Described herein are signatures that characterize a particular stromal cell state, type, and/or subtype. In some embodiments, the signatures can characterize a dysfunctional stromal cell. In some embodiments, the signatures can be used to diagnose, treat, and/or prevent a disease. In some embodiments, the signatures can characterize remodeling in a bone marrow microenvironment. Also described herein are cell populations having a specific signature and modulated cells that can be modulate to have a specific signature.

Gene expression data provides a basis for more accurate identification and diagnosis of lymphoproliferative disorders. In addition, gene expression data can be used to develop more accurate predictors of survival. The present invention discloses methods for identifying, diagnosing, and predicting survival in a lymphoma or lymphoproliferative disorder on the basis of gene expression patterns. The invention discloses a novel microarray, the Lymph Dx microarray, for obtaining gene expression data from a lymphoma sample. The invention also discloses a variety of methods for utilizing lymphoma gene expression data to determine the identity of a particular lymphoma and to predict survival in a subject diagnosed with a particular lymphoma. This information will be useful in developing the therapeutic approach to be used with a particular subject.

The present disclosure includes biomarkers, methods, devices, reagents, systems, and kits for the evaluation of risk of a caradiovascular (CV) Event within 5 years. In one aspect, the disclosure provides biomarkers that can be used alone or in various combinations to evaluate risk of a CV event within 5 years. In another aspect, methods are provided for evaluating risk of a CV event within 5 years in an individual, where the methods include detecting, in a biological sample from an individual, at least one biomarker value corresponding to at least one biomarker selected from the group of biomarkers provided in Table 1. In a further aspect, methods are provided for evaluating the risk of a CV, where the methods include detecting, in a biological sample from an individual, at least one biomarker value corresponding to at least one biomarker selected from the group of biomarkers provided in Table 2. In a further aspect, methods are provided for evaluating the risk of a CV event in an individual, generally within 5 years, where the methods include detecting, in a biological sample from an individual, at least one biomarker value corresponding to at least one biomarker selected from the group of biomarkers provided in Table 3.

Methods and compositions are provided for the selective activation of a BMP-dependent response in certain cell types. Methods include identifying a ligand or ligand combinations as well as cell receptor profiles that result in selectively activating a ligand-dependent response through interactions with ligand receptors on a first cell type that do not activate the ligand-dependent response in a second cell type.

The present invention relates to a method for assessing myocardial infarction comprising the steps of determining the amount of a first biomarker in a sample of a subject, said first biomarker being cMyBPC, determining the amount of a second biomarker in a sample of the subject, wherein said second biomarker is selected from the group consisting of: a BMP10-type peptide (Bone Morphogenic Protein 10-type peptide), FGF23 (Fibroblast growth factor 23), a BNP-type peptide (Brain natriuretic peptide type peptide), GDF-15 (Growth differentiation factor 15), ANG2 (Angiopoietin 2), CRP (C-reactive protein), ESM1 (endothelial cell specific molecule 1), or a lipid biomarker, such as Cholesterol, LDL (Low Density Lipoprotein) or APOAT (Apolipoprotein A-1) comparing the amounts of the biomarkers to references for said biomarkers and/or calculating a score for assessing myocardial infarction based on the amounts of the biomarkers, and assessing said subject based on the comparison and/or the calculation. The invention also relates to the use of a first biomarker being cMyBPC and a second biomarker selected from the group consisting of: a BMP10-type peptide, FGF23, a BNP-type peptide, GDF15, ANG2, CRP (C-reactive protein), ESM1, or a lipid biomarker, such as Cholesterol or LDL, or at least one detection agent for said first biomarker and at least one detection agent for said second biomarker for assessing myocardial infarction. Moreover, the invention further relates to a computer-implemented method for assessing myocardial infarction and a device and a kit for assessing myocardial infarction.

A method of preparing a cantilever sensor for measuring biochemical interactions and their associated stress wherein a cantilever having two sides is coated on one side with at least a gold layer and both sides of the cantilever are functionalized with a self-assembled monolayer (SAM) of a probe molecule by incubating the cantilever in a solution having a concentration of the probe molecule of between 1 to 1000 M. The unpassivated cantilever sensor comprising a layer coated on one side with a coating comprising gold and being unpassivated on the opposite side, wherein both surfaces comprises a self-assembled monolayer of a probe molecule in which the surface area occupied per probe molecule varies in the range 0.4-1.5 nm2, enabling the stress at the gold top surface that is not cancelled out by a counter stress from the bottom surface so that accurate quantitation of a target molecule is achieved.

Methods and compositions are provided for the selective activation of a BMP-dependent response in certain cell types. Methods include identifying a ligand or ligand combinations as well as cell receptor profiles that result in selectively activating a ligand-dependent response through interactions with ligand receptors on a first cell type that do not activate the ligand-dependent response in a second cell type.

A method of preparing a cantilever sensor for measuring biochemical interactions and their associated stress wherein a cantilever having two sides is coated on one side with at least a gold layer and both sides of the cantilever are functionalized with a self-assembled monolayer (SAM) of a probe molecule by incubating the cantilever in a solution having a concentration of the probe molecule of between 1 to 1000 M. The unpassivated cantilever sensor comprising a layer coated on one side with a coating comprising gold and being unpassivated on the opposite side, wherein both surfaces comprises a self-assembled monolayer of a probe molecule in which the surface area occupied per probe molecule varies in the range 0.4-1.5 nm.sup.2, enabling the stress at the gold top surface that is not cancelled out by a counter stress from the bottom surface so that accurate quantitation of a target molecule is achieved.

The disclosure provides a method of predicting the responsiveness of a wet AMD patient to anti-VEGF therapy comprising (1) determining the level of at least one marker protein selected from the group consisting of TGF-beta, BMP9, angiopoietin-1, and angiopoietin-2 in a blood, plasma or serum sample obtained from the patient, and (2) predicting the responsiveness of the patient to the anti-VEGF therapy with reference to the level determined in step (1), as well as a diagnostic agent for use in the method.

This disclosure provides data showing that LEFTY inhibits differentiation-promoting pathways such as BMP7/pSMAD5 in breast cancer cell lines, over and above its known role of inhibiting Nodal/pSMAD2. LEFTY competes with BMP7 to bind to its cell surface receptor BMPR2, leading to inhibition of pSMAD5. The LEFTY-BMPR2 interaction is dominant over BMP-BMPR2 in tumorigenic cells, resulting in diminished pSMAD status, whereas in non-tumorigenic cells, there is minimal LEFTY-BMPR2 interaction, increased BMP7-BMPR2 association, and elevated pSMAD. Compositions and methods for inducing or inhibiting expression and/or the activity of LEFTY and BMP proteins are described, which can be used in diagnosis and therapy of cancer and other conditions, and to promote proliferation of stem cells.