Masquerade syndrome is a collective term for various ocular diseases presenting with clinical features resembling intraocular inflammation. Delays in definitive diagnosis and treatment can not only lead to irreversible vision loss but also impact the patient's prognosis regarding survival. We report the case of a 26-year-old male patient who presented with impaired vision in the right eye, which had persisted for six months; neuroretinitis was diagnosed. Although infectious neuroretinitis was suspected, tests for pathogens such as Mycobacterium tuberculosis, Toxoplasma, Toxocara, and Bartonella were all negative. Treatment with betamethasone eye drops alone resulted in a fluctuating course of improvement and worsening of the neuroretinitis. Ten months after the initial visit, the patient's headache-which had begun one month prior-worsened and was accompanied by vomiting and a pulsating sensation, leading to a consultation with our department of neurosurgery. Magnetic resonance imaging (MRI) revealed a lobulated mass extending from the right midbrain to the right thalamus, causing narrowing of the cerebral aqueduct and hydrocephalus. Four days after the neurosurgical consultation, the patient underwent endoscopic third ventriculostomy (ETV) and a brain biopsy, leading to a definitive diagnosis of germinoma. The headache improved the day after surgery, and by one month after the operation, the hydrocephalus had resolved, while neuroretinitis also showed improvement. The patient received carboplatin and etoposide (CARE) treatment in the second, third, and fourth months post-surgery, whole-ventricle radiotherapy (24 Gy/15 fractions) in the fifth and sixth months, and ifosfamide (IFO), cisplatin (CDDP), and etoposide (VP-16) (ICE) treatment in the seventh, ninth, and 11th months. No recurrence of the brain tumor has been observed since then. At the final follow-up visit five years post-surgery, the neuroretinitis had resolved. When neuroretinitis is observed in a young patient and infectious causes have been ruled out, intracranial germinoma should be considered in the differential diagnosis.

Primary pericardial SMARCB1-deficient tumors with rhabdoid morphology are exceptionally rare. We present an adult case of a primary SMARCB1-deficient pericardial tumor showing concurrent loss of INI1 (SMARCB1) and BRG1 (SMARCA4) expression, representing the third documented tumor with co-loss of these SWI/SNF subunits across tumor sites. Targeted RNA sequencing detected no pathogenic sequence variants or fusion transcripts and showed reduced SMARCB1 and SMARCA4 transcript abundance. DNA-based whole-exome sequencing (WES) identified no pathogenic or likely pathogenic sequence variants in either gene. High-resolution SNP microarray demonstrated a homozygous SMARCB1 deletion with intact SMARCA4, establishing biallelic SMARCB1 inactivation; BRG1 loss was accompanied by marked SMARCA4 transcript downregulation in the absence of a detectable SMARCA4 genomic alteration. In the clinicopathological context, the overall findings supported classification as a SMARCB1-deficient pericardial tumor with rhabdoid morphology. Following resection, postoperative imaging suggested residual or recurrent disease. Combined doxorubicin-ifosfamide chemotherapy and radical radiotherapy achieved a complete radiologic response. However, imaging 18 months after resection suggested multifocal pericardial recurrence, with disease control regained following similar treatment. This course is hypothesis-generating and may suggest sensitivity to DNA-damaging therapy in the setting of dual SWI/SNF deficiency.

Primary synovial sarcoma of the prostate is exceptionally rare. Its nonspecific presentation and often normal or low prostate-specific antigen (PSA) levels may delay diagnosis. A 49-year-old man presented with lower urinary tract symptoms and gross hematuria. Digital rectal examination revealed a markedly enlarged, firm, irregular prostate. The serum PSA level was 0.34 ng/mL. Pelvic magnetic resonance imaging showed a 9.4 × 7.4 × 6.5 cm heterogeneous prostatic mass with loss of the rectoprostatic fat plane, without definitive evidence of metastatic disease on staging. Transrectal ultrasound-guided biopsy demonstrated a monophasic spindle-cell neoplasm with immunohistochemical findings consistent with synovial sarcoma. Robot-assisted radical prostatectomy was converted to an open approach to facilitate resection. Tumor was identified in tissue from the rectoprostatic margin, while the overall margin status was indeterminate because of tumor fragmentation, raising concern for microscopic residual disease. The patient received adjuvant pelvic radiotherapy followed by doxorubicin and ifosfamide chemotherapy. At 20 months, he remained alive without radiologic evidence of recurrence or metastasis. Primary prostatic synovial sarcoma should be considered in younger to middle-aged patients with obstructive urinary symptoms, a large prostatic mass, and a normal or low PSA level. Diagnosis relies on histopathologic assessment, supported by immunohistochemistry and molecular testing whenever available. Management should be individualized through multidisciplinary discussion.

