Abstract: As described herein, chromosomal missegregations, chromosomal micromodel, cytosolic DNA, and combinations thereof are indicative of metastatic cancer. Methods and compositions are described herein that are useful for detection and treatment of patients with chromosomal instabilities such as chromosomal missegregations, chromosomal micromilei, cytosilic DNA, and combinations thereof. For example, some of the methods and compositions include use of kinesin-13 proteins such as Kif2b, MCAK/Kif2 or KIF13A. The methods and compositions can also include is of STING, ENPPI, cGAS, NF-kB transcription factor p52, NF-kB transcription factor ReIB, or any combination thereof. Methods are also described for identifying compounds that are effective for treatment of cancer, including metastic cancer.

Abstract: As described herein, chromosomal missegregations, chromosomal micronuclei, cytosolic DNA, and combinations thereof are indicative of metastatic cancer. Methods and compositions are described herein that are useful for detection and treatment of patients with chromosomal instabilities such as chromosomal missegregations, chromosomal micronuclei, cytosolic DNA, and combinations thereof. For example, some of the methods and compositions include use of kinesin-13 proteins such as Kif2b, MCAK/Kif2c, or KIF13A. The methods and compositions can also include inhibitors of STING, ENPP1, cGAS, NF-kB transcription factor p52, NF-kB transcription factor RelB, or any combination thereof. Methods are also described for identifying compounds that are effective for treatment of cancer, including metastatic cancer.

Abstract: As described herein ingestion of high amounts of sugar, especially fructose, can increase the growth of intestinal tumors. Such cancer growth can be inhibited or prevented by limiting the amounts of sugar and amino acids ingested, by inhibiting ketohexokinase (KHK), fructose transport (via GLUT5), fatty acid synthesis (via FASN), phosphoinositide 3-kinases (PI3K), or by limiting amounts of sugar and amino acids ingested while also receiving KHK inhibitors, GLUT5 inhibitors, FASN inhibitors, PI3K inhibitors, or a combination of such inhibitors.

Abstract: As described herein, phosphatidylinositol-5-phosphate 4-kinases (PIP4Ks) have an allosteric function in addition to their catalytic activity. The allosteric function suppresses PIP5K-mediated PI(4,5)P2 synthesis and insulin-dependent conversion to PI(3,4,5)P3. Further described herein are methods for treatment of diabetes, metabolic syndrome, insulin resistance, a obesity, cancer, immune deficiency, autoimmune disease, infection, or a combination thereof.

Abstract: The present disclosure provides materials and methods for CUB domain-containing protein 1 (CDCP1)-targeted therapy.

Abstract: Described herein are compositions and methods for treating a disease or disorder associated with PI3K signaling. For example, such compositions can include use of modulators of glucose metabolism, use of at least one kinase in the insulin-receptor/PI3K/O AKT/mTOR pathway, and/or use of diet that influences the subjects metabolic state.

Abstract: Provided herein are methods for treating cancer that is resistant to treatment with an anti-ErbB therapeutic agent and which is associated with an activating MET gene mutation or a MET gene amplification. The methods involve administering to a subject a combination of an anti-ErbB therapeutic and an anti-MET therapeutic. Also provided are methods for reducing ErbB mediated signaling or PI3 kinase mediated signaling in a cancer cell.

Abstract: As described herein, chromosomal missegregations, chromosomal micronuclei, cytosolic DNA, and combinations thereof are indicative of metastatic cancer. Methods and compositions are described herein that are useful for detection and treatment of patients with chromosomal instabilities such as chromosomal missegregations, chromosomal micronuclei, cytosolic DNA, and combinations thereof. For example, some of the methods and compositions include use of kinesin-13 proteins such as Kif2b, MCAK/Kif2c, or KIF13A. The methods and compositions can also include inhibitors of STING, ENPP1, cGAS, NF-kB transcription factor p52, NF-kB transcription factor RelB, or any combination thereof. Methods are also described for identifying compounds that are effective for treatment of cancer, including metastatic cancer.

Abstract: Embodiments of the present invention are directed to small molecule inhibitors of PHGDH. Other embodiments of the present invention relate to methods of treating cancers using the small molecule inhibitors of PHGDH disclosed herein. Still other embodiments of the present invention relate to methods for using the small molecule inhibitors of PHGDH to study serine metabolism.

Abstract: Embodiments of the present invention are directed to small molecule inhibitors of PHGDH. Other embodiments of the present invention relate to methods of treating cancers using the small molecule inhibitors of PHGDH disclosed herein. Still other embodiments of the present invention relate to methods for using the small molecule inhibitors of PHGDH to study serine metabolism.

Abstract: Provided herein are methods for treating cancer that is resistant to treatment with an anti-ErbB therapeutic agent and which is associated with an activating MET gene mutation or a MET gene amplification. The methods involve administering to a subject a combination of an anti-ErbB therapeutic and an anti-MET therapeutic. Also provided are methods for reducing ErbB mediated signaling or PI3 kinase mediated signaling in a cancer cell.

Abstract: The invention features methods for identifying compounds that modulate the activity of phosphatidylinositol 5-phosphate 4-kinase (PI5P4K). Inhibitors of PI5P4K can be used in, for example, the treatment or prevention of cell proliferation disorders (e.g., the prevention of tumor cell growth in p53 mutated cancers).

Abstract: The invention features methods and compositions feature lapatinib and/or rapamycin for treating or preventing a cardiac condition induced by anthracycline treatment.

Abstract: Methods and compositions for treating and evaluating subjects having a neoactive mutation at residue 97 of IDH1 or 137 of IDH2.

Abstract: Provided herein are methods for treating cancer that is resistant to treatment with an anti-ErbB therapeutic agent and which is associated with an activating MET gene mutation or a MET gene amplification. The methods involve administering to a subject a combination of an anti-ErbB therapeutic and an anti-MET therapeutic. Also provided are methods for reducing ErbB mediated signaling or PI3 kinase mediated signaling in a cancer cell.

Abstract: The present invention relates to pharmaceutical compositions that contain PI3K inhibitors (e.g., PBKa-specific inhibitors) and PARP inhibitors. The invention also provides methods for the treatment of proliferative diseases such as cancer (e.g., breast cancer) by administering the composition(s) to a subject.

Abstract: Provided herein are methods for treating cancer that is resistant to treatment with an anti-ErbB therapeutic agent and which is associated with an activating MET gene mutation or a MET gene amplification. The methods involve administering to a subject a combination of an anti-ErbB therapeutic and an anti-MET therapeutic. Also provided are methods for reducing ErbB mediated signaling or PI3 kinase mediated signaling in a cancer cell.

Abstract: The invention features methods for identifying compounds that modulate the activity of phosphatidylinositol 5-phosphate 4-kinase (PI5P4K) Inhibitors of PI5P4K can be used in, for example, the treatment or prevention of cell proliferation dis orders (e.g., the prevention of tumor cell growth in p53 mutated cancers).

Abstract: The invention features methods and compositions feature lapatinib and/or rapamycin for treating or preventing a cardiac condition induced by anthracycline treatment.

Abstract: Methods and compositions for treating and evaluating subjects having a neoactive mutation at residue 97 of IDH1 or 137 of IDH2.