This disclosure provides kits and methods for detecting markers in a sample from a subject with unknown status and generating a risk assessment of the presence or absence of cancer, such as colorectal cancer. In embodiments, a kit comprises at least four reagents, each specifically binding to one of at least four polypeptides in a sample from the subject. The polypeptides include GDF15, keratin 1-10, and two or more of hepsin, IL-8, CEA, L1CAM, MCP-1, and OPG. The kit further includes at least one standard comprising a known amount of at least one of the polypeptides. The kit can also include computer readable media comprising instructions to analyze the detected amounts of the at least four polypeptides using a machine learning algorithm to determine whether a subject has an increased risk of the presence of colorectal cancer.

Described herein are materials and methods for stratifying risk for reactivation of a latent viral infection, such as CMV infection. The methods are particularly useful for immune compromised subjects. Also described herein are interventions, including therapeutic, prophylactic, and monitoring interventions, for subjects determined to be at elevated risk.

Two patients diagnosed with KLS were treated. One patient had severe KLS that progressed to the equivalent of pediatric Kawasaki Disease Shock Syndrome (KDSS). The second patient had a typical KLS presentation and clinical course. Cytokines and chemokines provide inflammatory signatures in the serum that reflect the polarity of the immune response and the affected cell types. Multiplex ELISA technology was used to define the cytokine milieu in the serum of the two adult HIV patients with KLS during the acute and convalescent phases. Those sera were compared with sera from asymptomatic HIV subjects and a normal serum control. Those comparisons suggest that HIV KLS is a dysfunctional Th2 response to an unknown inciting agent in the vascular wall, and that a multiplex ELISA or similar technology based a limited combination of KLS/KD pathogenesis-related cytokines (IL-6, IL-13, sTNFRII) and endothelial/smooth muscle chemokines (CCL1, CCL2, CxCL11) may provide an objective tool for diagnosing KLS and Kawasaki Disease. Because KD and HIV KLS are the only known Th2 vasculitidies that spare the lungs (unique clinical presentation) and include plasma cell infiltration of the vascular wall as a prominent histopathologic feature (unique pathophysiology), a diagnostic test based on combinations of the above analytes will be highly specific and therefore clinically useful.

Methods are disclosed that are based on the finding that serum and plasma levels of eotaxin, MIP1?, and CRP act as important biomarkers that are useful for determining the feasibility in instigating immunotherapeutic treatment of cancer when immunizing with the GV1001 peptide (EARPALLTSRLRFIPK; derived from human telomerase protein), optionally when combined with state of the art combination treatment with Gemcitabine and Capecitabine. In particular, the present invention provides methods for determining whether patients should be treated GV1001 and for determining whether instigated treatment should be continued.

Methods for identifying patients susceptible to treatment with checkpoint inhibitors are provided herein. Also provided are reagents for analyzing T cell responses for understanding resistance to checkpoint inhibitor therapy and understanding therapeutics for overcoming that resistance. Therapeutic strategies, for instance, for treating cancer, are also provided.

A method for diagnosing of or for determining the risk of developing Alzheimer's disease, as well as for determining the presence of severe AD in a subject involves at least four specific biomarkers being measured. A kit or an array comprising a detecting means, in particular antibodies, for at least four specific biomarkers can be used for the diagnosis. Further, a computer program product and a computer implemented method for diagnosing of or determining the risk of developing Alzheimer's disease may be employed.

Compositions and methods are provided for modifying diagnosing and treating inflammatory disease. The methods and compositions can be used to ameliorate the effects of a deficiency in the LAP pathway for clearing dead cells. Thus, methods are further provided for modulating dead cell clearance using an effective amount of a pharmaceutical composition that targets the LAP pathway. Accordingly, pharmaceutical compositions that target the LAP pathway re provided herein. The methods and compositions described herein can be used to treat inflammatory disease, such as systemic lupus erythematosus (SLE).

The methods disclosed herein relate to an improved tool incorporating platelet count into a multi-biomarker based outcome risk stratification model for evaluating mortality risk in pediatric patients having sepsis. The methods described here are useful for treating sepsis, for point of care clinical decision support, for stratifying septic shock patients based on baseline mortality risk, and for clinical trial design, among other uses.

The present invention includes methods, systems, and kits, for identifying and modifying the treatment of a systemic lupus erythematosus (SLE) patient prior to the presence of autoantibodies, comprising: (a) obtaining a dataset representing protein expression level values for cytokines and molecules; (b) assessing the dataset for protein expression levels of at least one innate serum mediator; (c) assessing the dataset for protein expression levels of at least one adaptive serum mediator; and (d) determining the likelihood that the patient will develop SLE prior to the onset of autoantibodies when compared to a control.

The invention provides methods, kits and reagents for diagnosing fibromyalgia (FM) in an individual by determining whether the levels of one or more cytokines in the individual are altered, as compared to control levels. The altered level(s) or patterns of expression of the cytokines measured in the affected individual compared to the level from the control is predictive/indicative of FM in the individual.