News & Comment

Pittet and collaborators show that macrophages can remove anti-PD1 antibodies from T cells, blunting their response, whereas Weissman and colleagues demonstrate that macrophages also express PD1 on their surface, which impairs their phagocytic activity.

Anti-LAP antibodies show promising anticancer properties.

Giustacchini, Thongjuea,et al. have developed a method to sensitively detect somatic mutations and analyze whole transcriptomes of the same single cell. Application of this technique to chronic myeloid leukaemia (CML) patient samples revealed heterogeneous CML stem cell populations with likely roles in CML progression and resistance to therapy.

To advance preclinical research, two groups have developed mouse models of metastatic colorectal cancer using the transplantation of engineered organoids.

ZEB1-mediated epithelial-mesenchymal transition (EMT) and cellular plasticity promotes metastasis in pancreatic cancer.

A paper inScienceby Tomasetti, Li and Vogelstein develops their 'bad luck' model further and explores how different sources of DNA mutation influence different cancer types.

Most of our current knowledge of melanoma is derived from the study of patients from populations of European descent, for whom public health, sun protection initiatives and screening measures have appreciably decreased disease mortality. Notably, some melanoma subtypes that most commonly develop in other populations are not associated with exposure to ultraviolet (UV) light, suggesting a different disease aetiology. Further study of these subtypes is necessary to understand their risk factors and genomic architecture, and to tailor therapies and public health campaigns to benefit patients of all ethnic groups.

Using gene expression analyses of cancer-resistant differentiated muscle cells, Keckesovaet al. identify a mitochondrial protein, lactamase β (LACTB), that affects lipid metabolism and can induce differentiation and suppress proliferation of breast cancer cells in vitro and in vivo.

Boireet al. describe a mechanism by which cancer cells can survive and grow in the leptomeninges of the brain by upregulating complement component 3 (C3) to disrupt blood–cerebrospinal fluid barrier function, allowing entry of growth-promoting factors.

Two papers find that the histone acetylation reader function of the YEATS domain of ENL is required to sustain oncogenic transcriptional programmes for the growth and disease maintenance of acute leukaemias.

Using data from The Cancer Genome Atlas, Carteret al. find that germline variations can influence tumour sites of origin and somatic mutations.

Mechanical coupling of cancer-associated fibroblasts and cancer cells through a heterotypic E-cadherin–N-cadherin adherens junction promotes cancer cell invasion.

A report inScience Translational Medicineprovides the first example of using universal engineered chimeric antigen receptor (CAR) T cells from human leukocyte antigen (HLA)-mismatched donors.

How similar are metastases to the primary tumour and other metastases in the same patient? And what does that tell us about the evolution of metastatic ability? Two papers investigated these questions in pancreatic ductal adenocarcinoma (PDAC).

Two papers demonstrate that centrosome amplification can cause cancer in mammals and that a PIDDosome–p53-dependent control mechanism acts to prevent cell proliferation in the presence of extra centrosomes.