Methods for diagnosing a subject as a candidate for removal of a solid tumor without preoperative chemoradiation therapy, and methods for treating patients having solid tumors, who have one or more of genomic instability, elevated double stranded DNA breaks, elevated gamma-H2AX foci, or elevated replication stress and/or double stranded break-signalling (DSB-signalling) biomarkers in peripheral blood lymphocytes (PBLs) are provided herein.

Methods for diagnosing a subject as a candidate for removal of a solid tumor without preoperative chemoradiation therapy, and methods for treating patients having solid tumors, who have one or more of genomic instability, elevated double stranded DNA breaks, elevated gamma-H2AX foci, or elevated replication stress and/or double stranded break-signalling (DSB-signalling) biomarkers in peripheral blood lymphocytes (PBLs) are provided herein.

The technology described herein is directed to methods of treating and diagnosing bronchial premalignant lesions, e.g. by determining the lesion subtype using one or more biomarkers described herein.

The technology described herein is directed to methods of treating and diagnosing bronchial premalignant lesions, e.g. by determining the lesion subtype using one or more biomarkers described herein.

The present disclosure provides methods of identifying patients who have partial or total resistance to HIF-2 inhibitors or who develop partial or total resistance to HIF-2 inhibitors after treatment and providing suitable treatment to these patients.

The invention is directed to biomarkers for predicting a patient's response, both therapeutic and toxic, to immunotherapy.

The invention is directed to biomarkers for predicting a patient's response, both therapeutic and toxic, to immunotherapy.

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.

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.

Provided are methods of selecting a patient with cancer and/or treating a patient with cancer that comprises a deleterious alteration in FBXW7 and/or an amplification of CCNL1 for CDK11 inhibitor and/or ATR inhibitor treatment. For example, the method of selecting a patient afflicted with a cancer likely to benefit from a CDK11 inhibitor and/or ATR inhibitor treatment, the method comprising: obtaining a biological sample; testing the sample for i) loss of function FBXW7, optionally for a deleterious mutation in F box WD-repeat containing protein (FBXW7) substrate binding domain and/or ii) upregulated CCNL1, optionally a gain or amplification of CCNL1; and selecting the patient having i) loss of function FBXW7, optionally a deleterious mutation in the FBWX7 substrate-binding domain or ii) upregulated CCNL1, optionally a gain or amplification of CCNL1, as likely to benefit and/or for treatment with the CDK11 inhibitor and/or ATR inhibitor.