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Aguirre-Ghiso and colleagues discuss the current status of the cancer dormancy field, including challenges and opportunities for monitoring and targeting dormant cancer.
The pre-metastatic niche is a complex microenvironment formed by the influence of tumor-derived factors on stromal and immune cells at distant sites of disseminated tumor-cell colonization. Signaling through the kinase p38α and regulation of the type I interferon receptor are now linked to formation of the pre-metastatic niche.
The approval of anti-TNF therapy for colitis over 20 years ago represented a paradigm shift for the treatment of this disease. Anti-TNF therapy is now shown to prevent colitis-associated colon cancer in mice by modifying the gut microbiota composition and transcriptional activity, including genes in Escherichia coli that control colibactin synthesis.
Bozic and Wu discuss how quantitative mathematical models elucidate the various stages of tumor evolution, from premalignancy to malignant progression, and the response to therapy.
KEAP1 is a tumor suppressor encoded by a gene commonly mutated in lung cancer. A systematic search for Keap1-mutant cancer vulnerabilities now reveals that Slc33a1 is a context-specific essential gene that represents a promising new anti-cancer target.
Natural killer (NK) cells serve a critical role in the control of metastasis. NK cells are now shown to preferentially control monoclonal metastases derived from single circulating tumor cells rather than polyclonal metastases derived from cell clusters. These findings provide further evidence that NK cells are linked to metastatic cell immunoediting.
Garnett and colleagues review principles that underpin the pre-clinical development of genomics-guided cancer medicines, challenges that limit their impact, and new opportunities, such as CRISPR-based screening, for refining and extending their use.
Immune-checkpoint blockade holds great promise in cancer therapy; however, T cell–specific checkpoint inhibitors are not effective for all patients with cancer. The transcription factor c-Rel is now shown to regulate pro-inflammatory polarization of myeloid cells and modulate anti-tumor immune responses.
Studies of the tumor microenvironment have provided fundamental insights into cancer progression. A new study now delineates the dynamics of immune-cell alterations at the single-cell level and across stages of multiple myeloma, elucidating the microenvironmental changes involved in the precursor states of the disease.
Although cancer genomics is a powerful tool to understand cancer and develop diagnostic tools, the contribution of the microbiome in cancer diagnosis and clinical assessment is much less studied. Elinav, Greten and colleagues provide their respective views on how studying cancer metagenomes could facilitate identification, diagnosis and staging of different tumor types.
Small-cell lung cancer rapidly develops resistance to standard-of-care therapy. Two papers now establish xenograft models derived from patient-derived circulating tumor cells and show that initially homogeneous, chemoresponsive tumors rapidly recur as heterogeneous drug-refractory disease.
Despite recent advances in cancer treatment, metastasis and therapy resistance remain among the major causes of cancer-related deaths worldwide. A recent pan-cancer study provides a comprehensive molecular profile of advanced and post-therapy tumors, integrating whole-genome and transcriptomic analysis with clinical outcomes.
Dysregulation of innate immune signaling in cancer can be pro-tumorigenic and can promote adaptive resistance to targeted therapies. Type I interferon signaling is now shown to promote survival following inhibition of the kinase EGFR, even in cells that are not ‘addicted’ to EGFR signaling.
Although many metabolic dependencies of cancer cells are well documented, altered cancer metabolism has not always been considered an active driver of tumorigenesis. Restrictive glutamine availability is now shown to promote colorectal cancer by lowering α-ketoglutarate levels and thereby promoting DNA hypermethylation, Wnt signaling and cellular de-differentiation.
A new suite of studies from the Pan Cancer Analysis of Whole Genomes (PCAWG) Consortium provides the most detailed resolution of cancer genomes to date, extending our knowledge of driver genes, mutational features, structural alterations and more. Kreisberg, Ideker, Mills and Meric-Bernstam discuss the foundational and translational insights gained from this project.
Evaluation of circulating tumor DNA in blood has emerged as a powerful technology for oncology research. Lillian Siu and colleagues review the potential applications of liquid biopsy, highlighting clinical-trial designs to establish its clinical utility.
To demonstrate the long-range effects of CD8+ T cell–secreted interferon-γ on bystander tumor cells, two studies now use mosaic models of antigen loss in tumors combined with intravital imaging. Factors that influence the length scale of diffusible signals could shape disease progression in cancer and autoimmunity.
Filtered through the analytical power of artificial intelligence, the wealth of available biomedical data promises to revolutionize cancer research, diagnosis and care. In this Viewpoint, six experts discuss some of the challenges, exciting developments and future questions arising at the interface of machine learning and oncology.
Discerning and analyzing the mutational patterns that arise in the cancer genome can provide essential information on the process of tumorigenesis. An analytical framework and web-based tool now aim to aid in mutational signature assignment for improved tumor stratification.
Tumor heterogeneity remains an obstacle to effective clinical management of breast cancer. Two new studies use high-dimensional imaging of single-cell protein expression in situ in clinical samples to link genomic alterations to multi-cellular features of the tumor microenvironment and reveal breast-cancer phenotypes associated with clinical outcome.