AIM:Abemaciclib, a cyclin-dependent kinase 4/6 inhibitor, is a standard treatment for hormone receptor-positive and HER2-negative breast cancer. However, liver dysfunction induced by abemaciclib is a significant clinical issue. METHODS:We report three cases of drug induced liver injury caused by abemaciclib with characteristic liver atrophy. Case 1: A woman in her seventies developed acute liver failure 2 months after initiation of letrozole and abemaciclib for breast cancer and bone metastases. A contrast-enhanced CT (CECT) scan revealed liver atrophy accompanied by Chilaiditi syndrome. Despite steroid pulse therapy, she progressed to coma. Her liver failure improved, but she died due to worsening of the underlying disease. Case 2: A woman in her seventies developed liver dysfunction 2 months after initiation of anastrozole and abemaciclib to prevent recurrence. A CECT scan revealed liver atrophy and Chilaiditi syndrome. After admission, she progressed to acute liver failure and coma, and steroid pulse therapy was initiated. Hepatic encephalopathy improved with conservative treatment, and liver failure resolved with continued steroid administration. Case 3: A woman in her fifties. After breast cancer surgery, tamoxifen and abemaciclib were started as adjuvant therapy. Blood tests revealed liver dysfunction 2 months later. A CECT scan revealed liver atrophy and Chilaiditi syndrome, which improved with liver support therapy alone without progressing to liver failure. RESULTS AND CONCLUSION:This report is the first highlighting the imaging characteristics of rapid-onset hepatic atrophy associated with abemaciclib-induced liver injury. These findings may provide useful insights for distinguishing abemaciclib-induced liver injury from other etiologies.

Primary urothelial carcinoma of the prostate is a rare malignancy that is often under-recognized because of its nonspecific clinical presentation and imaging features. Herein, we report a case of a 76-year-old man who was incidentally found to have multiple pulmonary and hepatic nodules and pelvic lymphadenopathy during preoperative imaging for valvuloplasty. These findings raised suspicion of metastatic disease. The primary origin was initially suspected to be bladder or rectal cancer. Gastrointestinal evaluations were unremarkable. Cystoscopy revealed multiple bladder tumors but no abnormalities in the prostatic urethra. Prostate-specific antigen (PSA) levels were within the normal range. Magnetic resonance imaging showed no distinct prostatic mass; however, diffusion-weighted imaging revealed diffuse diffusion restriction in the prostate, suggestive of malignancy. The patient underwent simultaneous transurethral resection of the bladder tumor and transperineal prostate biopsy. Both specimens revealed high-grade urothelial carcinoma. Immunohistochemical staining was positive for cytokeratin (CK) 7, CK20, and GATA3, and negative for PSA, consistent with urothelial origin. The tumor showed more extensive and aggressive involvement in the prostate than in the bladder, suggesting that the prostate was the primary site. This case highlights the importance of careful prostate evaluation when assessing urothelial carcinoma, particularly in cases with normal PSA levels and without bladder wall invasion. As the prostate is a potential primary site of urothelial carcinoma, clinical awareness of this rare malignancy is necessary.

Primary adenoid cystic carcinoma (ACC) of the thymus is extremely rare. Although thymic ACC is generally slow growing, complete surgical resection is essential due to its tendency for local invasion. Here, we report a case of primary thymic ACC successfully treated by complete resection using a single-port subxiphoid thoracoscopic approach. A 63-year-old asymptomatic male patient was referred after an anterior mediastinal mass was incidentally detected during a routine health screening. Imaging revealed a small, well-circumscribed tumor without evidence of invasion. At 2.2 cm, the lesion was among the smallest thymic ACCs reported to date. Thymoma was suspected and single-port subxiphoid thoracoscopic thymectomy was performed. The patient’s postoperative course was uneventful. The histopathological and immunohistochemical findings were consistent with ACC, and no other primary lesion was identified. Complete resection was achieved with minimally invasive thymectomy. This case illustrates that thymic ACC may rarely present as a small, early-stage tumor indistinguishable from thymoma, and it highlights the importance of complete resection with negative margins and long-term surveillance given the potential for delayed recurrence.

