Metabolic dysfunction-associated steatohepatitis is emerging as a leading cause of hepatocellular carcinoma in individuals whose lifestyle and dietary habits promote a positive energy balance. Here, we reviewed the role of free fatty acids in mediating lipotoxicity and its implications for organellar stress and genome alteration in hepatocytes. Additionally, we discussed the pathogenic processes underlying the malignant transformation of hepatocytes in obese patients.

The glioblastoma microenvironment is dominated by tumour-associated macrophages (TAMs). In the tumour core, monocyte-derived TAMs accumulate and exhibit anti-inflammatory and immune-suppressive expression profiles. At the periphery of the tumour, brain microglia-derived TAMs predominate and exhibit pro-inflammatory and interferon states. Depletion or repolarisation of selected TAM subsets may be key to effective immunotherapy.

Through unbiased drug screening experiments in the context of pancreatic cancer, we observed that KRAS^G12C inhibitors combine favorably with inhibitors of the tyrosine phosphatase SHP2, a broad-acting kinase inhibitor, and inhibitors of the guanine nucleotide exchange factor SOS1. These combinations are effective in a novel KRAS^G12C-driven patient-derived organoid model.

This study presents a glioblastoma-cerebral organoid assembloid (GCOA) model to investigate tumor cell invasion. The GCOA integrates patient-derived GBM tumoroids with cerebral organoids, enabling real-time 3D imaging of tumor cell behavior, intercellular interactions, and gene expression differences between invading and non-invading tumor cells.

Wang et al. found that a novel USP24 inhibitor, NCI677397, as a ferroptosis inducer (FIN) promoted ferroptotic cell death in drug-resistant cancers by increasing lipid peroxidation. Moreover, incomplete autophagy, HO-1 induction and reduced anti-oxidant levels by NCI677397 led to lipid ROS accumulation.

Cancer cachexia is a wasting disease associated with many cancers that leads to alterations in systemic metabolism, a loss of muscle and adipose tissue, and inflammation. In the current review, key mechanisms of cachexia are introduced, and how they relate to current knowledge on cachexia biomarkers. The interplay between ageing and cancer cachexia regarding potential links and biomarkers is discussed.

In this explorative biomarker analysis, we assessed serial sampling of circulating tumor cells (CTCs) with CellSearch in two randomized trials testing immune checkpoint inhibitors (ICIs) in metastatic breast cancer. Our data demonstrate a prognostic potential of CTCs, most apparent 4 weeks into ICI therapy. Furthermore, higher CTC counts were associated with increased markers of tumor immune activity.

Metabolic dysfunction-associated steatohepatitis is emerging as a leading cause of hepatocellular carcinoma in individuals whose lifestyle and dietary habits promote a positive energy balance. Here, we reviewed the role of free fatty acids in mediating lipotoxicity and its implications for organellar stress and genome alteration in hepatocytes. Additionally, we discussed the pathogenic processes underlying the malignant transformation of hepatocytes in obese patients.

Several studies have demonstrated the prognostic value of ctDNA, with mean tumor molecules (MTM)/ml and mean variant allele frequency (mVAF, %) as two validated metrics for quantifying tumor burden. However, the agreement between these two metrics with clinical parameters is yet to be understood. Here, we assessed the performance of mVAF and MTM/ml for predicting survival after definitive treatment.

This review introduces the ‘Alcatraz-Strategy’ for malignant brain tumours, drawing parallels to Alcatraz's isolating barriers. By disrupting cellular tumour networks through supramarginal resection and targeted pharmacological therapy, it aims to decouple tumour cells, akin to the prison's spatial and functional inmate isolation. This approach offers a promising framework to counteract the malignant connectivity of brain tumour networks.

The androgen receptor (AR) antagonist TAS3681 is effective against AR mutations, which leads to agonistic activity of AR signal inhibitors, and had an antitumor effect in an AR-splice variant 7 (AR-V7)-positive enzalutamide-resistant xenograft model. TAS3681 suppresses aberrant AR activation, including AR overexpression and expression of constitutively active nuclear-localized AR-V7, via downregulation of AR and AR-V7.