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Uric acid is the end product of purine metabolism and plays a dichotomous role in the human body. On one hand, it exerts antioxidant and neuroprotective effects; on the other hand, chronic hyperuricemia has been strongly associated with diseases beyond gout, affecting the cardiovascular, renal, metabolic, autoimmune, and central nervous systems (CNS). Excess uric acid promotes oxidative stress, endothelial damage, neurodegeneration, inflammasome activation, and impairs energy metabolism. It exacerbates autoimmune diseases, such as Systemic Lupus Erythematosus (SLE) and antiphospholipid syndrome (APS), by increasing inflammatory and oxidative damage, leading to greater end-organ damage. The British Society for Rheumatology, European League Against Rheumatism, American College of Rheumatology, and National Institute for Health and Care Excellence (NICE) have all established a "treat-to-target" approach for hyperuricemia with serum urate levels below 6 mg/dL and below 5 mg/dL in severe cases. Allopurinol and Febuxostat, xanthine oxidase inhibitors, are used as first-line pharmacological therapies for the treatment of hyperuricemia, whereas uricosurics and Interleukin-1 (IL-1) inhibitors are preferred in cases of refractory hyperuricemia. Lifestyle modifications, such as the Dietary Approaches to Stop Hypertension (DASH) diet, weight reduction, and smoking cessation, are also recommended for the long-term management of the disease. Sodium-Glucose Cotransporter 2 (SGLT2) inhibitors, selective urate transport inhibitors, and plant-derived anti-inflammatory compounds have emerged as new treatments with promising responses. This review synthesizes the current literature on the multifaceted role of uric acid and emphasizes its systemic implications in chronic diseases. It also outlines the already established management options and new innovative therapies for managing this disease. Understanding this dichotomous role is essential for adopting a precise management approach that balances the protective and pathological effects of uric acid.

Teledentistry has evolved from asynchronous communication to real-time consultations, with adoption accelerating during and post-COVID. Concurrently, AI has been leveraged to enhance diagnostic accuracy, efficiency, and accessibility using machine learning, GANs, and connected devices. This scoping review, conducted using Arksey and O'Malley framework and Joanna Briggs Institute guidance, explores the ethical, legal, and economic considerations of AI-driven teledentistry. Following a PRISMA-ScR compliant screening process by two independent reviewers, 137 studies published between 2018 and 2025 were included. Unlike previous reviews that have primarily focused on clinical applications or the general use of AI in healthcare, this review addresses the ethical, legal, and economic considerations of AI in teledentistry in a single paper. It underscores the importance of explainable AI, explores cross-border regulatory challenges, and discusses possible cost models for adoption in smaller practices. This review indicates that AI-powered teledentistry could enhance diagnostic accuracy, facilitate early detection, improve monitoring, and increase accessibility. Nonetheless, these advantages come with critical concerns including data privacy, potential biases, patient autonomy, accountability, and cost. Addressing these issues through governance, oversight, transparency, and economic viability is essential. AI-enabled teledentistry has the potential to transform dental care delivery, but its integration must be approached with careful consideration of its associated challenges.

Metformin-associated lactic acidosis (MALA) is a rare but life-threatening complication of metformin therapy that most commonly occurs in the setting of acute kidney injury (AKI) and impaired drug clearance. Given the widespread use of metformin for type 2 diabetes mellitus, recognition of precipitating factors for MALA remains critically important. We report a case of severe euglycemic diabetic ketoacidosis (DKA) with refractory lactic acidosis in a patient with previously unrecognized obstructive uropathy due to recurrent nephrolithiasis causing bilateral hydronephrosis and severe AKI while on metformin therapy. The patient developed profound metabolic derangements that were unresponsive to conventional medical therapy, with resolution only after emergent hemodialysis. This case highlights the importance of early recognition of AKI from obstructive uropathy as a reversible precipitant of metformin accumulation and emphasizes the role of prompt renal replacement therapy in patients with severe MALA and refractory metabolic acidosis.

