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Canale et al. engineered the bacterial strain Escherichia coli Nissle 1917 to recycle ammonia into arginine, and showed synergistic responses with anti-programmed cell death 1 ligand 1 therapy in tumour-bearing mice when injected intratumourally or given systemically.

Wang et al. have developed a diagnostic tool (based on the widely used Papanicolaou (Pap) test) to detect endometrial and ovarian cancer in patients by using PCR-based analyses of genetic mutations and aneuploidy.

A recent study published in Science Translational Medicine generated a mouse model to study the link between surgical wounding and distant tumour growth, showing that the systemic wound healing response induced by surgery can promote tumour growth.

Two studies describe distinct mechanisms of resistance to anti-CD19 chimeric antigen receptor (CAR) T cell therapy in relapsed leukaemia patients

A recent study, published in Nature, identifies the methylcytosine dioxygenase 2 (TET2) as an epigenetic modifier that is regulated in response to glucose availability and mechanistically links higher cancer susceptibility in patients with diabetes to high blood glucose levels.

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.

New research published inNaturenow demonstrates that immune checkpoint blockade can alleviate hepatocellular carcinoma progression in patients with nonalcoholic steatohepatitis (NASH) by inhibiting immunosuppressive immunoglobulin A-producing cells in the liver.

North, Benbarche et al. engineered synthetic introns that were spliced specifically in cancer cells expressing the mutant spliceosome factor SF3B1. This led to expression of herpes simplex virus-thymidine kinase and vulnerability of cancer cells to treatment with the antiviral drug ganciclovir.

Somasundara, Moss, Feigman et al. show that γδ natural killer T-like (NKT) cells expand during the late stages of pregnancy in mice because of changes in mammary epithelial cell surface protein expression, which was associated with suppressed mammary oncogenesis induced by BRCA1 loss or MYC-overexpression.

Asrir et al. show that tumour-associated high endothelial venues (TA-HEVs) in tumour-bearing mice are points of entry for lymphocytes, and increasing TA-HEVs frequency and maturation improves immune checkpoint blockade.

Bertocchi et al. show that tumour-resident bacteria in colorectal cancer disseminate to the liver via an impaired gut vascular barrier and promote the liver pre-metastatic niche.

Griffin, Wu, Iracheta-Vellve et al. identified SETDB1 as an immunosuppressive epigenetic modulator in cancer.

Gao, Xia, Li, Zhang et al. show that a circular RNA-encoded variant of E-Cadherin stimulates EGFR signalling independently of EGF, and contributes to glioblastoma tumorigenesis and anti-EGFR therapy resistance.

Wang et al. showed that monoamine-oxidase A, a regulator of neuronal activity, functions as a negative feedback regulator of T cell activity in tumours.

Ruscetti, Leibold, Bott et al. show that the growth of Kras-mutant lung tumours is sensitive to combined blockade of KRAS effectors. This was dependent on induction of the senescence-activated phenotype in cancer cells, followed by natural killer cell-mediated cell clearance.

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.

Boettcher et al. show that missense mutations in the DNA-binding domain of TP53 lead to a dominant-negative effect in leukaemia, where mutant p53, instead of activating de novo transcriptional programmes, inhibits the wild-type protein, thereby driving clonal selection.

Analyses of clinical trial patients with exceptional responses show that adoptive T cell therapy can be optimised to improve effectiveness in patients of chronic lymphocytic leukaemia and breast cancer.

The importance of 'Warburgian' metabolism in cancer is an increasingly disputed topic. By studying cancer metabolism in patients and mouse models, Faubertet al. now show that lactate is used as a respiratory fuel in non-small-cell lung cancer in vivo.

In a new study, researchers show that basal-like breast cancer can be converted into the luminal subtype by inhibiting platelet-derived growth factor (PDGF)-CC signalling in the tumour microenvironment, thereby potentially broadening treatment options for oestrogen receptor-negative breast cancer patients.

Mitogen- and stress-activated kinase 1 (MSK1) has been identified as an epigenetic modulator of luminal gene expression in breast cancer, maintaining latency of bone micrometastases.

The fusion gene consisting of fibroblast growth factor receptor 3 and transforming acidic coiled-coil-containing protein 3 is oncogenic and present in a small cancer subset. Frattini et al. have identified that this fusion gene drives peroxisomal and mitochondrial biogenesis.

Since mesenchymal-like properties in cancer cells are often associated with therapy resistance, Viswanathanet al. explored vulnerabilities of these cells. They identified an enzyme of the lipid peroxidase pathway, inhibition of which caused ferroptosis in a range of cancer types.

A recent study shows that smoking-induced epigenetic changes in lung epithelium occur even before malignant transformation, and sensitize the cells to allow a single key oncogenic event to initiate the growth of a tumour.

Both obesity and systemic inflammation promote cancer progression, although how obesity-associated inflammation affects cancer metastasis is poorly understood. Quailet al. now show that obesity induces cytokines that stimulate lung neutrophilia in mice, thereby promoting breast cancer metastasis.

Three studies published in Developmental Cell, Nature and Nature Medicine shed new light on mechanisms of cancer-associated cachexia in early and advanced disease.

Two papers recently published in Nature Medicine and Science Signaling highlight the various interdependent or independent ways by which YAP and TAZ can affect tumour growth.

Hoekstra et al. and Thibaut et al., both reporting in Nature Cancer, show that interferon-γ secreted by tumour-reactive T cells diffuses into the tumour microenvironment and acts on remote tumour cells to modify tumour behaviour.

Two studies by Park et al. and Papalarazou et al. explored mechanoresponses of cancer cell metabolism in the lung and pancreas, respectively. They identify distinct mechanisms of adaptation to changes in extracellular matrix stiffness, thereby maintaining the cells’ ability to grow or disseminate.

Vitamin C supplementation has shown limited benefits in patients with solid tumours. Two studies report that vitamin C supplementation can reduceTet-dependent leukaemia progression in mice, supporting the concept of high-dose vitamin C supplementation in certain patients with haematological malignancies.

Miller, Sen et al. show that exhausted T cells in tumours contain distinct subpopulations, one of which is long-lived and persistent and, in response to immune checkpoint blockade, can give rise to short-lived cytotoxic T cells that exert tumour control.

In a study published in Nature Medicine, Malehmir et al. have identified how platelet recruitment contributes to the development of nonalcoholic steatohepatitis and hepatocellular carcinoma in response to high-fat diets in mice.

PI3K inhibition in solid cancers driven by PI3K catalytic subunit-α has shown limited clinical benefit. This might be due to activation of a glucose–insulin feedback loop, which can be interrupted by dietary or pharmaceutical approaches, thereby improving therapy outcome.

Activation of TGFβ signalling in invasive margins of metastatic tumours can contribute to T cell exclusion and reduced immune checkpoint therapy response. Inhibition of TGFβ in non-responders can potentially help to improve outcomes in these patients.

Two groups have shown that personalized, neoantigen-based tumour vaccines elicit effective T cell responses in patients with advanced melanoma, leading to favourable clinical outcomes. Combination with checkpoint blockade can be of additional benefit.

Activation of TGFβ signalling in invasive margins of metastatic tumours can contribute to T cell exclusion and reduced immune checkpoint therapy response.

Torrino et al. report that extracellular matrix stiffening stabilizes microtubules by glutaminolysis-dependent microtubule glutamylation, thereby promoting breast cancer progression.

Liu et al. show that glycogen accumulates in pre-malignant liver cells by undergoing liquid–liquid phase separation and, by sequestering Hippo kinases MST1 and MST2, promotes YAP-driven tumorigenesis.