Articles in 2020

Allen, Hiam et al. have used mass cytometry to characterize the immune landscape over time in response to tumour development, demonstrating that tumour growth dynamically alters the systemic immune landscape and that this can be reverted by tumour removal.

Baksh et al. have delineated a pathway through which serine availability is integrated with stem cell fate decisions and can control the initiation of epidermal squamous cell carcinomas.

This Review discusses the key role that natural killer (NK) cells play in driving an antitumour immune response throughout the progression of cancer from its initial development to its metastatic spread and eventual treatment, defined herein as the cancer–NK cell immunity cycle.

Nejman et al. have comprehensively characterized the bacteria present in 1,526 human tumours and their adjacent normal tissues encompassing seven different solid tumour types. Their initial findings suggest that much like the gut microbiome, the tumour microbiome may impact many aspects of tumour biology.

Ostendorf et al. show that germline variants of human APOE play a role in melanoma that is opposite to that in Alzheimer disease, with APOE4 carrier status being associated with reduced melanoma growth in mice and improved outcome in patients with advanced melanoma.

This Review discusses intra-prostatic inflammatory processes and how they are induced and perpetuated, thereby driving prostate cancer development and progression. By discussing external inflammatory cues in connection to cancer cell-intrinsic factors in prostate tumorigenesis, the authors provide insight into potential preventative and therapeutic strategies.

This Review presents the evidence for the role of risk factors in breast cancer incidence and their inclusion in risk estimation tools as a step towards precision prevention to specifically target those women at increased risk for appropriate risk-reducing interventions.

This Review discusses recent advances in cohesin biology in cancer, providing insights into the role of cohesin inactivation in cancer pathogenesis and opportunities for exploiting these findings for the clinical benefit of patients with cohesin-mutant cancers.

The COVID-19 pandemic has broadly impacted biomedical research and health care. Here we discuss current challenges for the cancer research community as they apply to early career investigators (ECIs). We propose a series of collaborative initiatives aimed to sustain ECIs and preserve and accelerate the ability to innovate with long-lasting impact.

Ting Li, Xinyuan Li et al. determined that REL, a member of the nuclear factor-κB (NF-κB) family of transcription factors, has a key role in generating myeloid-derived suppressor cells (MDSCs) and that targeting REL might be used for cancer immunotherapy.

Normal tissues become colonized by clones, which have acquired somatic mutations in common cancer driver genes. Colom et al. have now shown that the fate of mutagen-exposed oesophageal epithelial cells in mice is governed by the genotype of their neighbours with implications for cancer development.

This Perspective proposes operational definitions to define the hallmarks of cancer cell dormancy and, based on the latest evidence pertaining to the role of the microenvironment in regulating dormancy, presents key stages in the life cycle of a dormant cancer cell that could be targeted.

In conflict-affected areas, people experience significant challenges in health-care delivery, and this situation is even more extreme for patients with cancer. Until now, research on access to cancer treatment and care as well as cancer disparities in war-torn and post-war regions has been limited. Therefore, we advocate coordinated, global action to address this issue and implement evidence-based solutions.

This Perspective advocates the study of tumour predisposition syndromes as an opportunity to better identify gene–environment interactions that influence cancer risk. Understanding syndrome-associated molecular mechanisms may provide new and more effective ways to prevent exposure-associated cancers in the general population.

Morral, Stanisavljevic et al. show that colorectal cancer (CRC) cell hierarchy is based on the capacity to perform biosynthesis. Undifferentiated CRC cells that have high capacity for protein synthesis were found immediately adjacent to the stroma, and this capacity was lost upon differentiation.

This Review outlines the ways in which leukaemic stem cells (LSCs) take advantage of normal haematopoietic stem cell properties to promote survival and expansion in myeloid leukaemogenesis. Opportunities for treatment of this disease by targeting LSC-specific mechanisms are also discussed.

This Perspective explores why TP53 is the most commonly mutated gene in cancer, discussing the evolutionary conservation of the p53 pathway in the context of tissue-specific functions and underlying reasons for the order of mutations which lead to p53-related cancer.

Chung et al. studied drivers of obesity-associated pancreatic ductal adenocarcinoma in a leptin-deficient mouse model and identified the hormone cholecystokinin, upregulated in islet beta cells in the context of obesity, to be promoting pancreatic tumorigenesis.