The present disclosure relates to a method for diagnosing in a subject the progression from myelodysplastic syndrome (MDS) to acute myelogenous leukemia (AML). Also disclosed are methods of treating AML in a subject diagnosed by the disclosed methods.

Provided is a peripheral blood biomarker for evaluating the antitumor immune effect of radiation therapy. Also provided is a method in which the composition of cell subpopulation in a sample obtained from a subject is used as an index for immune activation in the subject caused by a radiation therapy. By comparing, with a reference, the amount of CD4.sup.+ T cell subpopulation that correlates with dendritic cell stimulation in an antitumor immune response or the amount of dendritic cell subpopulation that correlates with the dendritic cell stimulation in an antitumor immune response, the presence or absence of, and/or the magnitude of, immune activation occurring in the subject as a result of a radiation therapy can be determined.

The invention provides methods of treating cancer and methods for selecting treatment approaches for cancer.

Disclosed by the present invention are an antibody targeting CTLA-4, a preparation method therefor and a use thereof. In particular, disclosed by the present invention is a novel fully human monoclonal antibody that targets CTLA-4. Further disclosed by the present invention is a method for preparing the monoclonal antibody. The monoclonal antibody of the present invention is capable of binding a CTLA-4 antigen with high specificity, has a high affinity, remarkable anti-tumor activity, and so on.

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 a method for diagnosing in a subject the progression from myelodysplastic syndrome (MDS) to acute myelogenous leukemia (AML). Also disclosed are methods of treating AML in a subject diagnosed by the disclosed methods.

The present disclosure relates to antibodies having the ability of binding to the immune checkpoint protein programmed death-1 (PD-1), such as human PD-1, or nucleic acids encoding such antibodies. The present disclosure also relates to compositions or kits comprising said antibodies or nucleic acids, as well as to the use of these antibodies or nucleic acids or compositions in the field of medicine, preferably in the field of immunotherapy, e.g., for the treatment of cancers. The present invention further relates to methods for inducing an immune response in a subject comprising providing to the subject an antibody having the ability of binding to the immune checkpoint protein PD-1, such as human PD-1, or a nucleic acid encoding such an antibody, or a composition comprising said antibody or nucleic acid.

The present invention provides a bispecific antibody and a use thereof. The bispecific antibody comprises a first protein functional zone and a second protein functional zone. TIM-3 full-length antibody of targeting TIM-3 corresponding to the targeting TIM-3 in the first protein functional zone has a low binding activity with Macaca TIM-3, has strong binding activity with Marmoset and human TIM-3, and can activate the killing effect of a human NK cell on the tumor cell. The bispecific antibody reserves the activity of a single TIM-3 antibody of activating PBMC(NK) to kill the tumor cell while reserving the original activity of the other protein functional zone, and can achieve the same activity of being combined with two molecules or better activate the activity of a T lymphocyte.

Provided herein are methods of detecting glycosylated proteins, such as immune checkpoint proteins. Further provided are methods of treating cancer, such as by administering immune checkpoint inhibitors.

Methods of treating cancer and improving immunotherapies comprising decreasing soluble immune receptor levels are provided. Agents that bind membranal immune receptor and inhibit proteolytic cleavage of the receptor and agents that bind soluble immune receptor and that are neither receptor agonists nor antagonists are also provided, as are methods of producing these agents.