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Showing posts from July, 2025

CPADS enables comprehensive analysis of drug resistance across 44 cancer types

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  CPADS integrates data from the Gene Expression Omnibus (GEO), The Cancer Genome Atlas (TCGA), and the Genomics of Drug Sensitivity in Cancer (GDSC) databases, encompassing over 29,000 samples across 44 cancer types and involving 288 drugs. It provides five main analysis modules: differential expression analysis, correlation analysis, pathway analysis, drug analysis, and gene perturbation analysis. These modules enable users to explore gene expression changes, correlations between genes or drugs, pathway enrichment, drug sensitivity, and the impact of genetic perturbations on drug resistance. The differential expression analysis module allows users to compare gene expression levels between control and drug-treated groups or between drug-sensitive and -resistant groups. The correlation analysis module supports both single-gene and multigene correlation studies, revealing how gene expression correlates with drug IC50 values. Pathway analysis is facilitated through Gene Set Enrichmen...

Senescent macrophages emerge as key drivers of tumor progression

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  Macrophages are versatile immune cells, tasked with cleaning up pathogens and maintaining tissue health. But within the tumor microenvironment, they often shift into an M2-like state—one that paradoxically helps tumors grow by weakening immune defenses and promoting inflammation. At the same time, cellular senescence, traditionally seen as a tumor-suppressive mechanism, can have the opposite effect in aged macrophages . These cells become chronic sources of inflammatory signals and lose their ability to destroy cancer cells. Because of these complexities, there is an urgent need to study senescent macrophages more deeply to uncover their full impact on cancer biology. A new review published (DOI: 10.20892/j.issn.2095-3941.2024.0589) in Cancer Biology & Medicine by researchers at Shandong University takes an in-depth look at how aging macrophages—once thought to be passive bystanders—actively drive tumor development. Drawing on molecular biology, immunology, and emerging thera...

Restoring mitochondria enhances immune response against lung cancer

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  While chemotherapy remains a cornerstone of lung cancer treatment, it often weakens the immune system it relies on for long-term control. Now, researchers have found a way to turn this weakness into strength—by transplanting healthy mitochondria into the tumor environment. In advanced non-small cell lung cancer (NSCLC), combining mitochondrial transplantation with cisplatin not only enhanced immune cell infiltration but also reversed tumor metabolism and improved the drug's effectiveness. This innovative approach transforms mitochondria from mere energy suppliers into active allies in cancer therapy, showing potential to reshape how we treat aggressive lung tumors. Lung cancer causes more deaths than any other cancer worldwide, with non-small cell lung cancer (NSCLC) accounting for 85% of cases. Chemotherapy is the first-line treatment for advanced NSCLC, yet its effectiveness is hampered by toxic side effects and emerging resistance. Moreover, chemotherapy damages immune cells a...

Hydrogels could be key to safer, smarter cancer drug delivery

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  Modern cancer therapies have resulted in higher survival rates in many cases. However, their delivery mode and generic action are associated with greater adverse effects and potentially lower efficacy. A recent review published in Frontiers in Immunology analyzed the potential for introducing hydrogels in cancer treatment, which could lead to personalized, more effective, and less toxic drug delivery platforms. Introduction Cancer treatments include surgery, radiation therapy, chemotherapy, and traditional Chinese medicine. Chemotherapy is very commonly used to increase survival time but is associated with a range of severe adverse effects. Usually, these arise because of the off-target effects of these highly cytotoxic molecules . Targeted drug delivery is the holy grail of cancer therapy. Newer systems are theorised which will direct drugs to act solely on the cancer cells, mediated by cell- or tumor-specific recognition mechanisms. Nanocarriers, one promising avenue, are used...

Deep-sea bacterial compound triggers pyroptosis to fight cancer

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  Promoting pyroptosis-an inflammatory form of programmed cell death-has become a promising treatment strategy for cancer. In research published in The FASEB Journal, investigators purified a long-chain sugar molecule, or exopolysaccharide, from deep-sea bacteria and demonstrated that it triggers pyroptosis to inhibit tumor growth. The compound, called EPS3.9, consists of mannose and glucose and is produced by the Spongiibacter nanhainus CSC3.9 bacterial strain and other members of the genus Spongiibacter. Mechanistic analyses showed that EPS3.9 can directly target 5 membrane phospholipid molecules and exert tumor toxicity by stimulating pyroptosis in human leukemia cells. EPS3.9 also had significant anti-tumor effects in the mice with liver cancer and activated anti-tumor immune responses. #ResearchChemistry, #ChemicalInnovation, #Science, #ScienceResearch, #ScientificResearch, #ResearchAndDevelopment, #ChemistryEducation, #ChemistryExperiments, #ChemistryLab, #ChemistryStudents, ...

Different anti-PD-L1 antibodies show varied results in tumor growth inhibition

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  Immune checkpoint inhibitors (ICIs), a powerful form of immunotherapy, have revolutionized cancer treatment by unleashing the body's own immune system to fight tumors. These compounds target the programmed cell death-ligand 1 (PD-L1), a surface protein typically found on tumor cells, which enables the tumors to avoid recognition by immune T cells. By disrupting PD-L1's function with specially tailored antibodies, ICI-based strategies have brought hope to countless patients with cancer. However, despite their undeniable success, these treatments do not work for everyone. Many patients remain unresponsive to immunotherapy , and scientists have been struggling to understand why some people benefit while others don't. While much research has focused on tumor and patient characteristics that could influence treatment response, less attention has been paid to how the drugs themselves might influence their treatment success. Different antibody drugs, even those targeting the sam...

