Abstract: The present disclosure relates to biomarkers and methods for determining or predicting survival of patients with low grade glioma (LGG) or pediatric neuroblastoma. Further disclosed are methods of diagnosing and treating patients with low grade glioma (LGG) or pediatric neuroblastoma.

Abstract: The present disclosure relates to methods of determining complementarity scores of antigen-binding proteins and proteins associated with cancers and uses thereof for diagnosing and treating cancers and for screening antigens and antigen-binding proteins.

Abstract: The present disclosure relates to methods of detecting, treating, and/or preventing the progression of diseases, such as Alzheimer's disease using a complementarity scoring method.

Abstract: The present disclosure relates to biomarkers and methods for determining or predicting survival of patients with low grade glioma (LGG) or pediatric neuroblastoma. Further disclosed are methods of diagnosing and treating patients with low grade glioma (LGG) or pediatric neuroblastoma.

Abstract: The present disclosure relates to biomarkers and methods for determining or predicting survival of patients with low grade glioma (LGG) or pediatric neuroblastoma. Further disclosed are methods of diagnosing and treating patients with low grade glioma (LGG) or pediatric neuroblastoma.

Abstract: The present disclosure relates to biomarkers and methods for determining or predicting survival of patients with low grade glioma (LGG) or pediatric neuroblastoma. Further disclosed are methods of diagnosing and treating patients with low grade glioma (LGG) or pediatric neuroblastoma.

Abstract: Provided herein is a method of modulating an APC peptidome comprising identifying an APC or an APC cell population that expresses an HDACi-associated polypeptide and administering an HDACi to the APC. Also provided herein is a method of identifying an HDACi-associated peptide comprising administering an HDACi to an APC, isolating the polypeptide from an APC MHC molecule binding cleft, and identifying the polypeptide.

Abstract: The present invention relates to a series of markers and a method of determining cause of death post-mortem by quantifying thymus integrity. An examination of thymuses from human infants suffering mortal head trauma revealed a disruption of the cortical-medullary organization of the thymus, particularly involving dissolution of the cortical-medullary border. A similar result was obtained for related mouse and rat models. The human thymuses from head trauma cases also displayed a higher percentage of Ki67-positive thymocytes.

Abstract: Numerous cancer fusion genes have been identified and studied, and in some cases therapy or diagnostic techniques have been designed that are specific to the fusion protein encoded by the fusion gene. However, there has been little progress in understanding the general features of cancer fusions genes in a way that could provide the foundation for an algorithm for predicting the occurrence of a fusion gene once the chromosomal translocation points have been identified by karyotype analyses. In this study, characterization of 59 cancer fusion genes indicated that all but a small percentage of the genes involved in fusion events are either relatively large, compared to neighboring genes, or are highly conserved in evolution. These results support a basis for designing algorithms that could have a high degree of predictive value in identifying fusion genes once conventional microscopic analyses have identified the chromosomal breakpoints.

Abstract: Oct-1 is shown to be an oncoprotein because of its known role as an activator of the histone H2B gene and the importance of this gene during DNA synthesis. To determine the role of Oct-1 as an oncoprotein, the cell line 5637 (ATCC HTB9) was transfected with the vector pcDNA3 containing full length, antisense Oct-1 cDNA. This cell line is Rb-defective and has been shown to have increased Oct-1 binding activity as compared to Rb reconstituted clones. After transfection, Oct-1 antisense clones were grown and assayed for the loss of oncogenic characteristics as compared to control transformants.

Abstract: A method of identifying genes that can be activated when methylated; as well as proteins that mediate such activation. The method allows identification of HLA-DRA silencing agents expected to be of therapeutic value in the treatment of inflammation associated with HLA-DRA expression.