Ewing's sarcoma is an aggressive small round cell tumour that usually arises from bone or soft tissues in children and young adults. Primary origin within the prostate is exceptionally rare, with only isolated cases documented. We describe a man in his 20s who presented with urinary obstruction, constipation and leg pain. Imaging revealed a bulky pelvic mass arising from the prostate and bilateral hydroureteronephrosis. Histology demonstrated a round cell neoplasm with strong CD99 and FLI1 positivity, confirming Ewing's sarcoma. Staging PET-CT identified widespread metastases involving lung, liver and bone. The patient underwent urinary and bowel diversion, followed by Vincristine, Adriamycin, Cyclophosphamide alternating with Ifosfamide and Etoposide (VAC/IE) chemotherapy. He achieved complete metabolic remission, allowing colostomy reversal and is currently under surveillance. This case illustrates the need to consider rare sarcomas in the differential diagnosis of pelvic masses in young men with normal serum PSA and highlights the potential for durable response with timely systemic therapy.

Ifosfamide (IFO) is an effective chemotherapeutic agent, but its clinical use is limited by dose-dependent nephrotoxicity. This study investigated the protective effects of 18β-glycyrrhetinic acid (18β-GA) against IFO-induced acute renal injury and explored the underlying molecular mechanisms. Twenty-eight male Wistar albino rats were divided into four groups: Control, 18β-GA, IFO, and IFO+18β-GA. 18β-GA was administered orally at 100 mg/kg/day for two consecutive days, while nephrotoxicity was induced by a single intraperitoneal injection of IFO at 500 mg/kg. Renal function markers, oxidative stress parameters, inflammatory and apoptotic gene expression, Wnt3a/IL-17 A/ACT1/TRAF6 and Notch/HES1 signaling pathways, histopathological alterations, ZO-1 integrity, and CHOP expression were evaluated. IFO markedly impaired renal function, increased serum urea and creatinine levels, enhanced lipid peroxidation, depleted antioxidant defenses, and induced severe histopathological damage. IFO also upregulated NF-κB, TNF-α, Bax, Caspase-3, Wnt3a, IL-17 A, ACT1, TRAF6, Notch, and HES1 expression, while reducing Bcl-2 expression. In addition, IFO increased CHOP immunoreactivity and disrupted ZO-1 expression in tubular epithelial cells. Co-treatment with 18β-GA significantly improved renal function, restored antioxidant capacity, and was associated with the suppression of inflammatory and apoptotic signaling, downregulation of Wnt3a/IL-17 A/ACT1/TRAF6 and Notch/HES1 activation, reduced CHOP expression, preserved ZO-1 immunoreactivity, and ameliorated renal histological injury. These findings suggest that 18β-GA exerts potential multi-target renoprotective effects against IFO-induced nephrotoxicity by modulating oxidative stress, inflammation, ER stress, apoptosis, developmental signaling, and epithelial junctional integrity.

Adolescent retroperitoneal sarcoma (RPS) poses significant decision-making challenges due to complex subtypes and limited molecular diagnosis. A 16-year-old male with a 13.8 cm retroperitoneal mass underwent R0 en bloc resection (with left adrenal gland). Pathology favored high-grade fibrosarcoma. He completed 5 cycles of adjuvant Ifosfamide and Doxorubicin. At 17 months post-surgery, surveillance shows no disease recurrence. When molecular testing is unavailable for large, high-grade adolescent RPS, combining R0 en bloc resection with intensive adjuvant chemotherapy remains an effective strategy for favorable outcomes.

