over-expression of MELK.

Abstract: The present invention relates to methods for treating PTEN deficient epithelial cancers using a combination of anti-PI3Kbeta and anti-immune checkpoint agents.

Abstract: Aspects of the disclosure provide fusion proteins that bind cells expressing one or more target molecules including, for example, one or more cell surface multisubunit signaling receptors (e.g.

Abstract: The present invention provides methods for measuring translation rates of RNA associated with a ribosome (e.g., mRNA in a rapid, cost-effective, and targeted manner.

Abstract: The present invention relates to use of pyrimido-diazepinone compounds that are able to modulate protein kinases such as PI3K-? and PI3K-?, which are members of the Class I Type IA and Class I Type IB family of phosphatidylinositol-4,5-bisphosphate 3-kinases, and the use of such compounds in the treatment of various diseases, disorders or conditions.

Abstract: The methods of the present invention, relate to the surprising determination that the level of phosphorylation of position 406 (e.g., a serine residue) of human eukaryotic initiation factor 4B (eIF4B), or a corresponding phosphorylatable amino acid of an ortholog thereof, serves as a biomarker for MELK enzymatic (e.g., kinase) and/or oncogenic activity. The methods of the present invention further relate to the surprising determination that the level of phosphorylation of position 3 (e.g., a threonine residue) and/or position 10 (e.g., a serine residue) and/or position 11 (e.g., a threonine residue) of human Histone M3, or a corresponding phosphorylatable amino acid of an ortholog thereof, also serves as a biomarker for MELK enzymatic (e.g., kinase) and/or oncogenic activity.

Abstract: The present invention relates to methods of treating brain metastases using synergistic combinations of anti-PI3K and anti-mTOR therapies. It has also been determined that blocking PI3K and mTOR provides therapeutic benefit for treating brain metastases.

Abstract: Provided herein are small molecule inhibitors of maternal embryonic leucine zipper kinase (MELK) having the structure of formula (I), wherein X and R1-R3 are defined in the specification. The compounds are useful for treating cancer and other conditions or diseases associated with aberrant MELK expression. Also provided herein are pharmaceutical compositions comprising a compound of formula (I) and a pharmaceutically acceptable carrier. The invention also provides methods of treating cancers associated with over-expression of MELK.

Abstract: The present invention is based, in part, on the identification of novel FI.3K-mTORCI-S6K 1 signaling pathway biomarkers predictive of responsiveness to anti-cancer therapies.