Ricerc@Sapienza

Precision oncology uses genomic evidence to match patients with treatment but often fails to
identify all patients who may respond. The transcriptome of these “hidden responders” may reveal
responsive molecular states. We describe and evaluate a machine-learning approach to classify
aberrant pathway activity in tumors, which may aid in hidden responder identification. The
algorithm integrates RNA-seq, copy number, and mutations from 33 different cancer types across
The Cancer Genome Atlas (TCGA) PanCanAtlas project to predict aberrant molecular states in

Prioritization of cell cycle-regulated genes from expression time-profiles is still an open problem. The point at issue is the surprisingly poor overlap among ranked lists obtained from different experimental protocols. Instead of developing a general-purpose computational methodology for detecting periodic signals, we focus on the budding yeast mitotic cell cycle.

Recent findings demonstrated that a subset of papillary thyroid cancers (PTCs) is characterized by reduced expression of the von Hippel-Lindau (VHL) tumor suppressor gene, and that lowest levels associated with more aggressive PTCs. In the present study, the levels of the two VHL mRNA splicing variants, VHL-213 (V1) and VHL-172 (V2), were measured in a series of 96 PTC and corresponding normal matched tissues by means of quantitative RT-PCR. Variations in the mRNA levels were correlated with patients' clinicopathological parameters and disease-free interval (DFI).

Aging is associated with cognitive decline and increased vulnerability to neurodegenerative diseases. The progressive extension of the average human lifespan is bound to lead to a corresponding increase in the fraction of cognitively impaired elderly individuals among the human population, with an enormous societal and economic burden.

Maintaining a stable and balanced histone pool is of paramount importance for genome stability and fineregulation of DNA replication and transcription. This involves a complex regulatory machinery, exploitingtranscription factors as well as histone chaperones, chromatin remodelers and modifiers. The functionaldetails of this machinery are as yet unclear. Previous studies report histone decrease in mammalianand yeast HMGB family mutants. In this study we find that Nhp6 proteins, the S.

The mouse neuroblastoma N18TG2 clone is unable to differentiate and is defective for the enzymes of the biosynthesis of neurotransmitters. The forced expression of choline acetyltransferase (ChAT) in these cells results in the synthesis and release of acetylcholine (Ach) and hence in the expression of neurospecific features and markers. To understand how the expression of ChAT triggered neuronal differentiation, we studied the differences in genome-wide transcription profiles between the N18TG2 parental cells and its ChAT-expressing 2/4 derived clone.