Latest Research
All publications from the Cancer3.AI database, newest first.
The Urinary Tract commensal Peptoniphilus spp. Encodes a Novel 17β-Hydroxysteroid Dehydrogenase.
Binion B, et al
Researchers have discovered that bacteria naturally residing in the male urinary tract possess previously unknown enzymes capable of producing testosterone, a finding with potential implications for prostate cancer treatment. The study focused on anaerobic bacteria from the genitourinary microbiome, particularly Peptoniphilus obesi and Anaerococcus species, and identified novel 17β-hydroxysteroid dehydrogenase (17β-HSDH) enzymes that convert the weak androgen androstenedione into testosterone using NADPH as a cofactor. These microbial enzymes were shown to act on a broad range of steroid substrates and are distinct from previously characterized enzymes performing similar reactions in the urinary tract. Critically, both bacterial genera harboring these enzymes have been repeatedly associated with prostate cancer, suggesting that the local microbiome may actively sustain testosterone levels in tumor tissue even when patients are undergoing androgen deprivation therapy, a standard treatment designed to starve hormone-sensitive prostate cancer of androgens. These findings broaden our understanding of how gut and urinary microbes extend the human hormonal system and may help explain why some prostate cancer patients develop resistance to hormone-blocking treatments.
bioRxiv : the preprint server for biology
Source →PHENOCAUZ: Linking Human Symptoms, Drug Side Effects and Efficacy to Their Molecular Causes Using Mendelian Disease Biology.
Zhou H, et al
Researchers developed PHENOCAUZ, a computational framework that connects clinical symptoms to the specific proteins responsible for causing them by drawing on genetic data from rare Mendelian diseases. The system integrates known gene-symptom relationships from Mendelian disorders with molecular protein features to train a machine learning model capable of predicting which proteins drive a given symptom even in complex, non-Mendelian diseases. Validated across 2,344 symptoms and nearly 5,000 proteins using rigorous cross-validation, the model achieved a precision of approximately 70% among its top predictions, and its outputs aligned well with known drug targets and disease mechanisms described in scientific literature. Beyond basic science, PHENOCAUZ demonstrated real-world utility by predicting severe drug side effects and identifying potential therapeutic targets for ovarian, prostate, and breast cancers, as well as for dementia and Crohn's disease. This work establishes that the biology of rare genetic diseases can serve as a powerful lens for understanding the molecular roots of common symptoms and accelerating the discovery of safer, more effective drugs.
bioRxiv : the preprint server for biology
Source →Folate Receptor α Contributes to Radiation Resistance in Neuroendocrine Prostate Cancer by Regulating Redox Homeostasis.
Goel HL, et al
Researchers investigated why neuroendocrine prostate cancer (NEPC), one of the most aggressive forms of prostate cancer, frequently resists ionizing radiation therapy, a treatment that is otherwise effective for less aggressive prostate cancers. Using mass spectrometry to compare cell surface proteins in prostate cancer cell lines before and after radiation-induced resistance, scientists identified folate receptor α (FRα) as a key driver of radiation resistance that also correlates with neuroendocrine differentiation. The study found that FRα expression is controlled by HIF-1α, a protein activated under low-oxygen conditions typical of the NEPC tumor microenvironment, establishing a direct mechanistic link between hypoxia, neuroendocrine identity, and treatment resistance. Crucially, the folate-FRα signaling axis was shown to sustain intracellular glutathione levels, a major antioxidant that neutralizes the surge of reactive oxygen species generated by radiation, thereby protecting cancer cells from radiation-induced death. These findings are clinically significant because FRα is already a validated therapeutic target, meaning that existing or emerging anti-FRα therapies could potentially be combined with radiotherapy to overcome resistance in NEPC patients and improve outcomes in this otherwise lethal disease.
bioRxiv : the preprint server for biology
Source →Comparative single-cell atlases reveal injury-driven tubal epithelial regeneration as a window for ovarian carcinoma initiation.
Ralston CQ, et al
Researchers conducted a large-scale comparative study to understand how high-grade serous carcinoma (HGSC), the deadliest form of ovarian cancer, originates in the Fallopian tube lining. Using single-cell genomic analyses of both human and mouse tubal tissue, combined with laboratory organoid experiments, the team mapped how immature progenitor cells develop into the two main cell types of the tube and found this process is largely conserved between species. Critically, the human distal Fallopian tube — the region most prone to cancer — showed strong signatures of ongoing injury and repair that were absent in mice, suggesting a biological vulnerability unique to humans. When mechanical injury was experimentally induced in mice, a population of pre-ciliated cells expanded dramatically, and disabling the tumor-suppressor genes Trp53 and Rb1 (both commonly mutated in HGSC) in these regenerating cells rapidly triggered cancerous transformation. These findings suggest that physical trauma to the Fallopian tube, such as from certain medical procedures or repeated ovulation-related injury, may create a window of vulnerability during which cancer-driving mutations can take hold. The results urge clinicians to consider the potential cancer risk of procedures that mechanically disturb the tubal epithelium and open new avenues for early prevention strategies.
bioRxiv : the preprint server for biology
Source →Trends in male breast cancer in Spain, 1999-2023: a nationwide analysis of incidence and mortality.
Cayuela L, et al
A new nationwide study from Spain analyzed trends in male breast cancer (MBC) incidence and mortality over a 25-year period from 1999 to 2023, using national death registry data and modeled incidence estimates from the Global Burden of Disease Study. Researchers found that while the age-standardized incidence rate remained largely stable across the study period, mortality dropped significantly — falling from 0.65 to 0.39 deaths per 100,000 men — representing an average annual decline of 1.8%. The mortality-to-incidence ratio also fell from 0.41 to 0.26, suggesting that men diagnosed with breast cancer are surviving longer thanks to improved clinical management. Reductions in mortality were most pronounced among men aged 55 to 64, and statistical modeling indicated that both period effects and lower cancer risk among more recently born cohorts contributed to the positive trends. These findings highlight the importance of continued investment in early detection programs, male-specific awareness campaigns, and adherence to evidence-based treatment guidelines to further reduce the burden of this rare but serious disease.
Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico
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