Herein is reported a polypeptide-polynucleotide-complex as therapeutic agent and its use as tool for the targeted delivery of an effector moiety. The polynucleotide part of the complex is essentially resistant to proteolytic and enzymatic degradation in vivo. Additionally the polypeptide part specifically binds to a compound or structure such as a tissue or organ, a process or a disease. Thus, one aspect as reported herein is a polypeptide-polynucleotide-complex comprising a) a polypeptide specifically binding to a target and conjugated to a first member of a binding pair, b) a polynucleotide linker conjugated at its first terminus to the second member of the binding pair, and c) an effector moiety conjugated to a polynucleotide that is complementary to at least a part of the polynucleotide linker.

Disclosed is a method comprising acquiring a value relating to VEGF-A of a subject, wherein the value is a measured value of total VEGF-A in a blood sample, or a value obtained by dividing a measured value of VEGF-A.sub.165b in the blood sample by a measured value of total VEGF-A in the blood sample (VEGF-A.sub.165b/total VEGF-A), and the value suggests prognosis of myocardial infarction of the subject or severity of coronary artery disease of the subject.

The invention provides biomarkers for predicting the response to checkpoint inhibitors. The inventors demonstrate that a PD-1/PD-L1 inhibitor exerts antitumor activity against tumor with low PD-L1 expression and immune-desert phenotype through blocking PD-L1 in the lymph nodes. The invention provides novel combinations of intratumoral markers for antigen cross-presenting cells and T cell chemokines which are expected to be superior efficacy-predicting biomarkers compared to existing methods.

Biomarkers for diagnosing the disease activity, disease severity or disease type of severe cutaneous adverse drug reactions (SCARs) such as drug-induced hypersensitivity syndrome and Stevens-Johnson syndrome/toxic epidermal necrolysis are provided. Also provided is a method of testing SCARs, comprising measuring the expression of at least one protein selected from the group consisting of stratifin, TNF receptor superfamily member 8 (CD30/TNFRSF8), interleukin-1 receptor antagonist (IL-1Ra), and TNF receptor superfamily member 6B (DcR3/TNFRSF6B) in a sample derived from a subject.

The present disclosure provides materials and methods for determining the presence of an N-terminal modification on a therapeutic protein, and/or the efficiency of N-terminal modification, such as PEGylation, at the N-terminus of a therapeutic protein such as Filgrastim (wherein the PEGylated version is therefore Pegfilgrastim).

The present invention relates to methods for treating an individual with high grade glioblastoma multiforme by preventing or disrupting the binding of CD95 to its ligand, CD95L, in vivo, whereupon that neutralization of CD95 activity reduces undesirable glial cell migration and invasion into body tissue.

Aspects of the present disclosure relate to genetically engineered organisms useful for the diagnosis and treatment of inflammatory bowel disease.

A method for characterizing stem cell differentiation includes harvesting differentiation media supernatant containing secreted analytes from key time points during a stem cell differentiation, performing at least one of a qualitative and a quantitative analysis of the differentiation media supernatant with respect to at least one secreted analyte, and identifying trends in analyte expression based on at least one of the qualitative and quantitative analysis of the differentiation media supernatant.

The present invention relates to methods and compositions for monitoring, diagnosis, prognosis, and determination of treatment regimens in subjects suffering from or suspected of having a renal injury. In particular, the invention relates to using a one or more assays configured to detect a kidney injury marker selected from the group consisting of Coagulation factor VII, CA 19-9, Insulin-like growth factor-binding protein 7, C—X—C motif chemokine 6, and C—C motif chemokine 13 as diagnostic and prognostic biomarkers in renal injuries.

The present invention relates to therapeutic and prophylactic methods based on inhibition of CIS in NK cells. In particular, the present invention relates to treating or preventing a NK-responsive condition by administering to a subject a CIS inhibitor, or administering CIS-inhibited NK cells. The invention further relates to methods for identifying a CIS inhibitor, and for determining a likelihood of cancer response to treatment with CIS inhibition