Spina bifida is a neural tube defect (NTD) that arises when the neural tube fails to close properly during early development. This review focuses on myelomeningocele (MMC), the most common severe form of spina bifida, which often leads to motor and sensory impairments, including lower limb weakness or paralysis, as well as renal, urological, orthopedic, developmental, and psychosocial challenges. We explore the etiology, pathogenesis, prevention, diagnosis, and management of spina bifida, with a special emphasis on in-utero surgical repair. Over the past several decades, researchers and clinicians have made remarkable strides across all stages of care from prevention to postnatal outcomes. Widespread use of folic acid supplementation has significantly reduced the number of new cases. Advances in prenatal imaging and diagnostics now allow for earlier and more accurate detection, enabling timely intervention. In-utero surgical techniques continue to evolve, with innovative hybrid approaches that combine the strengths of open and minimally invasive methods. The momentum in this field shows no sign of slowing. Promising developments in stem cell therapy, biomaterials, robotic-assisted surgery, 3D printing, and enhanced imaging are redefining treatment goals in spina bifida. With each advance, clinicians gain better tools to improve outcomes for both mother and child, minimizing risks and maximizing long-term health and quality of life for both patients.

Epigenetic modifications, particularly aberrant DNA methylation, play an important role in the pathogenesis of both solid and hematologic malignancies. Global hypomethylation and promoter hypermethylation can silence numerous tumor suppressor genes identified in acute myeloid leukemia (AML) and myelodysplastic neoplasm (MDS). Among stemness-associated transcription factors, OCT-4 and SOX-2 are key regulators of pluripotency and stem cell maintenance and have been implicated in cancer stem cell biology and tumor progression. Although their abnormal expression and epigenetic regulation have been reported in various malignancies, limited data are available regarding their promoter methylation status specifically in AML and MDS. Therefore, this study aimed to evaluate the methylation patterns of the transcription factors, specifically OCT-4 and SOX-2, in patients with AML and MDS. The study involved 84 newly diagnosed AML and MDS patients and 16 age, and sex-matched healthy controls. DNA was extracted from blood or bone marrow using a QIAGEN RDNA extraction kit. The SOX-2 and OCT-4 genes were studied using PCR-specific primers for methylated and unmethylated targets. SOX-2 gene methylation was observed in a significantly higher proportion of AML (n=48/77) and MDS (n=4/7) as compared to Controls (n=3/16) (p<0.001). OCT-4 methylation was also observed in a significantly higher proportion of AML (n=44/77) as compared to MDS (n=3/7) and Controls (n=1/16) (p<0.001). Only a few cases in the AML group had both SOX-2 and OCT-4 gene methylation (n=25/77), compared with MDS (n=0/7) and Controls (n=0/16) (p<0.007). This study indicates that SOX-2 and OCT-4 gene methylation is significantly more prevalent in AML and MDS patients than healthy controls, suggesting their potential involvement in leukemogenesis. These findings highlight the potential role of methylation of stemness-associated transcription factors as a biomarker for disease characterization and identification of epigenetic therapeutic targets in AML and MDS.

CD36 functions as both a lipid transporter and scavenger receptor, integrating metabolic and inflammatory signaling pathways. It plays a critical role in maintaining cellular homeostasis and influencing disease progression. This review summarizes the structure, ligands, functions, regulation, and clinical implications of CD36 in renal and bladder cancer. Increased CD36 expression promotes enhanced fatty acid uptake, which supports tumor cell proliferation, migration and survival, by mediating metabolic reprogramming and interacting with the tumor microenvironment. In renal cancer, most frequently clear cell renal carcinoma (ccRCC), which has a typical metabolic phenotype, CD36 is involved in lipid accumulation and oxidative stress pathways. Pathogenic mechanisms include hypoxia-inducible factor (HIF)-driven pathways and carnitine palmitoyl transferase 1A (CPT1A) via the PPAR&#x3b1;/CD36 axis, which phosphorylate Akt. By using fatty acid oxidation, CD36 lead to the production of reactive oxygen species and to transcription of genes mediating a pro-tumor function, inducing tumor-associated macrophages (TAM). In bladder cancer, CD36 is implicated in tumoral cells proliferation, survival, and adaptation to metabolic stress, epithelial-mesenchymal transition (EMT) and influences the tumor microenvironment, through interactions with tumor-associated macrophages and inflammatory signaling pathways. Although multiple studies propose CD36 as a prognostic biomarker, inconsistencies across cohorts limit its clinical translation. Notably, advances have revealed the regulatory networks governing distinct physiological properties of CD36, thereby identifying targeting CD36 as a potential strategy for cancer treatment. Inhibition of CD36-mediated lipid metabolism and signaling pathways may reduce tumor growth and metastatic potential. However, further research is necessary to clarify its context-dependent functions and to develop effective CD36-targeted therapies. To our knowledge, this is the first review to systematically examine the role of CD36 across both renal and bladder cancer. It could be the first step toward identifying new mechanisms mediated by CD36 in these malignancies.

