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Immunotherapy has undoubtedly become an effective treatment for many cancers, but how can we make the most of this approach? In this Review, Meleroet al. discuss how immune-targeted therapies can be synergistically combined to provide maximal benefit to patients.
Although most cancers exhibit some degree of intratumour heterogeneity, we are far from understanding the dynamics that operate among subclonal populations within tumours. This Review discusses the growing evidence that cooperative behaviour of tumour subclones can influence disease progression.
This Review discusses what we have learned about the biology of rhabdomyosarcoma using various model systems, and how these models might be used to discover new targetable pathogenic mechanisms.
'Cellular senescence' has been broadened to describe durable states of proliferative arrest induced by disparate stress factors. This Review discusses the limitations of senescence-associated biomarkers and provides suggestions for how to improve the phenotypic description of senescence.
In this Review, Barker and colleagues describe the mechanisms of radioresistance that are mediated by the tumour stroma and explore how these mechanisms can be targeted to improve radiotherapy responses.
Histone–lysineN-methyltransferase 2 (KMT2) family proteins, initially named the mixed lineage leukaemia (MLL) family, are altered in many types of cancers beyond MLL. Inhibitors of KMT2 function are being developed and could work as therapeutics in a variety of cancer types.
How can we improve the design of monoclonal antibodies (mAbs) to treat cancer? In this Review, George J. Weiner discusses the characteristics of mAbs that can affect their efficacy, the current approaches that use mAbs in cancer treatment and the numerous ways to enhance the potential of these mAb-based techniques.
The microRNA (miRNA) biogenesis pathway is frequently altered in cancer, leading to global downregulation of miRNA levels in some cancer types. This Review discusses the alterations that affect miRNA biogenesis in cancer.
The modern manufacture of tumour-selective antibodies bearing tumour-killing radioactive cargo has effectively harnessed the power of the atom to safely destroy cancer cells. This Review presents fundamental concepts of chemistry, physics and biology that are essential for the effective radioimmunotherapy of human cancer.
DNA damage can result in replication stress, which is a source of genome instability and a feature of cancer cells. Revealing the molecular basis of replication stress is crucial to the understanding of tumorigenesis and may provide potential targets for cancer therapy.
This Review discusses the mechanisms underlying resistance to aromatase inhibitor (AI) therapy of patients with oestrogen receptor-positive (ER+) breast cancer, and also assesses the possible therapeutic options for overcoming AI resistance.
Neurofibromatosis type 1 (NF1) is a cancer predisposition syndrome, and somaticNF1 mutations are also common in tumours. The neurofibromin protein (encoded by NF1) is a RAS GTPase-activating protein that activates RAS–MAPK signalling when lost. This Review discusses NF1 disease, neurofibromin signalling pathways and recent developments in NF1 therapeutics.
Caveolar lipid rafts are distinct regions of the cell membrane that can mediate diverse signalling events, including the regulation of autophagy, responses to oxidative stress and metabolism. What are the implications of caveolae in cancer cells and associated stromal cells?
Haematological malignancies have provided both initial proofs of concept and an informative testing ground for various immune-based cancer therapeutics. The immune-cell origin of many of the blood malignancies provides a unique opportunity both to understand the mechanisms of cancer immune responsiveness and immune evasion, and to exploit the unique therapeutic opportunities they provide.
Protein-linked DNA breaks can be formed through the abortive activity of topoisomerases — this Review discusses the roles of such breaks during transcription and in triggering gene deletions and translocations in cancer.
Mutations in the gene encoding DNA methyltransferase 3A (DNMT3A) have been reported in patients with various haematological malignancies, suggesting that DNMT3A could be a tumour suppressor. In this Review, Yanget al. put data from basic science studies into clinical context, opening stimulating discussions regarding possible new therapeutic avenues.
Although dysregulation of histone methylation has been widely studied in cancer, accumulating evidence suggests that cancer-relevant non-histone proteins such as p53, RB1 and signal transducer and activator of transcription 3 (STAT3) are also regulated by lysine methylation. This Review summarizes the possible functions of non-histone protein lysine methylation in cancer.
The S100 family of proteins modulates cellular responses by acting both as intracellular Ca2+sensors and as extracellular factors. Expression of several members of this family is dysregulated in cancer, and each cancer shows a unique S100 protein profile or signature. In this Review, Anne Bresnick and colleagues highlight new findings regarding the role of S100 proteins in cancer diagnosis and treatment.
The RUNX transcription factors seem to have dichotomous roles in cancer, sometimes being oncogenic and sometimes acting as tumour suppressors. This Review discusses the many roles of the RUNX family in cancer biology.
