Preterm birth is the leading cause of death among children aged under 5 years of age worldwide. Maternal genitourinary tract infections (GUTIs) are among the few modifiable risk factors for spontaneous preterm labor (sPTL), yet the gap between association and effective intervention remains unresolved. This narrative review consolidates recent evidence on GUTIs and sPTL, integrating pathogens, ascending and hematogenous pathways, and prevention. MEDLINE, Embase, the Cochrane Library, and Scopus were searched (January 2000-January 2026); evidence was synthesized narratively and stratified by preterm-birth subtype where possible. Pooled estimates showed increased odds of preterm birth with urinary tract infection (odds ratio [OR] 1.92, 95% confidence interval [CI] 1.62-2.27), asymptomatic bacteriuria (ASB; OR 1.62, 95% CI 1.30-2.01), bacterial vaginosis (OR 1.79, 95% CI 1.32-2.43), Ureaplasma colonization (OR 2.76, 95% CI 1.63-4.68), Trichomonas vaginalis (relative risk 1.42, 95% CI 1.15-1.75), and Chlamydia trachomatis (OR 1.57, 95% CI 1.11-2.22). A 2026 Swedish register cohort (n = 684 595) demonstrates that the hazard for preterm birth after urinary tract infection (UTI) diagnosis is highest in the first 6 days and declines with advancing gestation (adjusted hazard ratios 18.5, 13.5, and 6.7 at 22-27, 28-31, and 32-36 weeks). Gene-environment analyses further indicate that preterm birth subtypes differ in susceptibility to UTI versus vaginal infection. Antibiotic treatment of ASB reduces pyelonephritis (RR 0.24), but its effect on preterm birth in unselected populations is uncertain. Ascending infection drives decidual cytokine release and premature myometrial activation; amniotic-fluid sludge on transvaginal ultrasound is an accessible marker of subclinical intra-amniotic infection. Targeted screening, evidence-based antibiotic selection, and antimicrobial stewardship remain the practical priorities.

Depressive disorders and clinically significant depressive symptoms are common in women with breast and gynecologic cancers, although prevalence estimates range from approximately 12% to more than 50% depending on instrument, threshold, timing, and setting. This narrative review, structured according to SANRA criteria, examines evidence on depression and oncologic outcomes in breast and gynecologic cancers and grades each claim by type and strength of evidence. Meta-analyses of observational studies consistently associate depression with recurrence and with cancer-specific and all-cause mortality (pooled relative risks of approximately 1.2-1.3 in breast cancer), and with lower adherence to adjuvant endocrine therapy and radiotherapy. These are prognostic associations; residual confounding by stage, symptom burden, comorbidity, socioeconomic disadvantage, and access to care, and reverse causation, cannot be excluded. Neuroendocrine, inflammatory, and immune mechanisms are best characterized in ovarian cancer, largely in preclinical models and often in relation to chronic stress rather than clinical depression, and whether depression modifies the efficacy of immune checkpoint inhibitors in gynecologic cancers has not been studied. No adequately powered trial has tested whether treating depression improves cancer outcomes; available data come from broader psychosocial interventions and secondary analyses. We propose the Women's Biobehavioral Oncology Framework, an unvalidated conceptual model distinguishing depression as a prognostic marker, a possible causal contributor, and a treatment target, and a prioritized research agenda. Screening and treatment of depression are justified on clinical grounds; its use for risk stratification or treatment selection requires prospective validation.