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In response to tumour-derived signals, fibroblastic reticular cells within tumour-draining lymph nodes acquire a unique gene signature which in turn disrupts the composition and localization of lymph node immune cell populations.
Acquired resistance to programmed cell death 1 blockade in patients with melanoma is associated with defects in the pathways involved in interferon-receptor signalling.
Jianget al. show that inhibition of focal adhesion kinase (FAK) reduces immunosuppression and fibrosis in pancreatic ductal adenocarcinoma (PDAC) and can improve the efficacy of both chemotherapy and immunotherapy in PDAC mouse models.
Papaemmanuilet al. have described new mutations that drive acute myeloid leukaemia and classify the disease in distinct subgroups associated with different diagnostic features and clinical outcomes
Whereas activation of p21 by p53 causes G1 cell cycle arrest, p53-independent expression of p21 can cause deregulation of DNA replication and genomic instability.
The identification of multiple independent cancer lineages in multiple bivalve species makes transmissible cancers a common event, not exclusively restricted to the species of origin.
A recent article published inNature describes a novel genetic mechanism of immune evasion in a number of cancers that is caused by structural variants (SVs) disrupting the 3′ regulatory region of programmed cell death ligand 1 (PDL1).
Luet al. identify a potential mechanism driving chondroblastoma and sarcoma development in patients with lysine-to-methionine mutations in histone H3 at position 36 (H3K36M).
Two new studies present novel insights into how cancer can control or be controlled by the body's circadian clock and suggest that chronotherapies could have a wider therapeutic impact.
The small-molecule inhibitor rigosertib acts as a RAS mimetic — by disrupting the association of RAS with RAF and other effector proteins, it inactivates RAS downstream signalling.
SMAD4-mutant pancreatic ductal adenocarcinomas (PDACs) with impaired transforming growth factor-β (TGFβ) signalling initiate a signal transducer and activator of transcription 3 (STAT3)-dependent signalling pathway that leads to increased stromal stiffening and aggressive disease.
Kauret al. show that in older patients, fibroblasts in the melanoma microenvironment produce the WNT–β-catenin inhibitor secreted frizzled-related protein 2 (SFRP2), which increases oxidative stress in melanoma cells, driving metastasis and therapeutic resistance.
Paeket al. report that the level of p53 required to induce apoptosis in human colon cancer cells increases with time following treatment with DNA damage-inducing agents.
