Abstract: The present disclosure provides methods for identifying subjects having a cancer or tumor that may be susceptible to treatment with a therapeutic agent used to EGFR-related cancer an/or NTRK-related cancer.

Abstract: An immune suppressor cell modified to include an innate immune effector is described. Methods of using the modified immune suppressor cell to treat cancer are also described.

Abstract: The present disclosure provides, for instance, a method of inhibiting resistance to a DDR inhibitor in a subject, the method comprising administering to the subject a GDF15 inhibitor, thereby inhibiting resistance to the DDR inhibitor in the subject. The disclosure also provides combination therapies for cancer, comprising co-administration of a DDR inhibitor and a GDF15 inhibitor.

Abstract: Methods and compositions relating to TIC10 are described according to aspects of the present invention. The compositions and methods have utility in treating disease, particularly cancer in a subject in need thereof, including a human subject as well as subjects of other species. The compositions have utility in treating brain cancer in a subject in need thereof.

Abstract: Prodigiosin analogs which reactivate the p53 pathway are provided, as well as compositions of these compounds, and methods for reactivation of the p53 pathway using these compounds are provided. The prodigiosin analogs may be used to treat cancer in which p53 mutation plays a role, including prostate cancer, breast cancer, kidney cancer, ovarian cancer, lymphoma, leukemia, and glioblastoma, among others.

Abstract: The present disclosure provides methods for identifying subjects having a cancer or tumor that may be susceptible to treatment with a therapeutic agent used to EGFR-related cancer an/or NTRK-related cancer.

Abstract: Described are improved therapies for the treatment of cancer including prostate cancer.

Abstract: A method of treating urinary tract cancer in a subject in need thereof is described. The method includes determining if there are loss-of-function mutations in the CDKN1A and RB1 genes in a biological sample from the subject; and treating the subject with a combination of a checkpoint kinase inhibitor and a DNA damaging agent if there are loss-of-function mutations in the CDKN1A and RB1 genes. Alternately, the method includes determining if there is a loss-of-function mutations in a CDKN1A gene in a biological sample from the subject; determining if there is a mutation in a second gene selected from the list consisting of RAB44, TERT, MUC16, HRNR, and FLG; and selecting specific anticancer treatment for the subject based on the identification of a mutation in the second gene.

Abstract: The present disclosure provides compositions comprising miR-3132 and one or more pharmaceutical agents that upregulate TNF-related apoptosis-inducing ligand (TRAIL) or activate TRAIL signaling pathway, and methods for treating a cancer comprising administering miR-3132, or a composition comprising miR-3132 and one or more pharmaceutical agents that upregulate TRAIL or activate TRAIL signaling pathway, to a subject.

Abstract: Methods and compositions relating to TIC10 are described according to aspects of the present invention. The compositions and methods have utility in treating disease, particularly cancer in a subject in need thereof, including a human subject as well as subjects of other species. The compositions have utility in treating brain cancer in a subject in need thereof.

Abstract: The present disclosure provides miRNA mimics targeting CDK4 and/or CDK6, and compositions comprising the same. Methods for the treatment of tumors, including but not limited to colon cancer, comprising administering a modified oligonucleotide comprising a miRNA are also disclosed herein.

Abstract: The invention provides a method for optimizing the treatment of colorectal cancer in a subject comprising the steps of extracting colorectal cancer cells from the subject, determining the transcriptional response in colorectal cancer cells across four or more clinically used chemotherapeutic drugs in terms of gene identity, magnitude of change, and p53 dependence, and determining the gene signature to determine the optimal course of treatment for the subject.

Abstract: Prodigiosin analogs which reactivate the p53 pathway are provided, as well as compositions of these compounds, and methods for reactivation of the p53 pathway using these compounds are provided. The prodigiosin analogs may be used to treat cancer in which p53 mutation plays a role, including prostate cancer, breast cancer, kidney cancer, ovarian cancer, lymphoma, leukemia, and glioblastoma, among others.

Abstract: A method of treating a subject having colon cancer with a small molecule drug for treating colon cancer is described. The method includes determining the effect of the small molecule drug on the release of a plurality of immunomodulating factors by colon cancer cells; and treating the subject with a therapeutically effect amount of the drug if the effect of the drug on the release of immunomodulating factors indicates that the drug promotes anti-tumor immunity, or selecting a different drug for treating colon cancer if the effect of the drug on immunomodulating factor release indicates that the drug does not promote anti-tumor immunity. Methods of evaluating ongoing treatment using the method are also described.

Abstract: A method of treating a neuroendocrine tumor in a subject is described. The method includes determining the level of expression of neuroendocrine differentiation markers and/or TRAIL signaling pathway markers by the tumor, and either treating the subject with a therapeutically effective amount of an imipridone compound if the level of expression of one or more markers is high or treating the subject with a higher dose of the imipridone compound or a different neuroendocrine tumor treatment method.

Abstract: A method of treating cancer, where the biomarkers are predictive of response to PD-1/PD-L1 blockade and GSK-3 inhibition, and which can be used in the method of treatment.

Abstract: The invention provides small-molecule inhibition of GSK-3 to increase efficacy of ICB and improve response in patients with microsatellite stable colorectal cancer, and possibly other tumor types. These results demonstrate 9-ING-41 in combination with ?PD-1/PD-L1 therapy.

Abstract: The present disclosure provides miRNA mimics targeting CDK4 and/or CDK6, and compositions comprising the same. Methods for the treatment of tumors, including but not limited to colon cancer, comprising administering a modified oligonucleotide comprising a miRNA are also disclosed herein.

Abstract: A method of reducing toxic side effects in a subject undergoing cancer treatment is described. The method includes administering an effective amount of a TRAIL compound to the subject.

Abstract: The present disclosure provides compositions comprising miR-3132 and one or more pharmaceutical agents that upregulate TNF-related apoptosis-inducing ligand (TRAIL) or activate TRAIL signaling pathway, and methods for treating a cancer comprising administering miR-3132, or a composition comprising miR-3132 and one or more pharmaceutical agents that upregulate TRAIL or activate TRAIL signaling pathway, to a subject.