A method for treating cancer in a human subject includes initiating a cancer therapy on the human subject, preparing a biological sample from the human subject; (i) mixing the biological sample with an antibody or aptamer that specifically binds to an MEST protein, or (ii) obtaining mRNA of a nucleotide sequence encoding the MEST protein from the biological sample, and synthesizing and amplifying cDNA from the mRNA, detecting the MEST protein bound to the antibody or aptamer, or an expression of the cDNA, determining if the detected MEST or a level of the expression is higher than that in a normal human subject, determining responsiveness of the cancer to the cancer therapy by the detected MEST or the level of the expression, and continuing the cancer therapy to treat the cancer if it is determined that there is the responsiveness of the cancer to the cancer therapy.

An anticancer agent for cancers in which an abundance of cyclin D1 protein is greater than that in a control, the anticancer agent including a compound represented by the following Formula (1) as an active ingredient (in Formula (1), R.sup.1 to R.sup.11 each independently represent a hydrogen atom, an aliphatic group having 1 to 30 carbon atoms, or a group represented by Formula RCO— (where, R represents an aliphatic group having 1 to 30 carbon atoms, or an aromatic group or heteroaromatic group having 1 to 10 carbon atoms)). ##STR00001##

Isolated antibodies that bind specifically to R-spondin 3 (RSPO3) are described. Also described herein are compositions containing the antibodies and methods of using the antibodies to treat cancer and detect RSPO3.

The present disclosure is related to systems and methods to be used as aids in the diagnosis of risk for carcinoma, lesions, or dysplasia by identifying cellular phenotype characteristics of cell samples, including percentage of mature squamous cells, presence or absence of nuclear actin in mature squamous cells, percentage of non-mature squamous cells, percentage of small round cells, percentage of white blood cells, and percentage of lone nuclei.

Provided herein are methods of treating NMD-dependent tumors by administering an SMG1-inhibitor to a patient in need of such treatment and combination therapies comprising the same.

Provided are biomarkers for predicting the efficacy of MDM2 inhibitor or Bcl-2/Bcl-xL dual inhibitors or Bcl-2 inhibitor or Bcl-xL inhibitor in treating cancer patients. Also provided are compositions, e.g., kits, for evaluating gene levels of the biomarkers and methods of using such gene levels to predict a cancer patient's response to the MDM2 inhibitors or Bcl-2/Bcl-xL dual inhibitors or Bcl-2 inhibitor or Bcl-xL inhibitor. Such information can be used in determining prognosis and treatment options for cancer patients.

The present disclosure relates to compositions and methods for the diagnosis and treatment or prevention of cancers that exhibit elevated expression of the glutamate/cysteine transporter SLC7A11, reduced expression of the fatty acid transporter SLC25A45 and/or reduced expression of FAM3 metabolism regulating signaling molecule B (FAM3B). In particular, the instant disclosure provides for identification of a cancer as possessing elevated SLC7A11 expression, reduced expression of SLC25A45 and/or reduced expression of FAM3B, and selecting and/or administering a glutaminase inhibitor as a therapeutic agent for such a cancer and/or subject having or at risk of developing such a cancer. Methods and compositions for therapies that combine such selection of cancers/subjects for glutaminase inhibitor therapy with other cancer therapies and/or chemotherapeutic agents are also provided.

The present disclosure relates to the treatment of HPV-associated cancers by small molecule PD-L1 inhibitors.

Heritable mutations in the BRCA1 and BRCA2 and other genes in the DNA double-strand break (DSB) repair pathway increase risk of breast, ovarian and other cancers. In response to DNA breaks, the proteins encoded by these genes bind to each other and are transported into the nucleus to form nuclear foci and initiate homologous recombination. Flow cytometry-based functional variant analyses (FVAs) were developed to determine whether variants in BRCA1 or other DSB repair genes disrupted the binding of BRCA1 to its protein partners, the phosphorylation of p53 or the transport of the BRCA1 complex to the nucleus in response to DNA damage. Each of these assays distinguished high-risk BRCA1 mutations from low-risk BRCA1 controls. Mutations in other DSB repair pathway genes produced molecular phenocopies with these assays. FVA assays may represent an adjunct to sequencing for categorizing VUS or may represent a stand-alone measure for assessing breast cancer risk.

The present invention concerns a method for predicting the potential for aggressive growth and/or the risk to progress to high grade cancer for tumors in cell based detection procedures. In one aspect the invention concerns the detection of overexpression of cyclin-dependent kinase inhibitor gene products as a tool for predicting the progression risk and/or potential for aggressive growth of tumors. In a second aspect the invention concerns predicting the progression risk and/or potential for aggressive growth in tumors on the basis of the simultaneous co-detection of the presence of overexpression of cyclin-dependent kinase inhibitor gene products together with the expression of markers for active cell proliferation. Further the invention concerns preparations of probes for diagnosis namely for predicting the progression risk and/or the potential for aggressive growth of tumors.