The present invention provides, inter alia, methods for treating, preventing, or ameliorating the effects of a lymphoid malignancy, such as those associated with a mutated phosphatase and tensin homolog (PTEN) gene, or T-cell acute lymphoblastic leukemia (T-ALL). These methods include administering to a subject an effective amount of a phosphoinositide 3-kinase-delta (PI3K) inhibitor and a phosphoinositide 3-kinase-gamma (PI3K) inhibitor. The present invention also provides pharmaceutical compositions for treating the effects of a lymphoid malignancy. This invention further provides a method for identifying a subject who may benefit from co-treatment with a PI3K inhibitor and a PI3K inhibitor. This method includes determining from a sample of the subject whether the subject has a mutated PTEN gene. Additionally, this invention provides methods for identifying a compound that has both PI3K and PI3K inhibitory activity.

Disclosed is a kit for detecting drug resistance of cetuximab in the treatment of metastatic colorectal cancer. The kit comprises a substance used for detecting gene mutations in Exon 19 of the PIK3CA gene, and may further comprise a specification recording the following contents: if Exon 19 in the PIK3CA gene of a patient with metastatic colorectal cancer as a subject to be tested, who is intended to receive cetuximab treatment or is receiving cetuximab treatment and does not have drug resistance, has at least one of K944N, F930S, V955G, V955I, and K966E mutations, the subject to be tested will develop drug resistance or will be a candidate to develop drug resistance when receiving or continuing to receive cetuximab for treating metastatic colorectal cancer.

Disclosed herein are polypeptide fragments and polynucleotides based on mutant capicua transcriptional repressor (CIC), catenin beta 1 (CTNNB1), v-erb-b2 erythroblastic leukemia viral oncogene homolog B (ERBB2), kirsten rat sarcoma (KRAS), phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha (PIK3CA), phosphatase and tensin homolog (PTEN), splicing factor 3b subunit 1 (SF3B1), SRY-box transcription factor 17 (SOX17), tumor protein 53 (TP53), and cytomegalovirus (CMV) sequences, vectors, host cells, viruses, methods for generating CD8+ T-cells, and methods of treatment. Also disclosed herein are T-cell receptors (TCRs), polynucleotides, vectors and cells comprising the TCRs, and methods of treatment.

Use of p55 as a therapeutic target for aortic dissection (AD) is provided, belonging to the technical field of biomedicine. Over-expression of the p55 inhibits formation of the AD and degradation of elastic fibers in mice induced by -aminopropionitrile fumarate (BAPN); whereas knockdown of the p55 in vascular smooth muscle cells (VSMCs) promotes the formation of the AD and the degradation of the elastic fibers induced by the BAPN. Mechanistically, the p55 plays a role by maintaining phenotypic switching of the VSMCs, and knocking down the p55 promotes phenotypic switching of the VSMCs from a contractile phenotype to a synthetic phenotype. The p55 is used as a target in screening a drug for prevention and/or treatment of AD, such that a selected drug can effectively prevent and/or treat the AD, thus providing a new target for treating the AD.