The present application discloses a lentiviral transfer system which includes: (i) a self-inactivating transfer vector comprising: multiple gene units, wherein each gene unit includes a heterologous nucleic acid sequence operably linked to a regulatory nucleic acid sequence; and (ii) a helper construct which lacks a 5 LTR, wherein the 5 LTR has been replaced with a heterologous promoter, in which the helper construct further comprises: a lentiviral env nucleic acid sequence containing a deletion, wherein the deleted env nucleic acid sequence does not produce functional env protein; and a packaging signal contains a deletion, wherein the deleted packaging signal is nonfunctional.

A new system for identification and treatment against cancer, specifically the mutation or deletion of an antioncogene. An ideal candidate is a patient with family history for hereditary mutations in a known antioncogene. The first method of this system identifies the mutation of a patient's at-risk antioncogene by causing a natural fluorescence only when the specific at-risk antioncogene has mutated or deleted. The second method of this system utilizes a virus to attack and dissolve cancer cells with special markers to avoid the damage to normal cells, thereby achieving the purpose of treating cancer.

The present invention relates to the identification of p53 biomarker profiles that predict response in patients with hyperproliferative disease such as cancer to a therapy, and their use in methods of treating such patients with an anti-hyperproliferative disease gene therapy.

The present invention relates to engineered cells that enable exosome-mediated delivery of therapeutic cargoes, in particular protein therapeutics and RNA therapeutics. The present invention also relates to inventive polynucleotides, polypeptides and pharmaceutical compositions.

A peptide sequence of a guide protein for the production of a peptide of interest; a peptide sequence that has a similarity of at least 90% to SEQ. ID. NO 1; a nucleotide sequence encoding the guide protein; an expression vector comprising the nucleotide sequence; a host cell that expresses a fusion protein comprising a peptide of interest; a method of production of a peptide of interest, comprising the steps of A) constructing an expression vector; B) inserting the expression vector into a host cell; C) expressing the fusion protein, culturing the host cell in a culture medium; D) recovering the accumulated fusion protein in the host cell; E) cleaving the fusion protein; F) purifying the peptide of interest.

The present disclosure is directed to methods and compositions for inhibiting a cancer cell using nucleic acid sequences encoding elephant p53 or elephant p53 amino acid sequences.

This invention is generally related to modified peptidic oligomers that have an increased ability to reach the cytosol or nucleus. In some embodiments, the modified peptidic oligomer molecules deliver an associated cargo molecule to the cytosol or nucleus. Other embodiments of the invention relate to modified peptidic oligomer fusion molecules that reach the cytosol or nucleus.

The present invention relates to a method for determining sensitivity to a simultaneous inhibitor against poly ADP ribose polymerase (PARP) and Tankyrase. According to the present invention, a colorectal treatment effect can be maximized by sorting patients having sensitivity to the simultaneous inhibitor against PARP and Tankyrase.

The invention relates to novel peptides having an HDM-2 targeting sequence that target the human minute binding protein-2. The invention also relates to fusion proteins comprising a HDM-2 targeting sequence. The invention also relates to methods of using the peptides to treat cancer.

Disclosed are methods of isolating T cells having antigenic specificity for a mutated p53 amino acid sequence encoded by a cancer-specific p53 mutation, the method comprising: inducing autologous APCs of the patient to present the mutated p53 amino acid sequence; co-culturing autologous T cells of the patient with the autologous APCs that present the mutated p53 amino acid sequence; and selecting the autologous T cells. Also disclosed are related methods of preparing a population of cells, populations of cells, pharmaceutical compositions, and methods of treating or preventing cancer.