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 molecular profiling can include analysis of a sequence of a nucleic acid. The invention provides a method of identifying at least one treatment associated with a cancer in a subject. In still another related aspect, the invention provides use of a reagent in carrying out the methods of the invention, and/or use of a reagent in the manufacture of a reagent or kit for carrying out the methods of the invention. In an aspect, the invention provides a system for identifying at least one treatment associated with a cancer in a subject.

The application provides polypeptides comprising or essentially consisting of at least one heavy chain variable domain of a heavy chain antibody (V.sub.HH) or a functional fragment thereof, wherein said V.sub.HH or a functional fragment thereof specifically binds to a target protein that is present on and/or specific for a solid tumor, e.g. HER2. The application further provides nucleic acids encoding such polypeptides; methods for preparing such polypeptides; host cells expressing or capable of expressing such polypeptides; compositions, and in particular to pharmaceutical compositions, that comprise such polypeptides, nucleic acids and/or host cells. The application further provides such polypeptides, nucleic acids, host cells and/or compositions, for use in methods for detection, imaging, prognosis and diagnosis of cancer as well as for predicting patient response(s) to therapeutics.

Disclosed herein are methods for treating a cancer and a method for sensitizing a cancer to a chemotherapeutic agent. Each method administers an agent that selectively inhibits HDAC1 and HDAC2 to a subject in need thereof. Also disclosed herein are methods for determining if a cancer is sensitive to an agent that selectively inhibits HDAC1 and HDAC2 and methods for monitoring the efficacy of a treatment for a cancer that includes administration of an agent that selectively inhibits HDAC1 and HDAC2.

The present invention provides methods of treating cancer by inhibiting MECP2 and identifying cancers that will respond to therapy using MECP2 as a biomarker.

Disclosed herein are a method and a biomarker for predicting efficacy and prognosis of or resistance to an immunotherapy. The use of the biomarkers (TCTP, EGFR, AKT, MCL1, and/or CXCL10) of the present disclosure allows the prediction of resistance to or prognosis of a cancer immunotherapeutic agent and the selection of a therapy guaranteeing therapeutic benefit, thereby finding advantageous applications in treating cancers or tumors resistant to cancer immunotherapeutic agents.

The present invention relates to peptides, proteins, nucleic acids and cells for use in immunotherapeutic methods. In particular, the present invention relates to the immunotherapy of cancer. The present invention furthermore relates to tumor-associated T-cell peptide epitopes, alone or in combination with other tumor-associated peptides that can for example serve as active pharmaceutical ingredients of vaccine compositions that stimulate anti-tumor immune responses, or to stimulate T cells ex vivo and transfer into patients. Peptides bound to molecules of the major histocompatibility complex (MHC), or peptides as such, can also be targets of antibodies, soluble T-cell receptors, and other binding molecules.

A method for targeting cancer cells is described. The method uses immunizing a dromedary camel or llama with a WNT16B molecule to generate anti-WNT16B antibodies, then preparing a set of anti-WNT16B IgG blocking antibodies from the camel or llama. Cancer cells are targeted with the blocking anti-WNT16B IgG antibodies, which can be used for more effective chemotherapy and radiotherapy. The anti-WNT16B IgG antibodies can also be used in vitro or in vivo to detect cancer cells.

The present invention relates to a method for the prognosis of bone metastasis in triple negative (including basal-like) breast cancer or, alternatively, ER+ breast cancer (including luminal A and B) which comprises determining if the c-MAF gene is amplified in a primary tumor sample. Likewise, the invention also relates to a method for determining the tendency to develop bone metastasis with respect to metastasis in other organs, which comprise determining the c-MAF gene expression level, amplification or translocation. The invention also relates to a method for predicting early bone metastasis in a subject suffering breast cancer. The invention also relates to a c-MAF inhibitor as therapeutic agent for use in the treatment of triple negative (including basal-like) breast cancer metastasis or, alternatively, ER+ breast cancer (including luminal A and B) metastasis. The invention relates to kits for predicting bone metastasis and predicting the clinical outcome of a subject suffering from bone metastasis. Finally, the invention relates to a method for typing of a subject suffering breast cancer and for classifying a subject from breast cancer into a cohort.

The invention relates to an anti-GREM1 antagonist for use in a method for the treatment or prevention of a cancer.

The present invention relates to a method of detecting clustering of Rat Sarcoma Vims (Ras) protein in a cell comprising culturing the cells on an array of nanostructures and detecting the clustering of Ras protein around the nanostructures by using optical microscopy. In one embodiment, the nanostructures are nanobars. The invention further relates to the use of the method in identifying the isoform or mutation status of Ras protein, and anti-Ras drug screening.