Volume 2 Issue 2, February 2021

The COVID-19 pandemic, caused by the SARS-CoV-2 coronavirus, poses a clear and present danger to the health and well-being of populations. Here we discuss its indirect impact on global cancer prevention and control efforts, particularly for cervical cancer. We suggest some comparisons between the COVID-19 pandemic and the human papillomavirus–induced cancer burden, as well as opportunities for translating pandemic-control strategies into effective cancer control.

The complexity of glioblastoma is becoming increasingly recognized. Three recent studies used single-cell approaches that integrate cellular states, transcriptional trajectories, and metabolic alterations to uncover multiple dimensions of cellular and molecular heterogeneity and provide a framework for additional functional investigation and therapeutic development.

Metabolic reprogramming mediates resistance to therapy and rewires cancer-cell-signaling networks, paving the way to the discovery of enhanced treatment strategies through acquired vulnerabilities. A study now points to lipotoxicity dependent on Raf-1 kinase that occurs after activation of the liver receptor LXRα as a therapeutic intervention for the treatment of hepatocellular carcinoma.

Garofano et al. use single-cell RNA-sequencing data to classify glioblastomas along a metabolic axis of mitochondrial and glycolytic/plurimetabolic states and a neurodevelopmental axis of proliferative/progenitor and neuronal states.

Pugh and colleagues use single-cell RNA sequencing, CRISPR screens and functional assays to define a gradient of developmental and wound-response cell states in glioblastoma stem cells, revealing insights into glioblastoma origins and potential therapeutic targets.

Piccolo and colleagues perform integrated single-cell analyses and identify YAP/TAZ regulation of glioma stem cell differentiation as a core dependency for tumor maintenance.

Zhang and colleagues report that targeting GLS1 alleviates the glutamine dependence of ARID1A-mutated ovarian clear cell carcinomas, thereby suppressing their growth.

Zender, Dauch and colleagues demonstrate that pharmacologically induced lipotoxicity by activating LXRα and Raf-1 inhibition provides a metabolic therapeutic strategy for hepatocellular carcinoma.

Magrini et. al. study sarcoma development and antitumor immune response in complement-deficient murine hosts, demonstrating a role for the C3a–C3aR axis in promoting immunosuppressive macrophages.

Ma et al. apply few-shot learning to train a neural network model on cell-line drug-response data, and they subsequently transfer it to distinct biological contexts including different tissues and patient-derived tumor cells and xenografts.