Cancer cachexia involves more than a caloric deficit. A recent study by Cross et al. in Science shows that dietary lipid composition exacerbates cachexia in LKB1/STK11-deficient lung cancer through local prostaglandin E2 production and pulmonary sensory neuron activation. By linking local lipid metabolism to anorexia and wasting, these findings support precision nutritional interventions for cancer cachexia.

The tumour suppressor LKB1 (STK11) is implicated in diverse cancers, yet its transcriptomic role in breast cancer remains poorly defined. Here, we integrate bulk-tumour genomic analysis of the METABRI...

The algorithm is partially aligned with current metastatic squamous NSCLC practice in its emphasis on broad molecular testing and guideline-directed targeted therapy when actionable drivers are presen...

Suzuki and Yoshioka et al. show that the garlic-derived metabolite S-1-propenyl-L-cysteine (S1PC) increases circulating eNAMPT, a key NAD+ biosynthetic enzyme, in mice and humans by activating a criti...

IntroductionThe tumor suppressor kinase liver kinase B1 (LKB1) is known to regulate the activity of the metabolic sensor AMP-activated protein kinase (AMPK),...

Thyroid transcription factor-1 (TTF-1) expression, routinely assessed through immunohistochemistry (IHC) in the diagnostic evaluation of lung adenocarcinomas (LUAD), is negative (TTF-1Neg) in ∼15-20% ...

Cellular & Molecular Immunology - Obesity disrupts ILC2 metabolic and functional homeostasis by inhibiting mTORC1 signaling

Building custom data analysis platforms has traditionally required extensive software engineering expertise, limiting access for many researchers. Here, I demonstrate that modern large language models...

CRISPR screens in iPSC-derived neurons reveal that the E3 ubiquitin ligase CRL5SOCS4 ubiquitinates tau, that CUL5 expression is correlated with resilience in human Alzheimer’s disease, and that electr...

Pancreatic ductal adenocarcinoma (PDAC) has one of the lowest cancer survival rates. Recent studies using RAS inhibitors have opened the door to mo...

Alternative educational movements offer insights about how to help university students find purpose and hope as they navigate an increasingly complex world.

Academic publishing system often allows scientific errors to persist because it prioritises profit and prestige over timely correction.

Cell Death & Disease - Regulation of cell surface protease receptor S100A10 by retinoic acid therapy in acute promyelocytic leukemia (APL)☆

STK11 acts as a key regulator in M2 polarization through coordinating IL-4 signaling and glutamine metabolism.

PDF | Single-cell RNA sequencing (scRNA-seq) is an innovative technology that can be used to characterize transcriptome heterogeneity at the single-cell... | Find, read and cite all the research you n...

Multiple sclerosis (MS) is a chronic autoimmune disorder. Dendritic cells (DCs) represent a promising therapeutic target for restoring immune homeostasis. In this study, the CLAN platform was used to

Join Drs. Ma’n Zawati & James Tsui as they lead a thought-provoking session on the use of AI in research and innovation.

Recent developments in cancer research have illuminated crucial insights into the mechanisms that render lung adenocarcinomas resistant to immunotherapy. A study led by Parker, R.E. and colleagues has revealed that high levels of the protein PER1 are closely associated with mutations in the STK11 gene—a common occurrence in lung adenocarcinoma. This correlation not only underscores the vital relationship between molecular alterations and immunotherapy effectiveness but also proposes a potential pathway for targeted therapeutic strategies.

Welcome to This is Epigenetics!—a bilingual podcast, produced by the CEEHRC trainee committee, where we interview renowned Canadian scientists about their career, their research and, more importantly,...

Despite the development of new classes of therapeutics in oncology, patients with tumors harboring mutations in the tumor suppressor gene STK11/LKB1 continue to exhibit poor clinical response and therapeutic resistance. Recent advances in the understanding of LKB1-mutant tumor biology have illuminated how metabolism and the tumor microenvironment (TME) function as effectors of the aggressive nature of this tumor type. New findings have revealed how metabolic reprogramming, a hallmark of LKB1-mutant tumor biology, can be exploited as a potential targetable liability in these tumors. Characterization of the distinctly immunosuppressive LKB1-mutant TME has motivated multiple discoveries of new approaches for rewiring the microenvironment to overcome immunotherapy resistance. Indeed, overcoming therapeutic resistance in LKB1-deficient tumors continues to be a major research focus, and some preclinical studies have advanced to clinical trials. In this review, we critically analyze these findings and discuss therapies in development that aim to leverage this new understanding for clinical benefit.

Sun et al. report that high-dose ascorbic acid selectively induces pyroptosis in lung cancer with LKB1 deficiency via the ROS-caspase-3-GSDME axis. This promotes dendritic cell activation and progenitor-exhausted T cell expansion, ultimately sensitizing immunotherapy in LKB1-deficient lung cancer.