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People from minority racial and ethnic groups continue to experience disproportionate cancer incidences and cancer-associated mortality rates. In this Comment, Byrd and Wolf explore the contribution of non-medical factors to the composition of the gut microbiome, and how this may be an actionable target for reducing these disparities.
Although childhood cancer survival rates have increased globally, there is a markedly inequitable distribution of these advances. Here, Monica Gramatges summarizes these challenges and provides the reader with strategies and solutions that begin to address factors that contribute to these inequities.
Epidemiologic cohorts of cancer have contributed to the current understanding of cancer risk factors. In this Comment, Gomez and Cheng advocate for a new generation of cohorts that include underserved and understudied populations, and also address the roles of structural and social determinants of health.
In this Tools of the Trade article, Xiwen Tang describes the development of in vivo reporters detecting mutant p53 at the protein level, which enables the visualization of precancerous cells during cancer initiation.
In a recent Developmental Cell paper, Falvo et al. establish a role for epigenetic memory of inflammatory injury in promoting pancreatic tumorigenesis.
In a comprehensive study in acute myeloid leukaemia, Ozga et al. demonstrate sex-specific differences in the frequency and prognostic effect of genetic alterations.
In this Viewpoint article, we asked six scientists working in the field of cancer dormancy to provide their opinions on the current state of the field and the challenges associated with translating dormancy research into the clinic.
Although hyperactivation of BRAF has been well-established to drive tumour progression and drug resistance, the role of CRAF in cancer is becoming increasingly relevant. Here, Riaud et al. summarize the various oncogenic roles of CRAF and the potential for CRAF-targeted therapies to improve the clinical outcome for RAF1 altered tumours.
Transposable elements, also known as junk DNA, constitute nearly half of the human genome. This Review by Liang et al. discusses how tumours exploit these transposable elements during their evolution but also how they represent a vulnerability that could be targeted through immunotherapeutic approaches.
In this Review, Sato and colleagues provide an overview of the clinicopathological and phenotypical impact of lineage commitment and plasticity during tumorigenesis and progression of human epithelial cancer and discuss the molecular mechanisms that underlie histological lineage transition.