Diuretic resistance is a major therapeutic challenge in acute decompensated heart failure (ADHF). Acetazolamide, a carbonic anhydrase inhibitor, has emerged as a potential adjunct to conventional loop diuretics, as demonstrated in the ADVOR trial. We present a 74-year-old woman with acute coronary syndrome complicated by cardiogenic shock and refractory pulmonary edema despite inotropic support and guideline-directed therapy. The patient received intravenous acetazolamide 500 mg daily for three days, resulting in marked diuresis and radiographic resolution of pulmonary edema within 72 hours. The patient improved clinically. This case supports the potential utility of acetazolamide as an adjunctive strategy for overcoming diuretic resistance in ADHF.

Preliminary data for the Cellular Therapy for In Utero Repair of Myelomeningocele (CuRe) Trial have recently been published. These data showcase innovation in fetal surgery but introduce ethical questions regarding tissue sourcing. The CuRe Trial utilizes early gestational placental mesenchymal stromal/stem cells (PMSCs) in the repair technique. The ethical implications of this approach vary depending on whether they are sourced from miscarriage or elective abortion. The specific source of the PMSCs is unclear, but evidence suggesting that they might be sourced from elective abortion is presented, along with an overview of ethical implications if this is the case. Key questions considered include 1) whether research such as this is impacted by the recent decision by the National Institutes of Health (NIH) to cease funding of research using fetal tissue from elective abortion; 2) what ethical alternatives currently or may plausibly exist; and 3) whether scientific justifications exist for the use of tissue sourced from elective abortion over more ethical alternatives.

Ischemic heart disease (IHD) remains the leading cause of cardiovascular mortality worldwide. Although age standardized death rates have declined over the past two decades, the absolute number of deaths continues to rise due to population growth and demographic aging. This Perspective examines the resulting paradox of progress, in which improving mortality rates coexist with an expanding global burden. Emerging evidence from recent global analyses highlights widening disparities across regions, sexes, and age groups. Global Burden of Disease (GBD) studies suggest an increasing burden of early onset IHD among adults aged 15 to 49 years, associated with rising incidence and prevalence, with notable regional variability and links to metabolic and dietary risks. While high income settings continue to achieve sustained mortality reductions, low- and middle-income regions face persistent gaps in prevention and care. These disparities reflect differences in health system capacity, including limited screening, delayed access to acute cardiac care, and suboptimal use of secondary prevention. Scalable strategies such as task-sharing and simplified treatment approaches offer practical solutions but remain underused. A strategic shift toward implementation, life-course prevention, and equity-focused policy reform is essential. Importantly, this perspective bridges the gap between epidemiological trends and health policy, linking epidemiologic trends to scalable implementation strategies for clinicians and policymakers to address the global burden of IHD.

Recent progress in translational neuroscience has significantly advanced our understanding of neurological diseases. Research progress closely went in line with innovations in research methods, which have expanded our insights considerably beyond previous limits. However, despite the development of disease-modifying treatments, therapeutic options in brain diseases still lag behind fundamental discoveries in basic neuroscience. This perspective examines the factors that hinder clinical progress in translational neuroscience and provides solutions on how to overcome them. Editorial board members of Exploration of Neuroscience were interrogated about the most prominent challenges they see in translational neuroscience and about possible ways to overcome these issues. Key challenges were seen at the interface between experimental research and clinical studies by several members, both from the basic and applied neuroscience fields, which include the selection of appropriate study readouts and endpoints. The establishment of refined study endpoints, combined with biomarkers capable of predicting treatment responses in human patients, will be crucial for the successful clinical implementation of new therapies. Further obstacles were found in the standardization of experimental models, interventions, and assessments both in animals and humans, as well as in the development of personalized treatment strategies. These challenges can be addressed through more clearly defined experimental procedures that closely match clinical conditions and precision-based approaches that ensure efficient therapeutic responses. As a great opportunity, treatment options targeting pathophysiological processes in multiple brain diseases and disease processes in different organ systems were noted. Significant barriers remain in the funding of investigator-driven clinical trials through public research programs, as well as the education of translational and clinician scientists dedicated to clinical translation. Enhanced communication between experimental neuroscientists and clinicians, with a shared understanding and common language, will be essential for the success of future research endeavors.

