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Lim et al. show that there is an association between germline genetic variants and the immune features of a tumour, and that genetic background might affect responses to immunotherapy.
New findings published in Nature Medicine highlight a role for the anti-CTLA4 antibody ipilimumab when combined with radiotherapy in treating metastatic NSCLC.
Two studies published in Cell have characterized the inhibitory immune receptor NKG2A expressed on cytotoxic lymphocytes, such as natural killer cells and CD8+ T cells, as a novel checkpoint for cancer immunotherapy.
Lane et al. have shown that interferon-γ (IFNγ)-mediated activation of the lymphatic vasculature, as a non-haematopoietic component of the tumour stroma, serves to limit local CD8+ T cell accumulation in melanoma in mice as a mechanism of immune suppression.
Assi et al. have generated multi-omics data on leukaemic blasts from acute myeloid leukaemia (AML) patients with defined genetic alterations. These data provide a comprehensive overview of the specific transcriptional and signalling networks in certain AML subtypes.
Wang et al. demonstrate that increased flux of calcium derived from osteogenic cells into cancer cells promotes early-stage bone colonization. Calcium signalling in cancer cells can be targeted by arsenic trioxide, thereby reducing bone metastasis progression.
A study in Science reports the genome-wide chromatin accessibility profiles across 23 cancer types from The Cancer Genome Atlas and notably increases the number of known gene regulatory elements.
Grohmann, Wiede et al. report that obesity-associated nonalcoholic steatohepatitis (NASH) and hepatocellular carcinoma (HCC) can be driven by independent pathways. In particular, HCC can be driven by STAT3 signalling, independently from STAT1-driven NASH.
Song et al. show that in patients with ovarian cancer, intratumoural T cells and ascites-resident T cells experience endoplasmic reticulum stress triggered by activation of IRE1α–XBP1 signalling, leading to reduced antitumour activity.
Xie et al. have shown that a recently reported DNA modification in mammals, repressive N6-methyladenine, is enriched in human glioblastoma and targeting this modification can reduce cancer cell growth by restricting chromatin accessibility at oncogenic loci.
Martincorena, Fowler et al. have characterized the mutational landscape of normal oesophageal tissue during ageing, which has provided important insights into early cancer development.
Two studies from Ashani Weeraratna’s group have examined how changes in the skin microenvironment associated with ageing promote melanoma metastasis and modify immune infiltration.
Ye et al. show that leukaemia cells induce insulin resistance in the host to limit glucose consumption by healthy tissues, thereby augmenting the amount of available glucose for cancer growth.
Transcription elongation supported by the super elongation complex, and histone H3 lysine 9 methylation and gene repression by G9a mediate the oncogenic function of MYC.
Albrengues et al. have characterized a mechanism by which sustained lung inflammation can cause a switch from cancer dormancy to metastasis through the induction of neutrophil extracellular traps.
Orlando et al. and Ruella, Xu, Barrett et al. identified distinct mechanisms of resistance to anti-CD19 chimeric antigen receptor (CAR) T cell therapy in relapsed leukaemia patients, based on loss of CD19 surface expression.
Yang et al. have used genetically engineered mouse models of small cell lung cancer to show that the same genomic alterations in different cells of origin lead to the formation of tumours that follow distinct evolutionary paths to metastasis.