This case concerns a 39-year-old male with a history of adjustment disorder, and he had been using Ashwagandha-self-prescribed and self-imported online-for stress relief and vitality enhancement for the past 3 months. He visited the emergency department with symptoms of hyperventilation, and blood tests showed total bilirubin of 2.37mg/dL, ALT of 384U/L, and ALP of 92U/L, indicating hepatocellular-type liver dysfunction, thereby raising suspicion for drug-induced liver injury (DILI). Although ursodeoxycholic acid was initiated after referring to our hospital, his condition showed minimal improvement. A liver biopsy showed no infiltration of inflammatory cells, no dilation of the bile ducts, and no bile plugs, ruling out bile outflow obstruction. However, bilirubin deposition within hepatocytes and hepatocellular degeneration were noted. With a suspected defect in the hepatocellular bile transport, phenobarbital was started, resulting in rapid improvement of jaundice. Reports of DILI caused by Ashwagandha are rare, and this case exhibited clinical findings and test results different from those previously reported.

Obstructive uropathy (OU) during fetal development induces a fetal cystic dysplastic kidney. The mechanisms of cyst formation and the onset of renal dysfunction remain unclear. Determining whether nephrogenic potential persists during fetal life may suggest whether early intervention could preserve renal development. We aimed to evaluate residual nephrogenic activity in fetal cystic dysplastic kidneys using β-catenin and CD10 immunostaining, and to assess whether the site of obstruction influences cystogenesis. After appropriate approval, 20 timed-gestation fetal lambs had OU created at 60 days. Males underwent urethral and urachal ligation (n = 8, 3 lost), and females underwent unilateral ureteric ligation (n = 8, 1 lost). Fetuses were sacrificed at 80 days (n = 6) and 140 days (term, n = 10), comparing kidneys with normal controls of the same gestational age using immunohistochemical staining for β-catenin and CD10. Developing fetal cystic dysplastic kidneys were identified at 80 days. β-catenin staining showed the absence of granular cytoplasmic expression in cystic regions, indicating arrested nephrogenesis. In male models, cysts originated exclusively from proximal tubules. Female models exhibited mixed proximal and distal tubular involvement. CD10 staining confirmed the loss of proximal tubular markers. Renal development remained arrested at term. Cyst formation disrupts renal development early in gestation, which persists until term. Differences in cystogenesis between the models suggest that the site of obstruction influences pathogenic mechanisms.

Anti-glomerular basement membrane (anti-GBM) disease typically presents as rapidly progressive glomerulonephritis, however an atypical anti-GBM nephritis with various light microscopic findings without crescentic formation has been reported in recent years. The findings reported including cases with membranoproliferative glomerulonephritis (MPGN) pattern. Few reports have been able to follow the course of the disease over a long period of time. We report a case of MPGN associated with the spectrum of atypical anti-GBM nephritis that showed a slowly progressive course over more than eight years. A 49-year-old man underwent kidney biopsy because of hypertension, proteinuria, and mild renal insufficiency. The findings on kidney biopsy showed the findings of MPGN. Immunofluorescence microscopy revealed bright linear staining of IgG on the GBM. Electron microscopy showed subepithelial, intra-basement membrane, subendothelial, and paramesangial electron-dense deposits. Serum anti-GBM antibodies were negative. Proteinuria had been present for 4 years prior to the renal biopsy, however no worsening of renal function was observed. Because of worsening proteinuria and the presence of endocapillary hypercellularity in the tissues, the intravenous and oral steroids were started. Although the proteinuria showed slight improvement, the serum creatinine level was stable around 1.5–1.7 mg/dl. Although some indolent cases of atypical anti-GBM syndrome were reported previously, compared with these cases, our patient had more stable renal function for a long time. This is a rare case of resembling atypical anti–GBM disease that shows MPGN with linear IgG staining having a long-term indolent course and without secondary etiology.

Lymph node metastasis correlates with breast cancer prognosis; however, the cellular mechanisms underlying the earliest metastatic events remain unclear. In spatial transcriptomic analysis of a patient with breast cancer at single-cell resolution, we identified 30 tumor cells representing the initial metastatic seeding in a lymph node. These cells originated from multiple epithelial–mesenchymal (EM) transition status and included six distinct subpopulations with biological significance. Only cells exhibiting a metabolic shift toward fatty acid metabolism successfully established lymph node colonies, implicating this shift in metastatic fitness. The tumor microenvironment surrounding these cells showed immunosuppressive and tumor-promoting features, supporting metastasis establishment. Cross-referencing these expression profiles with public datasets revealed that poor prognosis correlated not with fully mesenchymal or metastatic populations, but with hybrid EM cells exhibiting epithelial and mesenchymal traits. These findings highlight the metabolic and phenotypic plasticity of metastatic cells and serve as translational bridges between the spatial evolution of tumor cells in the extremely early stages of lymph node metastasis and clinical prognosis in breast cancer.