Ischemic stroke (IS) remains a leading cause of disability and mortality in aging populations. Recovery trajectories are shaped not only by the acute vascular insult but also by pre-existing comorbidities, genetic predisposition, and age-dependent molecular remodeling. Common vascular risk factors, such as diabetes mellitus, atrial fibrillation, hypertension, and dyslipidemia, sustain systemic and cerebral inflammation, promote endothelial dysfunction, disrupt blood-brain barrier integrity, and impair neuroplasticity, collectively limiting neurovascular repair and recovery potential. Recent advances in genomic, epigenomic, and transcriptomic profiling have identified dynamic molecular networks that regulate neuronal survival, angiogenesis, and synaptic plasticity after stroke. However, most discoveries remain correlative. Establishing causality will require perturbation-based approaches, including genome and epigenome editing, patient-derived stem cell and organoid models, and longitudinal multi-omics analyses across diverse ancestries and comorbidity profiles. Such integration will clarify how metabolic and inflammatory states imprint the epigenetic and transcriptional landscape of the aging brain. Emerging evidence implicates DNA methylation, histone modifications, and noncoding RNAs, including circular RNAs, as pivotal regulators of ischemic resilience and neurovascular recovery. Translational studies combining genomic insights with epigenetic pharmacology have demonstrated proof-of-concept efficacy for genotype-guided therapies, RNA-based interventions, and histone deacetylase inhibition. Collectively, these strategies support a systems-level framework that unites vascular biology, multi-omics, and neurorestoration. Within this paradigm, aging is reframed not as a static risk factor but as a modifiable molecular trait, guiding the timing and intensity of interventions to enhance neurorepair, restore vascular integrity, and preserve cognitive resilience.

While traditional peer review offers advantages in academic publishing, it is often hampered by significant weaknesses, leading to frustration among many authors. Scientific discoveries after publication depend on thorough discussions and critiques, making post-publication peer review (PPPR) an essential tool for identifying errors and encouraging authors to make necessary corrections. PPPR is defined as a critical, ongoing, and public review conducted by the broader scientific community once research findings are formally published. Its goal is to enable more academic experts to continuously examine, question, and validate the work, identifying potential flaws or strengths that might have been missed during the initial review. This ongoing dialogue promotes transparency and motivates authors to make necessary corrections. Although the goal of PPPR is to enhance scientific integrity, the open nature of PPPR platforms makes them vulnerable to misuse. It can also be exploited to undermine colleagues, suppress differing viewpoints, or further personal or organizational interests. We also observe an increase in "hyper-skepticism," which differs from constructive criticism, reflecting an overly critical mindset that focuses on doubt rather than fostering understanding. To fully realize the benefits of PPPR and prevent misuse, the scientific community must build a more equitable and more responsible framework. Addressing these challenges requires a thoughtful strategy that integrates technological advancements, strengthens editorial policies, enhances transparency measures, and provides robust protections for good-faith scientific debate.

Ischemic stroke, the second leading cause of death worldwide and the leading cause of long-term disabilities, presents a significant global health challenge, particularly in aging populations where the risk and severity of cerebrovascular events are significantly increased. The aftermath of stroke involves neuronal loss in the infarct core and reactive astrocyte proliferation, disrupting the neurovascular unit, especially in aged brains. Restoring the balance between neurons and non-neuronal cells within the perilesional area is crucial for post-stroke recovery. The aged post-stroke brain mounts a fulminant proliferative astroglial response, leading to gliotic scarring that prevents neural regeneration. While countless therapeutic techniques have been attempted for decades with limited success, alternative strategies aim to transform inhibitory gliotic tissue into an environment conducive to neuronal regeneration and axonal growth through genetic conversion of astrocytes into neurons. This concept gained momentum following discoveries that in vivo direct lineage reprogramming in the adult mammalian brain is a feasible strategy for reprogramming non-neuronal cells into neurons, circumventing the need for cell transplantation. Recent advancements in glial cell reprogramming, including transcription factor-based methods with factors like NeuroD1, Ascl1, and Neurogenin2, as well as small molecule-induced reprogramming and chemical induction, show promise in converting glial cells into functional neurons. These approaches leverage the brain's intrinsic plasticity for neuronal replacement and circuit restoration. However, applying these genetic conversion therapies in the aged, post-stroke brain faces significant challenges, such as the hostile inflammatory environment and compromised regenerative capacity. There is a critical need for safe and efficient delivery methods, including viral and non-viral vectors, to ensure targeted and sustained expression of reprogramming factors. Moreover, addressing the translational gap between preclinical successes and clinical applications is essential, emphasizing the necessity for robust stroke models that replicate human pathophysiology. Ethical considerations and biosafety concerns are critically evaluated, particularly regarding the long-term effects and potential risks of genetic reprogramming. By integrating recent research findings, this comprehensive review provides an in-depth understanding of the current landscape and future prospects of genetic conversion therapy for ischemic stroke rehabilitation, highlighting the potential to enhance personalized stroke management and regenerative strategies through innovative approaches.

