The present invention includes compositions and methods for the treatment of cancer comprising an antineoplastic drug and an inhibitor of chromosome maintenance region 1 (CRM1) protein expression or activity, wherein the inhibitor of CRM1 enhances the anti-neoplastic effect of the antineoplastic drug.

Described herein are methods and compositions for treatment of immune-related diseases or disorders by modulating DD1 activity, alone or in combination with modulation of PD-1 activity. In some embodiments, the methods and compositions described herein are directed to treatment of cancer and/or infections (e.g., bacterial infection, and/or fungal infection). In some embodiments, the methods and compositions described herein are directed to treatment of autoimmune diseases and/or inflammation. In some embodiments, the methods and compositions described herein are directed to treatment of asthma, and allergy. Methods for identifying patients who are more likely to be responsive to and benefit from an immunotherapy that targets DD1 and/or PD-1 activity or expression are also described herein.

Disclosed herein are methods for treating subjects with breast cancer, comprising determining a therapeutic regimen for cancer by measuring the level (amount) of proteins of one or more biomarkers. Also disclosed are methods of treating a subject with breast cancer by predicting or assessing a therapeutic outcome for subject.

The present invention is in the field of oncology, and more particularly of cancer stem cells. It relates to a method for producing cancer stem cells based on overexpression of 133p53 isoform, 133p53 isoform, or both 133p53 and 133p53 isoforms; a method for predicting the risk that treatment with a chemotherapeutic anti-cancer agent induces cancer stem cells in a subject suffering from cancer from a cancer sample of said subject, based on detection of an increase in 133p53 isoform, 133p53 isoform, or both 133p53 and 133p53 isoforms following chemotherapeutic anti-cancer treatment; to therapeutic uses of a combination of chemotherapeutic anti-cancer agent and an agent reducing 133p53 isoform, 133p53 isoform, or both 133p53 and 133p53 isoforms expression; and also to screening methods for anti-cancer stem cells agents.

The use and screening of modulators of apoptosis is disclosed. The modulators may be, for example, modulator of NF-B activity. The modulators may be used, for example, in the treatment of NF-B-mediated diseases, conditions, and injuries.

Methods are provided for predicting and diagnosing the presence of breast cancer in women with dense breasts, as well as for assessing the therapeutic efficacy of a cancer treatment and determining whether a subject potentially is developing cancer.

The use and screening of modulators of apoptosis is disclosed. The modulators may be, for example, modulator of NF-B activity. The modulators may be used, for example, in the treatment of NF-B-mediated diseases, conditions, and injuries.

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 invention is based on a finding that silencing CIP2A (KIAA1524) gene sensitizes cancer cells for apoptosis-inducing activity of certain small molecule chemotherapeutic agents. Thus, the invention is directed to a respective combination therapy, sensitization method and pharmaceutical compositions. The invention further relates to a method of selecting cancer therapy for a subject on the basis of CIP2A and p53 expression and/or protein activity in a sample obtained from said subject.

PDGFRb inhibitors and the use of such inhibitors to treat mutant p53-expressing tumors are described. The present disclosure encompasses the discovery that mutant p53-induced upregulation of the platelet-derived growth factor receptor b (PDGFRb) contributes to invasion and/or metastasis of tumors expressing mutant p53. Specifically, the present disclosure encompasses the discovery that mutant p53 can disrupt a p73/NF-Y complex (which can repress PDGFRB transcription), leading to transcription of PDGFRb. The present disclosure therefore provides, at least in part, PDGFRb modulators (e.g., activators or inhibitors) for use in medicine, and specifically in diagnosis, treatment and/or prevention (e.g., delay of onset) of certain disorders, e.g., cancer.