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This Review discusses recent advances in the molecular characterization of bladder cancer, which has provided insights into pathogenesis and subgroups of bladder cancers with different prognosis.
Hyperactivation of phosphatidylinositol 3-kinase (PI3K) signalling cascades is one of the most common events in human cancers. This Review discusses recent advances in our knowledge of the roles of distinct PI3K isoforms in normal and oncogenic signalling, and the current state and future potential of targeting this pathway in the clinic.
The TYRO3, AXL and MERTK (TAM) family of receptor tyrosine kinases (RTKs) are overexpressed in tumour cells, promoting cell survival and chemoresistance. These RTKs also function in normal innate immune cells to promote an immunosuppressive tumour microenvironment. Thus, TAM RTKs are implicated as dual therapeutic targets in cancer.
Recent analyses of cancer genomes have revealed the occurrence of mutation patterns, which indicate their source. This Review discusses what we have learned, and what is yet to learn, from these data and how our current understanding of cancer mutations fits into our understanding of tumorigenesis and tumour progression.
The aryl hydrocarbon receptor (AHR) is a ligand-activated transcription factor that is best known for mediating the toxicity and tumour-promoting properties of dioxin. AHR levels are increased with constitutive nuclear localization in many tumours. How might AHR facilitate tumour progression, and can it be therapeutically modulated?
The Janus kinases (JAKs) are major activators of signal transducer and activator of transcription (STAT) proteins, and this signalling axis is crucial for cancer development in both tumour cells and the tumour microenvironment. This Review discusses the new roles of JAK–STAT signalling in promoting cancer through inflammation, obesity, stem cells and the pre-metastatic niche, and the potential therapeutic strategies that these roles can offer.
Reactive oxygen species (ROS) are generated through various mechanisms. Accumulating evidence indicates that these moieties have important roles in promoting tumorigenesis and tumour progression; modulating the redox balance could be a strategy in targeting cancer.
Survival for patients with metastatic or relapsed osteosarcoma has remained virtually unchanged during the past 30 years, and new therapeutic options are needed. This Review discusses normal bone biology relevant to osteosarcoma, including the immunobiology of bone, model systems for studying osteosarcoma, genetic and genomic studies on germline predisposition and tumour landscapes, and recent clinical trials.
There has recently been a flurry of publications on the molecular and genetic basis of diffuse high-grade glioma, a devastating paediatric tumour. In this Review, Jones and Baker integrate these findings to provide new insight into this disease. In particular, the unique selective pressures driving the paediatric disease along with their associated mutations, potential molecular mechanisms and how this information could be harnessed therapeutically, are discussed.
CUT-like homeobox 1 (CUX1) is a homeobox gene that is implicated in both tumour suppression and progression. What are the functions of the CUX1 protein, and how might the opposite roles of CUX1 in cancer protection and progression be explained?
Germline mutations inDICER1 can lead to DICER1 syndrome, which is characterized by the predisposition of various types of cancer in childhood and during early adulthood. Additionally, specific DICER1 mutations occur in tumours. This Review discusses germline and somatically-acquired DICER1mutations and their effects on tumorigenesis.
The unfolded protein response (UPR) is an important pro-survival pathway that is often activated in tumour cells owing to endoplasmic reticulum stress that is caused by both intrinsic and extrinsic factors. Wang and Kaufman discuss the mechanisms of UPR activation in tumour cells, the importance of this pathway to cancer development and targeting strategies for therapeutic intervention.
Disseminated tumour cells that survive treatment may become dormant and their 'awakening' may be the source of metastases. This Review discusses the mechanisms and factors that regulate tumour dormancy, including the extracellular and stromal microenvironments, autophagy and epigenetics. The authors also discuss how this information could be used therapeutically for metastatic disease.
Focal adhesion kinase (FAK) can promote tumour growth and metastasis through various kinase-dependent and kinase-independent pathways. This Review discusses the roles of FAK in tumour cells and cells of the microenvironment, as well as the progress that is being made in the clinical development of FAK inhibitors.
Non-small-cell lung cancers (NSCLCs) are now appreciated to be a group of heterogeneous diseases. This Review discusses the biology of NSCLCs and what we know about their origins, diversity and the microenvironments surrounding them, with a view towards improving therapies.
Recent advances in understanding the biology of senescent cells, especially the secretory phenotypes and the role of immune cell clearance of senescent cells, has revealed more about the role of senescence induction in tumorigenesis and tumour progression. This includes the surprising findings that senescence may promote tumour growth in some contexts.
This Review discusses the role of the tumour microenvironment in the pathogenesis of B cell lymphomas, proposing three main types of lymphoma-associated tumour microenvironment.
Mutations in the RAF family have been associated with several types of cancer, with BRAF mutations being the most common. This led to the development of BRAF inhibitors, which initially improve clinical responses but frequently induce more aggressive, drug-resistant disease and secondary tumours. This Review discusses what we know about RAF mutants in cancer and the lessons learned about acquired drug resistance, especially feedback signalling and the effects of dosing regimens.
de Jonget al. provide an overview of recent developments in molecular imaging and oncological animal models in basic and translational cancer research, with an emphasis on how to improve the translational value of preclinical imaging studies.