Human metapneumovirus is a respiratory pathogen that infects children, the elderly, and immunocompromised individuals. Despite its global prevalence, underdiagnosis persists because of clinical overlap with other respiratory viruses. The current approach is mostly supportive, with oxygen therapy and hydration being crucial interventions. Ribavirin contains antiviral properties but has little clinical application. Vaccine development is moving forward, with prospects including live-attenuated, subunit-based, and virus-like particle vaccines. Molecular diagnostics, such as RT-PCR and metagenomic sequencing, have increased detection rates, which aids epidemiological monitoring. Monoclonal antibodies targeting the fusion (F) protein are being studied for passive immunity, while immunomodulatory treatments such as corticosteroids and intravenous immunoglobulins may help treat severe cases. Emerging treatments include fusion inhibitors and pan-pneumovirus vaccinations that protect against HMPV and RSV. Future research should concentrate on optimizing antiviral methods, increasing vaccination trials, and improving surveillance to detect outbreaks. A multidisciplinary approach that combines virology, immunology, and epidemiology is required to reduce HMPV's effect and improve patient outcomes. This review serves as a comprehensive literature about HMPV which provides all the crucial clinical perspectives and the latest advancements in management, antivirals, patient prognosis as well and diagnostic modalities.

Cancer remains a leading cause of global mortality, with annual incidence projected to exceed 35 million cases by 2050. Modern antineoplastic therapies have improved survival outcomes at the risk of increasingly associated cardiovascular complications, collectively termed cancer therapy related cardiac dysfunction (CTRCD). Anthracyclines and HER2-targeted therapies remain the most well-characterized cardiotoxic agents. Anthracyclines cause irreversible, dose-dependent myocardial injury through mechanisms including oxidative stress, iron dysregulation, mitochondrial dysfunction, and topoisomerase II&#x3b2; inhibition, leading to progressive ventricular dysfunction and heart failure. HER2-directed therapies, such as trastuzumab, interfere with cardioprotective ErbB signaling, typically producing reversible cardiac impairment. Other oncologic treatments - including tyrosine kinase inhibitors, VEGF antagonists, and immune checkpoint inhibitors - contribute to hypertension, ischemic injury, and immune-mediated myocarditis. Newer modalities, such as proteasome inhibitors, histone deacetylase inhibitors, and CAR T-cell therapy, have expanded the spectrum of treatment-associated cardiotoxicity. Early CTRCD detection through multimodal strategies - including echocardiographic assessment with global longitudinal strain, cardiac magnetic resonance imaging, and serial measurement of troponins and natriuretic peptides - facilitates timely intervention. Risk stratification tools such as the HFA-ICOS score enable personalized monitoring and therapeutic planning. Preventive and management strategies incorporate cardioprotective agents like ACE inhibitors, &#x3b2;-blockers, dexrazoxane, and emerging therapies such as SGLT2 inhibitors. Modern cardio-oncology emphasizes a multidisciplinary, precision-based approach integrating early detection, genetic risk assessment, and targeted prophylaxis to preserve cardiac function while maintaining oncologic efficacy, thereby enhancing both survival and quality of life for cancer patients.