Most meningiomas are classified as WHO CNS grade 1 and have a favorable prognosis when completely resected. In contrast, intracranial recurrence and metastasis are frequently observed in grade 2–3 meningiomas, although extracranial spread is rare. A 59-year-old Japanese male presented with numbness on the right side of face and diplopia, and imaging revealed a lesion extending from the right middle cranial fossa to the paranasal sinuses and right optic canal. Histology revealed epithelioid nests and spindle cells with high cellularity. The epithelioid component formed whorl-like structures resembling meningothelial cells, with focal necrosis, bizarre nuclei and lower mitotic activity, which is consistent with atypical meningioma of the meningothelial subtype. In contrast, the spindle cell component demonstrated poor morphological differentiation and high mitotic activity. Immunohistochemistry revealed that the meningothelial cells were positive for epithelial membrane antigen and were partially positive for progesterone receptor. The spindle cells were negative for these markers and weakly positive for smooth muscle actin. The final diagnosis was anaplastic meningioma (WHO CNS grade 3) with sarcomatous features showing smooth muscle differentiation. Extensive extracranial metastases via the sarcomatous element involved 12 extracranial organs, including common sites such as the lungs, bones, and liver, indicating unusually widespread dissemination. This report describes an anaplastic meningioma with multiple extracranial metastases. The extensive multiorgan involvement and rapid progression by the autopsy confirmation distinguish this as a rare case with markedly greater malignancy than typically reported.

Introduction Secondary bladder tumor is rare. We report a case of a bladder tumor initially thought to be a recurrence of non‐muscle invasive bladder cancer that was ultimately identified as metastasis from gastric cancer treated 16 years prior. Case presentation A 75‐year‐old male with a history of gastric, prostate, and recurrent non‐muscle invasive bladder cancer was diagnosed to have multiple bone metastases. Open bone biopsy and cancer gene panel testing identified the primary origin of the metastases as gastric cancer. Retrospective evaluation revealed that what was initially suspected as recurrent bladder tumors were actually metastases from the gastric cancer. Conclusion In cases of metastases with an unknown primary origin, detailed evaluation, including biopsy of the metastatic lesion and genomic testing, is recommended.

We report a case of pancreatic ductal adenocarcinoma (PDAC) in a 51-year-old woman with PRSS1-associated hereditary pancreatitis (HP) and a history of chronic alcohol and tobacco use. Following neoadjuvant chemotherapy, she underwent total pancreatectomy. Histological analysis of the entire pancreas revealed no high-grade PanINs and scattered low-grade PanINs, with and without KRAS mutations, indicating molecular heterogeneity. Genomic profiling identified multiple driver alterations, comprising both clonal and subclonal events, including mutations in KRAS, CDKN2A/B, SMAD4, ATRX, MSH3, and the TERT promoter. Immunohistochemistry showed strong nuclear p53 overexpression despite the absence of TP53 mutation, suggesting a chromosomal instability phenotype. These findings support the hypothesis of a chromothripsis-like catastrophic genomic event contributing to rapid oncogenesis, bypassing the conventional PanIN sequence. The background of chronic inflammation, advanced lipomatous atrophy, and environmental exposures may have facilitated this transformation. This case underscores the need to consider alternative, nonlinear pathways of PDAC development in genetically predisposed individuals and highlights the potential utility of molecular surveillance for early detection and risk stratification.

