Volume 22 Issue 6, June 2022

mRNA vaccines have proven safe and effective in preventing serious illness and death during the COVID-19 pandemic. In this Comment, Morris and Kopetz argue that these technologies offer a novel approach towards personalizing immune-based treatments for patients with cancer with the potential for immune activation beyond commonly utilized immunotherapies.

Guan, Polesso, Wang, et al. report that androgen receptor blockade, in addition to androgen deprivation therapy, enhances the response of T cells to anti-PD1 immune checkpoint inhibitors.

Lv, Liu, Mo and colleagues demonstrate that in pancreatic ductal adenocarcinoma cells, gasdermin E transports the transcription factor YBX1 to the nucleus, where it promotes the expression of mucins, thereby providing tumour cells with a barrier against digestive enzymes.

In this Tools of the Trade article, Eunhee Yi describes the development and use of a method called ecTag, which allows imaging and tracking of extrachromosomal DNA in live cancer cells.

In this Tools of the Trade article, Alejandro E. Mayorca-Guiliani describes the development and use of in situ decellularization, which allows native extracellular matrix to be preserved to address both tumour deconstruction and reassembly.

In this Tools of the Trade article, Christian Umkehrer describes the development and use of CaTCH, which enables therapy-naive cancer cell clones to be isolated and compared to their resistant counterparts.

This Review discusses mechanisms by which tumour ecosystems adapt to therapeutic stresses and how these could be exploited, as well as challenges associated with tumour heterogeneity. It provides an integrative framework to identify and target vulnerabilities that arise from adaptive responses to overcome cancer therapy resistance.

This Review discusses how senescence can be induced in cancer cells and how distinctive features of senescent cancer cells might be exploited for their selective eradication as a potential cancer therapy.

Dysregulation of cyclin-dependent kinase 4 (CDK4) and CDK6, regulators of the cell cycle, favours the growth and survival of several cancer types. Owing to this, CDK4 and CDK6 inhibitors were developed and are currently approved for the treatment of advanced hormone receptor-positive breast cancer. This Review describes how we are only now beginning to fully understand their mechanisms of action and provides a new framework for conceptualizing their activity, which might enable expansion of the clinical opportunities of these agents.