Endometrial cancer is one the most prevalent gynecological cancers and, unfortunately, has a poor prognosis due to low response rates to traditional treatments. However, the progress in molecular biology and understanding the genetic mechanisms involved in tumor processes offers valuable information that has led to the current classification that describes four molecular subtypes of endometrial cancer. This review focuses on the molecular mechanisms involved in the pathogenesis of endometrial cancers, such as genetic mutations, defects in the DNA mismatch repair pathway, epigenetic changes, or dysregulation in angiogenic or hormonal signaling pathways. The preclinical genomic and molecular investigations presented allowed for the identification of some molecules that could be used as biomarkers to diagnose, predict, and monitor the progression of endometrial cancer. Besides the therapies known in clinical practice, targeted therapy is described as a new cancer treatment that involves identifying specific molecular targets in tumor cells. By selectively inhibiting these targets, key signaling pathways involved in cancer progression can be disrupted while normal cells are protected. The connection between molecular biomarkers and targeted therapy is vital in the fight against cancer. Ongoing research and clinical trials are exploring the use of standard therapy agents in combination with other treatment strategies like immunotherapy and anti-angiogenesis therapy to improve outcomes and personalize treatment for patients with endometrial cancer. This approach has the potential to transform the management of cancer patients. In conclusion, enhancing molecular tools is essential for stratifying the risk and guiding surgery, adjuvant therapy, and cancer treatment for women with endometrial cancer. In addition, the information from this review may have an essential value in the personalized therapy approach for endometrial cancer to improve the patient’s life.

Endometriosis is a non-malignant, inflammatory condition that impacts individuals across various hormonal stages, including before their first menstruation, throughout their reproductive years, and after menopause. This condition arises when tissue resembling the uterine lining grows outside the uterus, resulting in inflammation and a range of symptoms, such as dysmenorrhea, pain during intercourse, chronic discomfort, and challenges with fertility. This review provides a comprehensive analysis of the medical strategies implemented to address the pathology of endometriosis, highlighting its significant impact on the quality of life of the individuals affected by this condition. Endometriosis can influence various aspects of life, including physical health, emotional well-being, social interactions, and professional performance. Usually, to assess the quality of life in women with endometriosis, validated instruments, such as different questionnaire types, are used to measure the physical, psychological, social, and reproductive health impacts. To improve the quality of life of the women experiencing endometriosis, several supportive strategies are proposed. The findings underscore the necessity of managing endometriosis through a multidisciplinary approach that encompasses both medical and surgical interventions, lifestyle modifications, and psychological support.

Head and neck squamous cell carcinoma (HNSCC) is an aggressive cancer with a complex molecular landscape. Despite extensive research, our understanding of the molecular mechanisms remains incomplete, hindering the development of effective therapeutic strategies for this disease. Long non-coding RNAs (lncRNAs) have emerged as crucial factors in cancer biology, regulating key networks across various malignancies. These molecules exert their regulatory functions through interactions with nucleic acids or proteins, thereby influencing signaling pathways within tumor cells. Consequently, lncRNAs play a significant role in key processes like cell proliferation, metastasis, immune evasion, and treatment resistance. This review offers a comprehensive overview of current knowledge regarding lncRNA-mediated mechanisms in HNSCC. The first section explores how lncRNAs influence tumor processes through various modulation mechanisms, including transcriptional and post-transcriptional regulation, chromatin remodeling, and epigenetic modifications. We also highlight the impact of lncRNAs on specific signaling pathways that control essential cellular functions (e.g., proliferation, apoptosis, angiogenesis, invasion, metastasis). Ultimately, this underscores the promising potential of lncRNAs as diagnostic biomarkers and therapeutic targets capable of enhancing patient care in oncology. Gaining a deep understanding of how lncRNAs modulate carcinogenic mechanisms may yield innovative approaches for early detection, personalized treatment, and improved clinical outcomes for HNSCC patients.

