Latest Research
All publications from the Cancer3.AI database, newest first.
miR-16-5p mediates E2-induced cell proliferation and EMT in benign prostate hyperplasia.
Kim J, et al
Researchers investigated the molecular mechanisms by which estradiol (E2), a major form of estrogen, drives abnormal cell growth in benign prostatic hyperplasia (BPH), a non-cancerous enlargement of the prostate gland that is highly prevalent in aging men. The study focused on miR-16-5p, a small non-coding RNA molecule known as a microRNA, and its role in regulating both cell proliferation and epithelial-mesenchymal transition (EMT), a cellular process in which epithelial cells acquire more mobile, mesenchymal-like properties that can contribute to tissue remodeling and disease progression. The findings demonstrate that miR-16-5p acts as a critical mediator of E2-driven cellular changes in prostate tissue, linking estrogen signaling to altered gene expression programs that promote BPH pathology. These results suggest that hormonal stimulation by estrogen is not merely a passive background factor in prostate enlargement, but actively reshapes cellular behavior through specific microRNA pathways. For clinicians and patients, this research highlights miR-16-5p as a potential biomarker and therapeutic target for BPH, which may eventually inform new non-surgical treatment strategies for millions of men affected by this condition worldwide.
Scientific reports
Source →Polygenic risk score and 20-year prostate cancer-specific mortality and survival.
Plym A, et al
A large study involving nearly 20,000 men from Sweden and the United States investigated whether a polygenic risk score (PRS) — a genetic tool combining 451 inherited DNA variants — is associated not only with prostate cancer incidence but also with long-term cancer-specific mortality and survival over 20 years. In full-cohort analyses, men with a PRS at or above the median had three times the risk of developing prostate cancer and an even greater risk of dying from it compared to men with lower genetic scores, with hazard ratios of 3.02 and 3.26 respectively. Case-only survival analyses, which compared men who died of prostate cancer against survivors, revealed a modest but meaningful elevation in risk that became statistically significant after excluding PSA-linked variants — particularly in men aged 65 to 74 at diagnosis, where the hazard ratio reached 1.72. The authors also found that standard case-only survival estimates may underestimate the true genetic influence due to age-dependent selection effects and differences in disease detection driven by PSA testing. These results demonstrate that inherited genetic risk captured by a comprehensive PRS may shape prostate cancer prognosis, not just susceptibility. Clinicians and researchers may need to integrate polygenic risk into prognostic models and personalized screening strategies for prostate cancer.
Communications medicine
Source →Electrophilic compound screening identifies GPX4-dependent ferroptosis as a senescence vulnerability.
D'Ambrosio M, et al
Researchers screened a library of 10,480 electrophilic compounds to identify new drugs capable of selectively killing senescent cells — aged, dysfunctional cells that accumulate in tissues and drive cancer progression and other age-related diseases. Among 38 active compounds discovered, a class of chemicals called chloroacetamides showed broad senolytic activity, and activity-based protein profiling revealed that their primary cellular target is GPX4, an enzyme that protects cells from a form of iron-dependent cell death known as ferroptosis. The study found that senescent cells exist in a precarious state: they accumulate elevated oxidative stress and intracellular iron that prime them for ferroptosis, yet simultaneously upregulate GPX4 to suppress this lethal process and survive. Blocking GPX4 with inhibitors or with senolytic chloroacetamides tips this balance, triggering selective ferroptotic death in senescent cells while leaving healthy cells largely unaffected. Crucially, combining established anticancer therapies with GPX4 inhibitors successfully eliminated senescent tumor cells in laboratory models of melanoma, prostate cancer, and ovarian cancer. These findings establish GPX4 as a critical survival dependency of senescent cells and position GPX4 inhibitors as a promising new class of senolytics with broad potential to improve cancer treatment outcomes.
Nature cell biology
Source →Shift happens: a fairness-oriented framework for medical classification under hidden bias.
To MN, et al
Researchers developed DPE-Former, a new artificial intelligence framework designed to reduce hidden biases in medical AI classification systems that can cause models to perform poorly for certain patient subgroups, even when those groups are not explicitly labeled in training data. The system combines prototype-based learning with a transformer attention mechanism, training multiple complementary classifiers on balanced data subsets and then adaptively merging their outputs to produce fairer predictions. Testing was performed across diverse medical datasets, including prostate ultrasound images, skin lesion photographs, and structured cardiac patient records. DPE-Former consistently achieved higher accuracy for underrepresented patient groups and more uniform overall performance compared to conventional AI training approaches. These findings are clinically significant because hidden bias in medical AI can silently worsen health disparities, particularly for minority populations, and the publicly released code may enable widespread adoption of fairer diagnostic tools in fields such as oncology and cardiology.
International journal of computer assisted radiology and surgery
Source →Diagnostic challenges and management of primary accessory axillary breast cancer.
Gonzalez J, et al
This case report from BMJ Case Reports describes the diagnostic and clinical management challenges surrounding accessory axillary breast cancer (AABC), a rare condition in which malignant tissue develops within residual embryonic breast tissue located in the armpit rather than the conventional breast. A perimenopausal woman presented with a slowly enlarging right axillary lump initially misidentified as a benign sebaceous cyst, but incisional biopsy ultimately revealed high-grade invasive ductal carcinoma arising from accessory breast tissue, with no tumor detected in the orthotopic breast on imaging. The patient was staged at cT1N0M0, underwent axillary lumpectomy and sentinel lymph node biopsy confirming pT1bN0M0 disease, and received adjuvant whole-breast radiotherapy along with hormonal therapy using anastrozole and goserelin. At two years post-treatment, she remains entirely disease-free, demonstrating that applying standard breast cancer protocols to AABC can yield excellent outcomes. The case serves as an important clinical reminder that physicians should maintain a high index of suspicion for malignancy when evaluating axillary masses, especially when routine breast imaging returns negative results, in order to avoid delayed diagnosis of this easily overlooked condition.
BMJ case reports
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