Latest Research
All publications from the Cancer3.AI database, newest first.
BRCA1 and BRCA2 pathogenic variants increase the risk of four less common cancer types.
Sasagawa H, et al
A large case-control study published in ESMO Open examined whether inherited mutations in the BRCA1 and BRCA2 genes increase the risk of nine less common cancer types, including bladder, bone, brain, head and neck, sarcoma, skin, testis, thyroid, and ureteral cancers. Researchers analyzed genetic data from 3,489 cancer patients and 38,842 cancer-free controls, identifying 105 disease-causing variants among nearly 1,000 germline mutations. The study found four statistically significant associations: BRCA1 mutations were linked to a more than fivefold increased risk of thyroid cancer, while BRCA2 mutations were associated with substantially elevated risks of bladder, head and neck, and skin cancers. Notably, the impact of BRCA2 mutations on bladder cancer risk was significantly greater in women than in men. These findings expand the known cancer risk profile of BRCA1 and BRCA2 carriers and support broader genetic counseling and surveillance strategies for individuals who carry these mutations.
ESMO open
Source →Insertion of SnCl2 into the Pd-Cl bond: mechanistic elucidation and antitumor evaluation of trichlorostannyl palladium-NHC allyl complexes in ovarian cancer models.
Botter E, et al
Researchers designed and synthesized a new class of dual-metal compounds combining palladium and tin, known as Pd(II)/Sn(II) η3-allyl complexes with N-heterocyclic carbene ligands, and evaluated their potential as anticancer agents against ovarian cancer. A total of thirteen complexes were prepared using a chemically elegant insertion reaction, and computational modeling revealed the precise step-by-step mechanism by which tin chloride inserts into the palladium-chlorine bond. All compounds showed strong cell-killing activity across multiple ovarian cancer cell lines, including those resistant to standard platinum-based chemotherapy, with two lead candidates demonstrating exceptional selectivity for tumor cells over healthy tissue. The most promising compound, designated 2i, remained highly active in patient-derived tumor organoids — miniature lab-grown tumors that closely mimic real patient biology — while sparing non-cancerous fallopian tube tissue, indicating a favorable safety profile. Mechanistic studies revealed that compound 2i works by targeting the thioredoxin reductase enzyme and disrupting mitochondrial function, triggering a cell death pathway fundamentally different from that of cisplatin, which helps explain its ability to overcome platinum resistance. These findings suggest that Pd(II)/Sn(II) allyl complexes represent a promising new direction for treating ovarian cancer, particularly in patients who have stopped responding to existing platinum-based therapies.
Dalton transactions (Cambridge, England : 2003)
Source →Are serum MOTS-c levels and MOTS-c m.1382A>C polymorphism related to polycystic ovary syndrome?
Filibeli BE, et al
A new study published in Archives of Endocrinology and Metabolism investigated whether the mitochondria-derived peptide MOTS-c and a specific genetic variant (m.1382A>C polymorphism) are associated with polycystic ovary syndrome (PCOS) in adolescent girls aged 12 to 18. Researchers measured serum MOTS-c levels using ELISA in 121 adolescents with PCOS and 125 healthy controls, and analyzed the m.1382A>C polymorphism through DNA sequencing. Although MOTS-c levels were slightly higher in the PCOS group, the difference did not reach statistical significance, and no meaningful associations were found between MOTS-c and metabolic or anthropometric parameters. Notably, all participants carried the wild-type genotype for the polymorphism studied, meaning no genetic variation was detected in this population. These findings suggest that MOTS-c plays at most a minor role in the development of PCOS in adolescents, and that this particular genetic variant is unlikely to serve as a useful biomarker for the condition in this age group. Clinicians and researchers may need to look beyond MOTS-c when investigating the metabolic and hormonal underpinnings of adolescent PCOS.
Archives of endocrinology and metabolism
Source →CSF3R signalling beyond granulopoiesis: new paradigms in female reproductive biology.
Ansari R, et al
A new comprehensive review published in Cytokine examines the expanding role of CSF3R, the receptor for granulocyte colony-stimulating factor (G-CSF), beyond its classical function in white blood cell production and into female reproductive health and gynaecological cancers. Researchers synthesized current transcriptomic and proteomic evidence showing that CSF3R is expressed in ovarian, endometrial, cervical, and placental tissues, where it regulates immunity, hormone signalling, and tissue remodeling through pathways such as JAK-STAT, PI3K-AKT-mTOR, and NF-κB. The review finds that dysregulated CSF3R activity contributes to a range of disorders including polycystic ovary syndrome, endometriosis, recurrent implantation failure, and ovarian and endometrial cancers, in each case driving inflammation, abnormal cell growth, or immune suppression. In cancer settings, CSF3R promotes tumour proliferation, epithelial-mesenchymal transition, angiogenesis, and the recruitment of immunosuppressive cells that help tumours evade detection. The authors highlight that therapeutic strategies targeting this receptor and its downstream pathways, including JAK inhibitors, STAT3 antagonists, and anti-G-CSF monoclonal antibodies, represent promising avenues for treating both gynaecological cancers and benign reproductive disorders. This work positions CSF3R as a clinically actionable molecular target that could reshape treatment strategies across reproductive medicine and gynaecologic oncology.
Cytokine
Source →Canagliflozin Alleviates Hyperandrogen-Induced Granulosa Cell Ferroptosis in Polycystic Ovary Syndrome Mice by Activating the AMPK/GSK3β/NRF2 Pathway.
Lin J, et al
Researchers investigated whether canagliflozin, a diabetes drug belonging to the SGLT2 inhibitor class, could alleviate symptoms of polycystic ovary syndrome (PCOS) by protecting ovarian cells from a damaging process called ferroptosis — a form of iron-dependent cell death driven by oxidative stress. Using a mouse model of PCOS with elevated androgens (male hormones), the team found that canagliflozin treatment restored normal estrous cycles, improved ovarian structure, lowered testosterone levels, and corrected metabolic problems such as insulin resistance and abnormal lipid levels. At the molecular level, the drug activated the AMPK/GSK3β signaling pathway, which in turn promoted the movement of the antioxidant master regulator NRF2 into the cell nucleus, boosted the protective enzyme GPX4, and reduced harmful lipid peroxidation and mitochondrial damage in granulosa cells. These findings reveal a previously unclear mechanism by which canagliflozin protects ovarian function and suggest it could serve as a valuable treatment option for women with PCOS, a condition affecting millions of women of reproductive age worldwide.
The Journal of steroid biochemistry and molecular biology
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