Search

Gliomas are the most common type of malignant brain tumor and are characterized by a plethora of heterogeneous molecular alterations. Current treatments require the emergence of reliable biomarkers that will aid personalized treatment decisions and increase life expectancy. Glioma tissues are not as easily accessible as other solid tumors; therefore, detecting prominent biomarkers in biological fluids is necessary. Cerebrospinal fluid (CSF) circulates adjacent to the cerebral parenchyma and holds promise for discovering useful prognostic, diagnostic, and predictive biomarkers. In this review, we summarize extensive research regarding the role of circulating DNA, tumor cells, proteins, microRNAs, metabolites, and extracellular vesicles as potential CSF biomarkers for glioma diagnosis, prognosis, and monitoring. Future studies should address discrepancies and issues of specificity regarding CSF biomarkers, as well as the validation of candidate biomarkers. [ABSTRACT FROM AUTHOR]

The article discusses the advancements in lung cancer vaccination, highlighting the challenges faced in targeting this disease effectively. It mentions the development of personalized vaccines targeting neoantigens and the use of mRNA technology, such as the BNT116 vaccine, to treat non-small-cell lung cancer. The article also explores the potential of combining vaccines with existing immunotherapies to enhance the immune system's ability to combat cancer cells. Ongoing research aims to reshape the future of lung cancer vaccination, offering hope for improved treatments and potential preventive vaccines in the future. [Extracted from the article]

The editorial "Leveraging the ROS–TME Axis for Cancer Treatment" explores the role of reactive oxygen species (ROS) in cancer biology, focusing on the delicate balance of ROS levels in the tumor microenvironment (TME). Elevated ROS levels in cancer cells promote proliferation and metastasis, while disrupting this balance can offer therapeutic opportunities. The article discusses strategies to target ROS production or scavenging mechanisms in cancer cells, highlighting potential approaches for cancer therapy. The research emphasizes the importance of understanding the ROS-TME axis for developing effective cancer treatments, although further studies are needed to translate preclinical findings into clinical applications. [Extracted from the article]

The article discusses the role of artificial intelligence (AI) in reshaping anticancer drug development, highlighting its potential to predict efficacy and toxicity, streamline clinical trials, and accelerate drug discovery timelines. AI tools like AlphaFold and PERCEPTION have shown promise in predicting drug responses and targeting specific molecules crucial for cancer cell survival. While AI has the potential to reduce health inequalities and democratize access to care, careful oversight is needed to prevent biases and disparities in patient outcomes. Collaboration among AI experts, cancer researchers, oncologists, and regulatory bodies is crucial to fully realize AI's potential in drug development while ensuring the human element of care is not overlooked. [Extracted from the article]

This article discusses the limitations of current preclinical studies in rheumatoid arthritis (RA) and proposes ways to improve their translatability and clinical relevance. The use of animal models of arthritis and conventional in vitro systems is common in RA research, but they have several weaknesses that compromise their effectiveness. Animal models only mimic certain aspects of RA and have poor translatability to human diseases. Conventional in vitro systems are too simplistic and do not accurately represent the complex pathogenesis of RA. The article suggests using more advanced ex vivo systems, such as 3D synovial organoid platforms, to better model the disease and identify disease-relevant pathogenic subsets. These advancements could lead to better preclinical validation of potential therapeutic treatments for RA. [Extracted from the article]

A recent study published in the Journal of Cellular & Molecular Medicine explores the role of a protein called Suv39h1 in liver fibrosis. The study found that Suv39h1 is involved in the transition of hepatic stellate cells to myofibroblasts, which contributes to liver fibrosis. The researchers also discovered that a natural compound called chaetocin can inhibit Suv39h1 and reduce liver fibrosis in a mouse model. However, further research is needed to develop more selective and less toxic inhibitors of Suv39h1 for potential therapeutic use. Additionally, combining Suv39h1 inhibitors with other drugs or mechanotherapeutics may be a promising approach for treating liver fibrosis. [Extracted from the article]

Pancreatic cancer represents a formidable challenge in oncology, primarily due to its aggressive nature and limited therapeutic options. The prognosis of patients with pancreatic ductal adenocarcinoma (PDAC), the main form of pancreatic cancer, remains disappointingly poor with a 5-year overall survival of only 5%. Almost 95% of PDAC patients harbor Kirsten rat sarcoma virus (KRAS) oncogenic mutations. KRAS activates downstream intracellular pathways, most notably the rapidly accelerated fibrosarcoma (RAF)/mitogen-activated protein kinase kinase (MEK)/extracellular signal-regulated kinase (ERK) signaling axis. Dysregulation of the RAF/MEK/ERK pathway is a crucial feature of pancreatic cancer and therefore its main components, RAF, MEK and ERK kinases, have been targeted pharmacologically, largely by small-molecule inhibitors. The recent advances in the development of inhibitors not only directly targeting the RAF/MEK/ERK pathway but also indirectly through inhibition of its regulators, such as Src homology-containing protein tyrosine phosphatase 2 (SHP2) and Son of sevenless homolog 1 (SOS1), provide new therapeutic opportunities. Moreover, the discovery of allele-specific small-molecule inhibitors against mutant KRAS variants has brought excitement for successful innovations in the battle against pancreatic cancer. Herein, we review the recent advances in targeted therapy and combinatorial strategies with focus on the current preclinical and clinical approaches, providing critical insight, underscoring the potential of these efforts and supporting their promise to improve the lives of patients with PDAC. [ABSTRACT FROM AUTHOR]