Surrogate co-receptors for T cells, including T cells expressing chimeric receptors comprising major histocompatibility molecules grafted onto T cell receptor molecules. The surrogate co-receptors feature a portion of CD8, wherein the Ig domains of CD8 are replaced with Ig domains that confer novel specificities (e.g. antibody Fv fragments specific for a target of interest.) The surrogate co-receptors may be used to help enhance CRM.sup.pMHC-CD3 signaling as part of a 5-module receptor system. The present invention also describes Lck fusions.

Disclosed herein are compositions and in vitro and in vivo methods for reprogramming lymphatic tissue to induce the lymphatic tissue to form a lymphovenous anastomosis with an adjacent vessel of the venous system.

Disclosed herein are methods of culturing immune cells in a medium comprising at least about 5 mM potassium ion, wherein the medium is capable of increasing the stemness of the immune cells. In some aspects, the immune cells which are cultured using the methods provided herein are modified to express a ROR1-binding protein and have increased level of c-Jun protein. In some aspects, the immune cells are administered to a subject in need thereof.

The invention relates to truncated isolated BRK peptides and functional peptides thereof that inhibit the phosphorylation of p27Kip1 and the resulting kinase activity of CDK2 and CDK4; and to pharmaceutical compositions thereof. The invention further relates to the use of the isolated peptides in methods of treating cancer in subject in need thereof.

The current invention relates to a chimeric polypeptide, a nucleic acid encoding such chimeric polypeptide, a cell comprising such chimeric polypeptide of nucleic acid, preferably a T cell, a CAR T cell, NK cell or a CAR NK cell, and method of treatment using such cell, polypeptide of nucleic acid in the treatment of cancer, in particular in immune cell therapy. The chimeric polypeptide according to the invention allows for the reversible and dose dependent control of T cell and NK cell function (cytokine release, cytotoxicity).

The present invention relates to methods of treating cancer patients carrying one or more specific fusion genes. It is based, at least in part, on the discovery that the protein encoded by the MAN2A1-FER fusion gene exhibits kinase activity and the use of tyrosine kinase inhibitors targeting MAN2A1-FER in a cancer other than prostate, for example hepatocellular cancer, led to dramatic improvement of survival of animals xenografted with the cancer.

Described herein is a compound selected from the group consisting of AZ960, CYC116, MI-3, Nexturastat A, TAK-901, Tubastatin A hydrochloride salt, and a small interfering RNA molecule comprising any one of SEQ ID No. 5 to SEQ ID No. 28 for use in the treatment of Hepatitis B. The compound may also be used in the manufacture of a medicament for the treatment of Hepatitis B. Also described is a method of treating a Hepatitis B infection in a subject, the method comprises administering to the subject a therapeutically effective dose of the compound as described above.

Provided herein are chimeric inhibitory receptor constructs and compositions, and cells comprising the same. Also provided are methods of using chimeric inhibitory receptor constructs and compositions, and cells comprising the same.

Receptor protein kinases (RPTKs) transmit extracellular signals across the plasma membrane to cytosolic proteins, stimulating formation of complexes that regulate key cellular functions. Over 5 half of the known tyrosine kinases are implicated in human cancers and are therefore highly promising drug targets. A large-scale loss-of-function analysis of tyrosine kinases using RNA interference in the clinically relevant Erb-B2 positive, BT474 breast cancer cell line showed that Bruton's tyrosine kinase (BTK), a cytosolic, non-receptor tyrosine kinase that has been extensively studied for its role in B cell development, is required, in altered form, for BT474 10 breast cancer survival. This alternative form contains an amino-terminal extension that is also present in tumorigenic breast cells at significantly higher levels than in normal breast cells.

The present invention relates to methods of treating cancer patients carrying one or more specific fusion genes. It is based, at least in part, on the discovery that the protein encoded by the MAN2A1-FER fusion gene exhibits kinase activity and the use of tyrosine kinase inhibitors targeting MAN2A1-FER in a cancer other than prostate, for example hepatocellular cancer, led to dramatic improvement of survival of animals xenografted with the cancer.