Morin (3,5,7,2',4'-pentahydroxyflavone) is a dietary flavonol with broad neuroprotective, anti-inflammatory, and antioxidant actions across central and peripheral nervous system models. This synthesis consolidates evidence from in vitro and rodent studies-covering neurodegenerative proteinopathies (Alzheimer's, Parkinson's, and Huntington's), neuropathic pain, epilepsy, stress- and schizophrenia-like phenotypes, and chemo-/toxicant-induced neurotoxicity-to evaluate morin's consistent benefits on survival, motor/cognitive performance, and biochemical normalization. Morin mitigated neurotoxicity induced by doxorubicin, ifosfamide, vincristine, acrylamide, heavy metals, and endocrine disruptors. Context-specific effects included modulation of disease-defining pathways (GSK3β/CDK5, mTORC1, PARP, and AMPK-ULK1-TFEB), microglial polarization, and normalization of neurotransmission (dopamine, GABA, 5-HT, and reduced AChE). Core mechanisms included the following: restoration of redox and mitochondrial homeostasis via Nrf2/HO-1 activation; replenishment of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), and glutathione (GSH); decreased reactive oxygen species (ROS), malondialdehyde (MDA), and nitric oxide (NO); and preserved mitochondrial potential/fusion; suppression of innate immune and inflammasome signaling through downregulation of TLR4/NF-κB and ERK-p65, reduced TNF-α, IL-1β/IL-6, iNOS/COX-2; inhibition of NLRP3/caspase-1; and rebalancing of cell-death programs (↓Bax/caspase-3, ↑Bcl-2; attenuation of RIPK1/RIPK3/MLKL-mediated necroptosis). Formulation strategies (intranasal microemulsions, pluronic micelles, and more soluble derivatives) have enhanced brain exposure and efficacy, but translation now warrants optimized delivery, pharmacokinetic-pharmacodynamic mapping, target engagement biomarkers, and rigorously controlled trials to define dose, route, and indications as adjunctive to standard care in neurodegeneration, neuropathic pain, and toxicant-related brain injury. Collectively, morin emerges as a multitarget neuroprotective scaffold with reproducible functional and mechanistic benefits.

Uterine adenosarcoma is a rare biphasic malignancy composed of benign epithelial and malignant stromal components. Adenosarcoma with sarcomatous overgrowth is an aggressive subtype associated with rapid progression and a poor prognosis. We report a case of uterine adenosarcoma with sarcomatous overgrowth diagnosed through the histopathological evaluation of a hysteroscopic polypectomy specimen. A 47-year-old woman presented to a local physician with abnormal uterine bleeding. Pelvic magnetic resonance imaging revealed a 5.5-cm polypoid lesion arising from the uterine corpus and protruding into the endometrial cavity, along with an intramyometrial mass. Hysteroscopic polypectomy was performed, and histopathological examination revealed uterine adenosarcoma, prompting referral to our institution. Positron emission tomography/computed tomography demonstrated fluorodeoxyglucose uptake in both the endometrial lesion and intramyometrial mass, without evidence of distant metastasis. The patient underwent total abdominal hysterectomy with bilateral salpingo-oophorectomy. Histopathological examination of the resected uterus showed mildly atypical glandular epithelium surrounded by densely cellular, high-grade malignant stromal cells, together with extensive high-grade sarcomatous overgrowth involving the myometrium. Immunohistochemical staining demonstrated strong CD10 positivity and focal weak h-caldesmon positivity. The final diagnosis was uterine adenosarcoma with sarcomatous overgrowth, International Federation of Gynecology and Obstetrics stage IC. The patient received three cycles of adjuvant doxorubicin plus ifosfamide chemotherapy and remained free of recurrence 18 months after surgery. This case highlights the diagnostic value of hysteroscopic polypectomy in patients with intracavitary uterine lesions and underscores the importance of careful histopathological evaluation for the early recognition of sarcomatous overgrowth.