Validation of a deep learning computer aided system for CT based lung nodule detection, classification, and growth rate estimation in a routine clinical population.

Objective: In this study, we evaluated a commercially available computer assisted diagnosis system (CAD). The deep learning algorithm of the CAD was trained with a lung cancer screening cohort and developed for detection, classification, quantification, and growth of actionable pulmonary nodules on chest CT scans. Here, we evaluated the CAD in a retrospective cohort of a routine clinical population.

The histone demethylase Jarid1b (Kdm5b) is a novel component of the Rb pathway and associates with E2f-target genes in MEFs during senescence.

Senescence is a robust cell cycle arrest controlled by the p53 and Rb pathways that acts as an important barrier to tumorigenesis. Senescence is associated with profound alterations in gene expression, including stable suppression of E2f-target genes by heterochromatin formation. Some of these changes in chromatin composition are orchestrated by Rb.

Screening for modulators of cisplatin sensitivity: unbiased screens reveal common themes.

Cisplatin is a widely used chemotherapeutic agent to treat a variety of solid tumors. The cytotoxic mode of action of cisplatin is mediated by inducing conformational changes in DNA including intra- and inter-strand crosslink adducts. Recognition of these adducts results in the activation of the DNA damage response resulting in cell cycle arrest, repair, and potentially, apoptosis.

Using large-scale RNAi screens to identify novel drug targets for cancer.

In recent years, the development and clinical implementation of targeted therapeutics have progressed significantly. The specific inhibition of components of signal transduction pathways controlling proliferation and survival has been a highly successful research strategy. However, cancer is a heterogeneous disease and, even within one type of cancer, different genetic alterations are associated with identical phenotypes.

Transforming growth factor-beta requires its target plasminogen activator inhibitor-1 for cytostatic activity.

The cytokine transforming growth factor beta (TGFbeta) has strong antiproliferative activity in most normal cells but contributes to tumor progression in the later stages of oncogenesis. It is not fully understood which TGFbeta target genes are causally involved in mediating its cytostatic activity. We report here that suppression of the TGFbeta target gene encoding plasminogen activator inhibitor-1 (PAI-1) by RNA interference leads to escape from the cytostatic activity of TGFbeta both in human keratinocytes (HaCaTs) and primary mouse embryo fibroblasts.