A 69-year-old Japanese man developed abdominal pain, purpura, proteinuria, and hematuria while receiving treatment for pulmonary tuberculosis. A skin biopsy revealed IgA-positive leukocytoclastic vasculitis, and a renal biopsy showed IgA-positive mesangial proliferative glomerulonephritis with crescent formation. Based on these findings, we diagnosed IgA vasculitis with nephritis (IgAVN) and initiated treatment. The patient’s abdominal symptoms improved following factor XIII supplementation and corticosteroids. Corticosteroids were administered, and after 5 months, the proteinuria was in complete remission. Although IgAVN often follows a prior infection, it is rarely complicated by tuberculosis. In this case, staining for galactose-deficient IgA1, which is specifically positive in IgA nephropathy and IgAVN, was positive. Nephritis-associated plasmin receptor staining was also positive, suggesting some involvement of infectious glomerulonephritis. Therefore, the patient was considered to have IgAVN associated with pulmonary tuberculosis. In adult-onset cases, IgAVN is often severe. This patient was presented with adult-onset nephrosis and International Study of Kidney Disease in Children grade IIIb IgAVN, suggesting a poor prognosis. Therefore, we immediately initiated treatment with corticosteroids, factor XIII supplementation, a renin-aldosterone-system inhibitor, and a sodium–glucose cotransporter 2 inhibitor. The patient recovered uneventfully with no worsening of tuberculosis.

Reports of glomerulonephritis associated with lymphoproliferative disorders are common, but reports of minimal change disease (MCD) accompanying non-Hodgkin’s lymphoma are rare. Here, we present a case of a 45-year-old woman diagnosed with primary Waldenström’s macroglobulinemia (WM) during MCD treatment. Her kidney biopsy revealed endothelial cell injury in parts of the MCD. Subsequently, she developed steroid-resistant nephrotic syndrome and temporary acute kidney injury, requiring dialysis. Remission of the nephrotic syndrome was achieved after initiating combination therapy with bendamustine and rituximab for WM. The renal histological findings and treatment course suggest a causal relationship between MCD and WM in this case. The pathogenesis of MCD associated with WM may involve the release of glomerular permeability factors derived from B lymphocytes. Although mild WM is often managed with observation, steroid-resistant nephrotic syndrome associated with WM should raise suspicion of a paraneoplastic syndrome, necessitating active chemotherapy targeting WM as a critical treatment approach.

In recent years, perioperative immune checkpoint inhibitors have become indicated for early-stage lung cancer, emphasizing the importance of high-resolution endoscopic evaluation of preoperative drug therapy. At the initial evaluation, a male patient in his 60s presented with a primary lesion obstructing the right upper lobe bronchus. After three courses of neoadjuvant immunochemotherapy, chest computed tomography and endoscopic examinations showed a near-complete response. Narrow-band imaging indicated that subepithelial vascular regularity and distribution patterns were within normal limits. However, autofluorescence imaging (AFI) revealed a magenta-colored area on the bronchial epithelium corresponding to the initial lesion site. Two months later, the magenta coloration faded, suggesting pathological normalization of the bronchial epithelium thickening. AFI enabled visualization of tumor progression in the bronchi otherwise completely obstructed by the lesion, potentially offering valuable information to determine bronchial resection lines during surgery.

A gastric neuroendocrine tumor (NET) with pancreatic acinar cell differentiation is extremely rare. We report the case of an 87-year-old woman with a submucosal tumor in the gastric body on a background of atrophic gastritis. She also had Sjögren's syndrome. Initially 17.8 × 6.5 mm, the tumor enlarged over 10 years, leading to wedge resection. The resected mass (45 × 40 × 30 mm) was solid with a pale yellow to gray-white cut surface. Histologically, it showed trabecular or solid nests of epithelial cells with round nuclei and eosinophilic cytoplasm. Immunohistochemistry showed positivity for CKAE1/3, VMAT2, neuroendocrine markers, and pancreatic acinar markers. Ki-67 index was 11.2%. The tumor co-expressed PDX1 and ARX and showed loss of menin and ATRX. These findings support a diagnosis of gastric ECL-cell NET G2 arising in autoimmune gastritis, with secondary pancreatic acinar differentiation. This tumor may represent a variant of type 1 gastric NET.

Acquired tracheomalacia (TM) following tracheostomy can hinder decannulation and affect the quality of life of pediatric patients. Therefore, a reproducible animal model of type III TM is required for further research and therapeutic development. We established a rabbit model of acquired TM by resecting the anterior walls of the 2nd to 4th tracheal cartilage rings, while preserving the mucosa. Bronchoscopic evaluations were conducted at three time points: before surgery (term 1), immediately after surgery (term 2), and 3–4 months post-surgery (term 3). The area of the tracheal lumen was measured under varying negative suction pressures using image analysis. Five of the six rabbits survived and successfully modeled TM. Progressive luminal narrowing was observed, particularly at term 3, where the area decreased to 15.0 ± 18.8