Background: Polypoid endometriosis is a rare variant of endometriosis that presents as a tumorous mass, making it difficult to differentiate it from a malignant tumor. It usually occurs in perimenopausal women or those undergoing hormone therapy, and its presence in a young pregnant woman is extremely uncommon. Case Presentation: This article describes a rare instance of polypoid ovarian endometriosis in a pregnant woman, a condition with few documented cases in the medical literature. An adnexal mass was discovered incidentally during a routine prenatal ultrasound, with imaging features that raised the suspicion of a neoplastic process and prompted surgery to exclude malignancy. However, histopathological examination of the excised lesion confirmed features compatible with polypoid endometriosis, without revealing evidence of cancer. This case highlights the diagnostic challenges of differentiating polypoid endometriosis from ovarian neoplasms, especially during gestation, where imaging findings can be ambiguous. In addition, the hormonal environment inherent in pregnancy may exacerbate the proliferative behavior of endometriotic lesions, thus complicating clinical evaluations. The presence of an adnexal mass in such a setting often requires careful evaluation to balance the risks of surgery with the potential consequences of delayed diagnosis. The data presented emphasize the importance of an accurate diagnosis. In conclusion, a well-coordinated approach ensures the protection of maternal and fetal health. Conclusions: By prioritizing accurate diagnosis and personalized treatment plans, physicians can minimize complications and improve outcomes for both mother and child.

Human Papillomavirus (HPV) infection is the leading cause of cervical cancer, presenting a significant global health challenge. While natural infection is widespread, the resulting immune response is often characterized by weak, delayed, and type-specific antibody production, offering unreliable protection against reinfection. This review provides a comparative analysis of natural versus vaccine-induced immunity, focusing on antibody kinetics, duration of protection, and cancer prevention efficacy. A comprehensive search of the literature from the last decade was conducted using PubMed, ScienceDirect, and Web of Science. The findings demonstrate that, unlike natural immunity, which is dominated by cellular responses with often incomplete seroconversion, prophylactic vaccination induces high titers of neutralizing IgG antibodies against the L1 capsid protein. These responses are durable, with protection persisting for over a decade, and recent data support the high efficacy of single-dose regimens. Furthermore, vaccination has shown utility in reducing infection persistence in HPV-positive individuals and provides critical protection in immunocompromised groups. Consequently, vaccine-induced immunity is consistently superior to naturally acquired immunity, supporting World Health Organization recommendations for universal vaccination as the primary intervention for reducing the global burden of HPV-related malignancies.

Understanding the complex molecular mechanisms behind gynecological cancers is crucial, as these diseases pose significant challenges to women’s health and are frequently diagnosed at advanced stages. Various genetic, epigenetic, and metabolic alterations play a vital role in tumor development, metastasis, and therapy. Exploring mitochondrial dysfunction and the role of lncRNAs may provide essential insights into how tumor cells evade apoptosis, alter their metabolic pathways, and adapt to stress. In gynecological malignancies, nuclear lncRNAs contribute to tumor progression, treatment resistance, and metastasis through mechanisms that include chromatin remodeling, microRNA modulation, and regulation of mitochondrial dynamics. More recently, the emerging role of mt-lncRNAs, derived from the mitochondrial genome, has attracted attention for their involvement in retrograde signaling, mitochondrial respiration, and regulation of apoptosis. Dysregulation of mt-ncRNAs may contribute to tumor bioenergetic reprogramming, mitochondrial integrity, and nuclear gene expression. The objective of this review is to consolidate the current understanding of the regulatory mechanisms of mitochondrial lncRNAs in ovarian, cervical, and endometrial cancers, thus identifying new opportunities of research. A thorough elucidation of the role of mitochondrial lncRNAs in mitochondrial–nuclear communication may facilitate the development of new interventions in gynecological oncology, highlighting the potential of these molecules as diagnostic biomarkers and therapeutic targets.