High mitochondrial ATP is a metabolic trait that confers hyper-proliferation, sternness, anchorage-independence, anti-oxidant capacity and multi-drug resistance in cancer cells. Under the present approach, intracellular ATP levels may be used as a metabolic biomarker to identify, separate, and purify an aggressive and hyper-proliferative cancer stem cell (“CSC”) phenotype. Further, ATP may be combined with other CSC markers, e.g., CD44 or ALDH-activity, to beneficially fractionate the CSC population into sub-populations. For example, ATP-high/ CD44-high CSC sub-populations showed twice the level of anchorage-independent growth compared to ATP-low/CD44-high CSC sub-populations. Also disclosed are complementary bioinformatic data that implicate mitochondrial ATP synthesis in stemness, metastasis, and the detection of circulating tumor cells (“CTCs”), and a five-member, ATP-related metastasis gene-signature (ABCA2, ATP5F1C, COX20, NDUFA2 and UQCRB). The gene signature of the present approach may be used to identify CSCs having a dramatic increase in cell migration and invasion in vitro capacity, as well as spontaneous metastasis in vivo. The present approach also provides a cellular platform for systematically targeting sternness, multi-drug resistance, and metastasis in cancer cells.

The present disclosure relates to the field of cancer. More particularly, the invention relates to methods of diagnosing and treating cancer, including determining a cancer type thereof. These methods involve the detection of markers in an exosome sample of the subject.

An automated method and system for determining the risk of developing a cancer in a subject, the method comprising preparing a tissue sample obtained from the subject for visually identifying at least one biological marker associated with the cancer, digitally scanning the prepared tissue sample, analyzing the scanned image of the tissue sample to identify regions of interest, quantifying at least one parameter associated with the marker, and executing an algorithm using the quantified parameter to calculate a risk score, wherein the risk score is representative of the risk of the individual developing the cancer.

A method for predicting susceptibility to stimulator of interferon genes (STING) agonists of a cancer patient is provided, comprising (1) obtaining at least one sample from the cancer patient; (2) detecting an expression level of S-methyl-5′-thioadenosine phosphorylase (MTAP) in the at least one sample by using at least one specific probe; and (3) if MTAP is expressed in the at least one sample, then predicting that the cancer patient has high-susceptibility to STING agonists and providing STING agonists to treat the cancer patient; otherwise providing non-STING agonists for treatment.

A method is disclosed for treating a cancer in a subject that involves administering to the subject a therapeutically affective amount of a geranylgeranyltransferase I (GGTase I) inhibitor, such as GGTI-2418, wherein the cancer comprises a defective PTEN, a hyperactivated FBXL2, or a low level of IP3R3. In some embodiments, the method further involves administering to the subject a therapeutically affective amount of an Akt inhibitor.

Methods and compositions are provided for oligonucleotides that bind targets of interest. The targets include cells and microvesicles, such as those derived from various diseases. The oligonucleotides can be used for diagnostic and therapeutic purposes. The target of the oligonucleotides can be a target such as PARP1, HIST1H1B, HIST1H1D, NCL, FBL, SFPQ, RPL12, ACTB, HIST1H4A, SSBP1, NONO, H2AFJ, and DDX21, or a complex, subunit or fragment thereof.

The present invention relates to methods for predicting the response of a breast cancer patient to a chemotherapy. The present invention further relates to a method of determining whether to treat a breast cancer patient with a chemotherapy. The present invention also relates to a kit for predicting the response of a breast cancer patient to a chemotherapy.

The present invention relates to the field of medicine and in particular to the treatment of cancer. More particularly, the invention relates to a method of assessing the sensitivity or resistance of a subject having a cancer to an oncolytic virus, to a method of selecting a treatment comprising an oncolytic virus efficient against the cancer of a subject and to a method of monitoring in a subject the response to a cancer treatment comprising an oncolytic virus. The description further relates to products including a therapeutic recombinant virus, in particular a recombinant oncolytic virus, typically a vaccinia virus, a pharmaceutical composition, and a kit comprising such a therapeutic virus, as well as preparation and uses thereof.

A method for detecting a tumor cell surface marker molecule PD-L1, comprising the following steps: providing a capture screen that has antibodies capable of specifically binding to tumor cells; making a sample to be tested flow through the capture screen, such that tumor cells in the sample to be tested bind to the capture screen; fixing captured tumor cells on the capture screen; and successively using a PD-L1 primary antibody solution, a PD-L1 secondary antibody solution labeled with a fluorophore AlexaFluor 647, a pan-CK-AlexaFluor 488 primary antibody solution, a CD45 primary antibody solution and a CD45 secondary antibody solution labeled with a fluorophore AlexaFluor 568, to incubate the cells fixed on the capture screen, and then labeling all cells on the capture screen with a nuclear fluorescent dye.

The present disclosure relates generally to methods and compositions for cancer immunotherapy, and more specifically, liquid markers for predicting effectiveness of cancer therapies. The disclosure features compositions and methods that are useful for predicting the efficacy of cancer treatment (e.g., a checkpoint inhibitor immunotherapy) and, in some embodiments, administering the cancer treatment such as immunotherapy.