Doxorubicin (DOX), an anthracycline antibiotic, is pivotal in managing osteosarcoma (OS). Although a cornerstone in the multimodal treatment regimen, its usage is limited by its associated toxicities, such as cardiotoxicity, myelosuppression, and neurotoxicity. This review provides an in-depth discussion of the emerging research aimed at enhancing the overall efficacy and mitigating the undesired side effects of DOX in treating OS. We explore the various drug delivery systems, including polymer-based injectable hydrogels, hydroxyapatite-based systems, and various nanoparticle-based systems such as calcium carbonate nanocrystals and cerium-substituted hydroxyapatite. We also discuss various innovative combination therapies, such as pegylated liposomal DOX with cisplatin and DOX with platinum nanoparticles. Moreover, emerging research into light-sensitive nano-micelles have been highlighted. These methods improve DOX's cytotoxicity and potentially reduce the need for high systemic doses and their associated side effects. The review aims to highlight the promising future in OS treatment by integrating these methodologies to maximize the therapeutic action of DOX and reduce its systemic side effects.

Acute scrotum in neonates is a rare condition with multiple causes, including incarcerated hernia, testicular torsion, birth trauma, gross hydrocele, and neonatal adrenal haemorrhage, the least common aetiology. Early diagnosis and intervention are essential to prevent testicular ischemia. Due to the continuity between the retroperitoneum and the scrotum via the processus vaginalis and inguinal canal, blood from an adrenal haemorrhage may track down into the scrotum, leading to swelling and discoloration.&#xa0; We report a case of a 1-day-old male neonate born via emergency caesarean section at 37 weeks due to foetal distress. The baby initially admitted to the NICU for transient tachypnoea, developed a right hemi-scrotal swelling with bluish discoloration on the second day of life. Scrotal ultrasound suggested testicular torsion, but Doppler imaging showed absent blood flow. Further abdominal ultrasound confirmed a right adrenal haemorrhage. The neonate was managed conservatively with intravenous fluids, antibiotics, oxygen support, and coagulation management. Serial ultrasounds showed gradual resolution, and he was discharged on the 17th postnatal day. Follow-up at 1 and 3 months showed complete recovery with normal growth.&#xa0; Neonatal adrenal haemorrhage should be considered in cases of acute scrotum, especially in neonates with birth asphyxia. Abdominal ultrasound can aid in diagnosis, preventing diagnostic delays, unnecessary surgery, and anaesthesia exposure. This case highlights the importance of thorough imaging and awareness of rare differential diagnoses, contributing to improved clinical practice and better neonatal outcomes.

Ganaxolone, a neuroactive steroid that increases GABAergic inhibition, has been tested in many trials for the resolution of different epileptic disorders. Based on these, our study implemented a systematic review to evaluate the general benefit of ganaxolone for seizures. Pubmed, google scholar, European PubMed Central, Cochrane Library, and U.S. National Library of Medicine Clinical Trials were searched for relevant randomized controlled trials (RCTs) up to March 2023 and 12 RCTs were included in this review. We included 1337 patients from 12 RCTs to evaluate the efficacy and safety of ganaxolone. As results showed, across all trials, 26.3% of participants reported >50% reduction from baseline in seizure frequency. The analysis revealed that the nervous system was the most impacted, with dizziness, somnolence, headache, and seizures being the most frequently reported treatment-related adverse events (TRAEs). The results of these trials suggest that ganaxolone may be effective in reducing seizure frequency in patients with various types of epilepsy, including CDKL5 deficiency disorder, Lennox-Gastaut syndrome, and Protocadherin 19. However, further studies are needed to determine its safety and efficacy in a larger patient population.

Clear cell adenocarcinoma of the cervix is a rare neoplasm that accounts for about 4-9% of all uterine cervical adenocarcinoma. It was first reported in young women with in-utero exposure of diethylstilbesterol (DES). However, many cases have been reported post-ban of DES that are not associated with diethylstilbesterol (DES). Here, we are reporting a case of clear cell adenocarcinoma in an 18-year-old woman without any exposure history of DES. An exophytic mass arising from the anterior lip was found in MRI. Biopsy from the mass was diagnosed as Clear cell adenocarcinoma of the cervix based on histopathological and immunohistochemical findings. The patient then underwent a total hysterectomy and bilateral salpingo-oophorectomy. One each of the right pelvic lymph nodes and external iliac lymph nodes showed metastatic deposits. The patient was staged as FIGO stage I [AJCC TNM staging (8th Edition): pT2b pN1]. Post 6 months follow up there is no evidence of any recurrence.