Metastatic spine disease alters spinal load-to-strength ratios in patients compared to healthy individuals.

Pathologic vertebral fractures (PVF) are common and serious complications in patients with metastatic lesions affecting the spine. Accurate assessment of cancer patients' PVF risk is an unmet clinical need. Load-to-strength ratios (LSRs) evaluated in vivo by estimating vertebral loading from biomechanical modeling and strength from computed tomography imaging (CT) have been associated with osteoporotic vertebral fractures in older adults.

An open annotated dataset and baseline machine learning model for segmentation of vertebrae with metastatic bone lesions from CT.

Automatic analysis of pathologic vertebrae from computed tomography (CT) scans could significantly improve the diagnostic management of patients with metastatic spine disease. We provide the first publicly available annotated imaging dataset of cancerous CT spines to help develop artificial intelligence frameworks for automatic vertebrae segmentation and classification. This collection contains a dataset of 55 CT scans collected on patients with various types of primary cancers at two different institutions.

Registration of Longitudinal Spine CTs for Monitoring Lesion Growth.

Accurate and reliable registration of longitudinal spine images is essential for assessment of disease progression and surgical outcome. Implementing a fully automatic and robust registration is crucial for clinical use, however, it is challenging due to substantial change in shape and appearance due to lesions. In this paper we present a novel method to automatically align longitudinal spine CTs and accurately assess lesion progression.

CDK5-cyclin B1 regulates mitotic fidelity.

CDK1 has been known to be the sole cyclin-dependent kinase (CDK) partner of cyclin B1 to drive mitotic progression. Here we demonstrate that CDK5 is active during mitosis and is necessary for maintaining mitotic fidelity. CDK5 is an atypical CDK owing to its high expression in post-mitotic neurons and activation by non-cyclin proteins p35 and p39.

Cyclin A/B RxL Macrocyclic Inhibitors to Treat Cancers with High E2F Activity.

Cancer cell proliferation requires precise control of E2F1 activity; excess activity promotes apoptosis. Here, we developed cell-permeable and bioavailable macrocycles that selectively kill small cell lung cancer (SCLC) cells with inherent high E2F1 activity by blocking RxL-mediated interactions of cyclin A and cyclin B with select substrates. Genome-wide CRISPR/Cas9 knockout and random mutagenesis screens found that cyclin A/B RxL macrocyclic inhibitors (cyclin A/Bi) induced apoptosis paradoxically by cyclin B- and Cdk2-dependent spindle assembly checkpoint activation (SAC).