Cervical cancer is rare in adolescent and pediatric populations, with adenocarcinoma being the most commonly reported. Clear cell adenocarcinoma of the uterine cervix accounts for only 4% of all adenocarcinoma cases, and about two-thirds are associated with intrauterine diethylstilbestrol (DES) exposure. We report the case of a 14-year-old virgin girl who presented with a 1-month-long history of abnormal vaginal bleeding and lower abdominal pain. Transabdominal pelvic ultrasound examination revealed the presence of an irregular, homogeneous cervical mass that was 7 cm in size. Therefore, a magnetic resonance imaging (MRI) scan was performed to establish the origin of the tumor and its relationship to adjacent pelvic organs. Furthermore, a vaginoscopy was performed to identify the tumor, and a cervical biopsy was performed. Immunohistochemical and anatomopathological studies resulted in the diagnosis of non-HPV(Human Papilloma Virus)-related clear cell adenocarcinoma of the cervix. Following the oncological examination, she was admitted for radiotherapy. The patient had no maternal history of DES exposure in utero. Even though the number of cases in the literature is low, most of the virgin girls diagnosed with clear cell adenocarcinoma of the cervix have a fatal prognosis because of the delay in making a correct diagnosis.

Background/Objectives: Hepatoblastoma, the most common pediatric primary liver cancer, is no longer regarded as a conventional malignancy but rather as a tumor emerging from disrupted hepatic developmental processes. Although improvements in chemotherapy, surgical techniques, and liver transplantation have markedly enhanced survival, therapeutic decision-making is still primarily guided by anatomical criteria and insufficiently reflects the biological heterogeneity that contributes to variable treatment response and disease recurrence. This narrative review integrates recent advances in molecular biology, tumor stemness, microenvironmental interactions, and translational research models in pediatric hepatoblastoma. We critically examine how developmental signaling pathways, cellular plasticity, and immune–vascular context shape tumor behavior and therapeutic vulnerability, with a focus on emerging targeted, anti-angiogenic, immune, and epigenetic strategies. Results: Hepatoblastoma is characterized by aberrant activation of key developmental pathways, including Wnt/β-catenin, Hippo–YAP, IGF, and mTOR signaling, which cooperate to sustain proliferation, stem-like phenotypes, and treatment resistance. Tumor heterogeneity is further reinforced by cancer stem cell populations and a predominantly immune-cold microenvironment. While innovative therapeutic approaches show promise, their clinical impact has been limited by biological complexity and insufficient integration into current treatment algorithms. Liquid biopsy biomarkers, advanced translational models, and multi-omics approaches offer new opportunities for biologically informed risk stratification and therapy adaptation. Conclusions: Future progress in pediatric hepatoblastoma will require a paradigm shift from purely clinicopathological management toward an integrated molecular and surgical framework. Incorporating biological stratification into therapeutic decision-making may enable personalized treatment, rational therapy de-escalation, and improved outcomes for high-risk disease. This review highlights the foundations and future directions for precision medicine in hepatoblastoma.

Celiac disease (CeD) is an enteropathy caused by the complex interaction between genetic, environmental, and individual immunological factors. Besides the hallmark of intestinal mucosal damage, CeD is a systemic disorder extending beyond the gastrointestinal tract and impacting various other organs, causing extraintestinal and atypical symptoms. The association between CeD and liver damage has been classified into three main categories: mild and asymptomatic liver injury, autoimmune liver injury, and liver failure. We present a case of severe liver damage with cirrhotic evolution in an obese 12-year-old boy who had been admitted due to generalized jaundice and localized abdominal pain in the right hypochondrium. In the course of investigating the etiology of severe liver disease, toxic, infectious, metabolic, obstructive, and genetic causes were excluded. Despite the patient’s obesity, a diagnosis of CeD was established, and in accordance with autoimmune hepatitis (AIH) criteria, the patient was diagnosed with autoantibody-negative AIH associated to CeD.

Introduction: Wilson’s disease (WD) and autoimmune hepatitis (AIH) are important causes of acute and chronic hepatitis; each can lead to serious complications. The coexistence of these two diseases in the same patient is rare and poses significant diagnostic and therapeutic challenges. The pathophysiological mechanism in WD involves hepatocellular necrosis and the exposure of intracellular antigens to the immune system, resulting in the production of low-titer autoantibodies, which may be misleading and complicate the differentiation between WD and AIH. Case Presentation: We report the case of an 11-year-old girl admitted with abdominal pain, fatigue, and scleral jaundice. Physical examination revealed mild hepatomegaly without splenomegaly. Laboratory investigations were consistent with Wilson’s disease, and treatment with D-penicillamine was initiated. The initial clinical course was favorable; however, six weeks later, the patient again presented with acute hepatitis. A liver biopsy with histochemical analysis revealed findings highly suggestive of both Wilson’s disease and autoimmune hepatitis, confirming a dual diagnosis. Conclusions: The overlap of clinical and biochemical features between AIH and WD can delay accurate diagnosis and treatment, potentially affecting patient outcomes. Although the coexistence of Wilson’s disease and autoimmune hepatitis in the same child is rare, clinicians should maintain a high index of suspicion, given the complex management and the risk of complications associated with both disorders.

Background and Clinical Significance: Childhood-onset Sjögren’s disease (cSjD) is a rare autoimmune disorder that remains challenging to diagnose because of its heterogeneous clinical presentation and the frequent absence of classic sicca symptoms at disease onset. Recurrent parotitis and systemic manifestations often predominate in pediatric patients, contributing to diagnostic delay and potential irreversible glandular damage. Early recognition is essential to prevent complications and improve long-term outcomes. Case Presentation: We report the case of a 17-year-old female diagnosed with primary Sjögren’s disease following a prolonged history of recurrent parotid involvement and progressive glandular dysfunction. Comprehensive evaluation revealed positive anti-SSA antibodies, hypergammaglobulinemia, characteristic salivary gland ultrasonography abnormalities, and a positive minor salivary gland biopsy, resulting in fulfillment of all domains of the 2016 ACR/EULAR classification criteria. The patient also exhibited unusual vascular findings, including carotid atheromatous calcifications in the absence of traditional cardiovascular risk factors. Conclusion: This case highlights the diagnostic complexity of cSjD and underscores the value of a multimodal diagnostic approach integrating clinical assessment, serology, imaging, and histopathology. The presence of early vascular abnormalities broadens the spectrum of potential extraglandular manifestations and emphasizes the need for comprehensive evaluation and long-term monitoring in affected patients.