Provided herein are methods and systems of molecular profiling of diseases, such as cancer. In some embodiments, the molecular profiling can be used to identify treatments for the disease, such as treatments that provide likely benefit or likely lack of benefit for the disease.

The present disclosure relates to methods of determining a treatment course of action. In particular, the present disclosure relates to compositions and methods for determining responsiveness to estrogen and estrogen blocking therapies for cancer.

The invention features diagnostic and therapeutic methods and compositions featuring androgen receptor variant proteins and nucleic acid molecules whose expression is increased in androgen related diseases or disorders.

The present invention falls within the field of the early diagnosis of tumours of the oral cavity. In particular, the invention relates to a method for the diagnosis and/or for predicting the risk of developing tumours of the oral cavity comprising the detection in cell extracts of certain markers of tumours of the oral cavity using immunological assays, for example ELISA (enzyme-linked immunosorbent assay). The invention also relates to the relative kit for the diagnosis and/or for predicting the risk of developing tumours of the oral cavity.

A method that includes testing for the presence of a phosphorylated Ser294 (phospho-Ser294) progesterone receptor (PR). A method that includes determining the expression level of a gene in a patient sample and comparing it to a control sample.

Acute exposure to estrogenic chemicals is shown herein to induce DNA damage mediated by formation of ERα-dependent R-loops. Disclosed herein are methods for evaluating the safety and activity of a xenoestrogen. Also disclosed are methods for identifying subject particularly susceptible to the genotoxic effects of endogenous estrogens or environmental xenoestrogens. This method can be used to select suitable hormone therapies, such as a selective estrogen receptor modulator (SERM), aromatase inhibitor, or selective estrogen receptor degrader (SERD).

Disclosed herein are methods and compositions for inactivation of the human glucocorticoid receptor (GR) gene by targeted cleavage of genomic DNA encoding the GR. Such methods and compositions are useful, for example, in therapeutic applications which require retention of immune function during glucocorticoid treatment.

The present invention relates to a cell as deposited under accession number DSM ACC332 and derivatives thereof. Furthermore, the present invention relates to methods for testing a compound of interest for potential estrogenic or anti-estrogenic activity as well as to methods for testing a cell for its potential to form discontinuous basolateral adherens junctions in presence of an anti-estrogenic compound. The application relates also to uses of a cell capable of forming discontinuous basolateral adherens junctions. The present invention relates furthermore to methods of analysing the morphology of adherens junctions in tissue of a subject and a respective kit.

A method that includes testing for the presence of a phosphorylated Ser294 (phospho-Ser294) progesterone receptor (PR). A method that includes determining the expression level of a gene in a patient sample and comparing it to a control sample.

The present invention is concerned with the detection of ligands which bind to and activate steroid hormone receptors. Specifically, the present invention provides test kits and assay methods for the selective identification of steroid hormone receptor ligands from a test sample. Importantly, the test kits and assay methods described herein are cell-free, and do not require expensive-to-manufacture nuclear extracts for their performance. Instead, the test kits and assay methods described herein employ single polypeptide polymerases, such as T7 RNA polymerase, linked to a reporter construct. Activity of the enzyme is inhibited, rather than activated, by ligand-bound steroid hormone receptor complexes which only form in the presence of a target ligand. Accordingly, a measured change in a physical property of the reporter construct (e.g. fluorescence output) may be used to determine the presence of a target ligand in a sample under investigation.