Fluorescent bacteria enable real-time tumor visualization during surgery

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  Accurate removal of tumors is the most critical aspect of cancer surgery, yet it remains a significant challenge in clinical practice. In breast cancer, for example, the positive margin rate-where cancer cells remain at the surgical boundary-can reach up to 35%, often requiring reoperation and increasing the risk of recurrence. Preoperative imaging or ultrasound is often insufficient to fully identify tumor boundaries, forcing surgeons to rely heavily on experience. These limitations highlight the urgent need for technologies that can provide real-time tumor visualization during surgery . A joint research team led by Dr. SeungBeum Suh (Center for Bionics) and Dr. Sehoon Kim (Center for Chemical and Biological Convergence) at the Korea Institute of Science and Technology (KIST, President Sang-Rok Oh), and Professor Hyo-Jin Lee at Chungnam National University Hospital, has developed a next-generation intraoperative imaging platform using engineered beneficial bacteria that emit flu...

Dual cancer drugs restore memory and rewire brain cells in Alzheimer’s mouse models

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  In a recent study published in the journal Cell, a group of researchers investigated whether combining the aromatase inhibitor letrozole and the topoisomerase I inhibitor irinotecan could reverse cell–type–specific transcriptomic disturbances and improve cognition and pathology in Alzheimer’s disease (AD) models. Background Every three seconds, someone develops dementia, and more than 50 million people worldwide now live with AD, a figure forecast to triple by 2050. Existing monoclonal antibodies slow amyloid beta (Aβ) accumulation yet leave most patients cognitively impaired, partly because AD involves intertwined neuronal and glial dysfunctions. Recent single-nucleus RNA sequencing (snRNA-seq) studies have revealed that excitatory neurons, inhibitory neurons, microglia, astrocytes, and oligodendrocyte precursor cells (OPCs) each follow distinct yet interacting degenerative programs. Repurposing approved drugs offers a faster, safer route to intervention, but single-target candi...

Blocking a single gene disrupts vitamin D metabolism and cancer pathways in new cell study

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  A recent study published in the journal Frontiers in Endocrinology investigated the role of the short-chain dehydrogenase/reductase 42E member 1 (SDR42E1) enzyme in regulating sterol metabolism and vitamin D. Vitamin D is a pleiotropic hormone vital for phosphorus and calcium homeostasis, immune function, and bone health. Deficiencies could arise from impaired absorption and metabolism, despite exposure to sunlight and the availability of dietary sources. The vitamin D receptor (VDR) mediates the biological effects of vitamin D, while the cytochrome P450 family 24 subfamily A member 1 (CYP24A1) enzyme regulates its inactivation. A genome-wide association study on vitamin D deficiency identified a nonsense variant, rs11542462, that produces a non-functional SDR42E1 enzyme. This variant correlates with increased levels of 7-dehydrocholesterol (7-DHC) and 8-DHC, precursors in vitamin D synthesis. Furthermore, the authors had previously identified these sterols in silico as potential...

Intratumoral microbiota reshape our understanding of cancer biology

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  Intratumoral microbiota-the microbial populations residing within solid tumors-have emerged as pivotal components of the tumor microenvironment (TME), influencing tumor initiation, progression, and therapeutic outcomes. In a comprehensive review published in Med Research, researchers from Southern Medical University and collaborating institutions systematically examine the heterogeneity of these microorganisms and their multifaceted roles in cancer biology. The authors categorize microbial heterogeneity at three distinct levels: among different tumor types, within individual tumors, and between tumors and adjacent non-tumorous tissues. Tumors such as colorectal, breast, gastric, and pancreatic cancers exhibit distinct microbial profiles, with notable diversity in both species composition and spatial localization. These microbial communities may be shaped by tumor subtype, anatomical location, stage of progression, or patient-specific factors such as age, diet, or comorbidities. F...

Researchers unveil drug complex that makes cancer cells self-report to immune system

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  Two junior research groups at Ruhr University Bochum, Germany, have developed a drug complex that kills cancer cells in such a clever manner that they raise a red flag as they die. They signal to the immune system that something is seriously wrong with this type of cell. This teaches the immune cells to destroy such cancer cells—even if they are not in the vicinity of the original tumor. This could remove metastases that develop at distant sites in the body. Dr. Johannes Karges from the Department of Chemistry and Biochemistry and Dr. Carlos Plaza-Sirvent from the Department of Medicine present their findings in the Journal of Medicinal Chemistry on July 17, 2025. Uncommon: Immunogenic cell death 90 percent of all deaths from cancer are due to metastases. This is why Karges and his team are looking for ways to train the immune system to target and eliminate cancer cells. They have found success with a drug that kills the cells in a sophisticated manner. "The gallium complex we...

Galectin-3 identified as key driver of chemoresistance in pancreatic cancer

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  Pancreatic cancer is often diagnosed at an advanced stage and is characterized by a poor prognosis and rising mortality. Galectin-3 (Gal-3), a chimeric protein, plays a multifaceted role in driving the progression of pancreatic adenocarcinoma (PAAD). While its interaction with tumor microenvironment cells is well-documented, the specific mechanisms by which Gal-3 mediates tumor-stromal interactions and promotes metabolic reprogramming linked to drug resistance remain unclear. This research, published in the Genes & Diseases journal by a team from Capital Medical University, Peking University Cancer Hospital & Institute, Shandong First Medical University, and Cardiff University School of Medicine elucidates whether the inhibition of Gal-3 expression in tumor or stromal cells can improve the efficacy of gemcitabine, a standard chemotherapeutic agent for PAAD. Analysis of multiple RNA sequencing public datasets revealed that Gal-3 is not only remarkably up-regulated in tumor...