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    Endometriosis as a Systemic and Complex Disease: Toward Phenotype-Based Classification and Personalized Therapy
    (MDPI AG, 2026-01-16)
    Daniel Simancas-Racines
    ;
    Emilia Jiménez Flores
    ;
    Martha Montalvan
    ;
    Raquel Horowitz
    ;
    Valeria Araujo
    Endometriosis is traditionally conceptualized as a pelvic lesion–centered disease; however, mounting evidence indicates it is a chronic, systemic, and multifactorial inflammatory disorder. This review examines the molecular dialog between ectopic endometrial tissue, the immune system, and peripheral organs, highlighting mechanisms that underlie disease chronicity, symptom variability, and therapeutic resistance. Ectopic endometrium exhibits distinct transcriptomic and epigenetic signatures, disrupted hormonal signaling, and a pro-inflammatory microenvironment characterized by inflammatory mediators, prostaglandins, and matrix metalloproteinases. Immune-endometrial crosstalk fosters immune evasion through altered cytokine profiles, extracellular vesicles, immune checkpoint molecules, and immunomodulatory microRNAs, enabling lesion persistence. Beyond the pelvis, systemic low-grade inflammation, circulating cytokines, and microRNAs reflect a molecular spillover that contributes to chronic pain, fatigue, hypothalamic–pituitary–adrenal axis dysregulation, and emerging gut–endometrium interactions. Furthermore, circulating biomarkers—including microRNAs, lncRNAs, extracellular vesicles, and proteomic signatures—offer potential for early diagnosis, patient stratification, and monitoring of therapeutic responses. Conventional hormonal therapies demonstrate limited efficacy, whereas novel molecular targets and delivery systems, including angiogenesis inhibitors, immune modulators, epigenetic regulators, and nanotherapeutics, show promise for precision intervention. A systems medicine framework, integrating multi-omics analyses and network-based approaches, supports reconceptualizing endometriosis as a systemic inflammatory condition with gynecologic manifestations. This perspective emphasizes the need for interdisciplinary collaboration to advance diagnostics, therapeutics, and individualized patient care, ultimately moving beyond a lesion-centered paradigm toward a molecularly informed, holistic understanding of endometriosis.
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    Obesity and breast cancer: exploring the nexus of chronic inflammation, metabolic dysregulation, and nutritional strategies
    (Informa UK Limited, 2025-06-23)
    Claudia Reytor-González
    ;
    Daniel Simancas-Racines
    ;
    Náthaly Mercedes Román-Galeano
    ;
    Martín Campuzano-Donoso
    ;
    Angelo Michele Carella
    The global prevalence of obesity has risen to epidemic proportions, posing significant health challenges across populations and contributing to increased morbidity and mortality from non-communicable diseases. Among its many consequences, obesity is now firmly established as a modifiable risk factor for breast cancer, particularly in postmenopausal women. The association between obesity and breast cancer is driven by complex and interrelated biological mechanisms, including chronic low-grade inflammation, hormonal imbalances, adipokine dysregulation, insulin resistance, and metabolic dysfunction. These factors collectively create a pro-tumorigenic environment that supports cancer initiation, progression, and recurrence. This review explores the multifaceted nexus between obesity and breast cancer, emphasizing the critical role of inflammatory, hormonal, and metabolic pathways in mediating disease risk and outcomes. Additionally, it highlights the emerging contribution of gut microbiome dysbiosis in modulating host immunity and systemic inflammation in the context of obesity. Nutritional strategies—ranging from dietary pattern modification to caloric restriction and time-restricted feeding (TRF)—are examined for their potential to reduce risk, enhance treatment efficacy, and improve survivorship in breast cancer patients.