The disclosure features systems and methods for measuring and diagnosing target constituents bound to labeling particles in a sample. The systems include a radiation source, a sample holder, a detector configured to obtain one or more diffraction patterns of the sample each including information corresponding to optical properties of sample constituents, and an electronic processor configured to, for each of the one or more diffraction patterns: (a) analyze the diffraction pattern to obtain amplitude information and phase information corresponding to the sample constituents; (b) identify one or more particle-bound target sample constituents based on at least one of the amplitude information and the phase information; and (c) determine an amount of at least one of the particle-bound target sample constituents in the sample based on at least one of the amplitude information and the phase information.

A method of detecting epithelial cancer is described that includes the steps of: (a) determining the level of beta defensin 3 (BD-3) and beta defensin 2 (BD-2) in a suspect sample obtained from a subject; (b) comparing the level of BD-3 to BD-2 determined in the suspect sample to obtain a suspect BD-3/BD-2 ratio, (c) comparing the suspect BD-3/BD-2 ratio to a healthy BD-3/BD-2 ratio to obtain a diagnostic BD-3/BD-2 ratio; and (d) characterizing the subject as having epithelial cancer if the diagnostic BD-3/BD-2 ratio is greater than 1. A microfluidic device for detecting epithelial cancer using the diagnostic BD-3/BD-2 ratio is also described.

The present invention relates to a eukaryotic initiation factor (eIF) modulating compound for use in the treatment of a tumor and in the diagnosis of a cancer. The present invention also relates to a method of diagnosing lung cancer in an individual and to a method of providing a prognosis to an individual suffering from lung cancer. Furthermore, the present invention relates to a method of diagnosing colorectal cancer in an individual, a method of differentiating between colon cancer (CC) and rectum cancer (RC) in an individual, a method of determining whether an individual responds to a therapeutic treatment of colorectal cancer, and to a method of determining the course of colorectal cancer in an individual. Furthermore, the present invention relates to a method of diagnosing a glioma in an individual, a method of grading a glioma in an individual, a method of differentiating between a low-grade glioma and a high-grade glioma in an individual, a method of determining whether an individual responds to a therapeutic treatment of a glioma, and a method of determining the course of a glioma in an individual. In addition, the present invention relates to a kit for conducting the above mentioned methods.

The present invention relates to method of therapy selection for patient suffering from glioblastoma. Using in vitro and in vivo approaches, the inventors demonstrated the critical role of CD90 in GBM migration/invasion. They showed that CD90 signaling though SRC, FAK and RhoA promotes cell migration and importantly, that high CD90 expression impacts on the cell response to the SRC inhibitor dasatinib. In particular, the present invention relates to a method for predicting whether a subject will be eligible to a treatment with a drug selected from the group consisting of SRC inhibitor, FAK inhibitor or RhoA inhibitor by determining the expression level of CD90 in a sample obtained from the subject.

Provided is an in vitro method for determining the metabolic status of a lymphoma comprising a step of determining the level of glyceraldehyde-3-phosphate dehydrogenase (GAPDH) expression in lymphoma cells, wherein a low level of GAPDH expression is indicative of oxidative phosphorylation (OXPHOS) status. Also provided is an in vitro method for predicting the responsiveness of a patient afflicted with a lymphoma to a treatment with a metabolic inhibitor selected from the group consisting of mitochondrial metabolic inhibitors and glutamine metabolism inhibitors comprising a step of determining the level of GAPDH expression in lymphoma cells obtained from said patient, wherein a low level of GAPDH expression is predictive of a response to a treatment with a metabolic inhibitor.

Disclosed is the in vitro use of at least one lectin for marking cancer stem cells of hormone-dependent cancer target organs, selected from the lectins Maackia amurensis lectin II (MAH-II), Euonymus europaeus lectin (EEL), Psophocarpus tetragonolobus lectin I (PTL-I) and Griffonia simplicifolia lectin II (GSL-II), in particular at least two lectins selected from MAH-II, EEL, PTL-I and GSL-II, in particular the two lectins MAH-II and EEL, in order to obtain cancer stem cells of labeled hormone-dependent cancer target organs in a biological sample.

The present invention is based on the identification of novel biomarkers predictive of responsiveness of esophagogastric cancers to inhibitors of the PD-1 pathway.

Provided by the disclosure are compositions and methods for modulating differentiation of regulatory T cells. In some embodiments, methods include selectively decreasing IL-23R activity and/or IL-23R expression without significantly decreasing IL-12RP activity and/or IL-12RP expression.

This invention provides antibodies directed against a highly specific and previously unrecognized marker for cancerous cells. In certain embodiments an isolated antibody or fragment thereof that specifically binds human placentally expressed ALPP and/or ALPPL2, but not ALPL and ALPI that are expressed outside the placenta is provided as well as immunoconjugates comprising such antibodies.

From gene expression analysis with a long-term recurrence-free group and a recurrence metastasis group of stomach cancer, CHRNB2 and NPTXR were identified as drug discovery targets. Tumor growth was successfully inhibited by an antibody medicine or a nucleic acid medicine targeting CHRNB2 or NPTXR. Furthermore, a polyclonal antibody and a monoclonal antibody linking to CHRNB2 or NPTXR are provided. Since these receptor molecules are novel molecular targets, treatment of cases which the existing therapeutic drugs have no effect on is made possible.