Adherence to antiviral therapy is essential for viral suppression in chronic hepatitis B (CHB), yet its effect on hepatocellular carcinoma (HCC) remains uncertain. We examined the association between nucleos(t)ide analog (NA) adherence and HCC risk, focusing on tenofovir alafenamide (TAF) versus entecavir (ETV). Treatment-naïve adults with CHB initiating TAF or ETV were identified from the Health Insurance Review and Assessment Service, Republic of Korea. Adherence was measured using the medication possession ratio, with high adherence defined as ≥ 90%, and the primary outcome was HCC incidence. A total of 28 448 patients were included, of whom 19 001 (66.8%) showed high adherence and 9447 (33.2%) showed low adherence. In the overall cohort, HCC incidence was comparable between the high- and low-adherence groups (14.89 vs. 13.76 per 1000 person-years; IRR, 1.08; 95% CI, 0.95-1.24). Among patients with claims-defined cirrhosis, however, high adherence was associated with lower observed HCC incidence (32.92 vs. 49.59 per 1000 person-years; IRR, 0.66; 95% CI, 0.57-0.78), and this association remained significant in multivariable Cox regression (HR, 0.77; 95% CI, 0.66-0.90) as well as in IPTW, landmark, and sensitivity analyses. In exploratory regimen-stratified analyses, high-adherence TAF users showed a lower observed cumulative HCC incidence than high-adherence ETV users, whereas no significant difference was observed in the low-adherence group. Logistic regression identified ETV use as a predictor of low adherence (OR, 2.80; 95% CI, 2.65-2.96). High adherence to antiviral therapy was associated with lower observed HCC incidence among patients with CHB and claims-defined cirrhosis. Although this association remained evident across multiple analyses, residual confounding, treatment-selection effects, time-related bias, and competing-risk issues cannot be fully excluded.

Fluoropyrimidines are widely used in the treatment of solid tumors but may cause severe toxicity in patients with reduced dihydropyrimidine dehydrogenase activity caused by specific DPYD variants. Although pretreatment DPYD genotyping is guideline supported, implementation remains inconsistent when testing, interpretation, and result reporting are not integrated into routine care pathways. This study evaluated the implementation of an in-house DPYD genotyping program embedded in prechemotherapy workflows at a multisite cancer center.

A prospective observational cohort study was performed from May 2024 through July 2025 at a multisite community-academic cancer center. Peripheral blood specimens underwent in-house DPYD genotyping for c.1905 + 1G > A, c.1679T > G, c.1236G > A as a proxy for c.1129-5923C > G, c.2846A > T, and c.557A > G using TaqMan allelic discrimination. Raw instrument output was processed through an internally developed automated pipeline that supported genotype calling, quality control review, phenotype and activity assignment, and generation of a note with this information for release into the electronic health record after medical director review. Of 617 genotyped patients, 505 who received systemic fluoropyrimidine-based therapy were included in the primary analysis.

Among 505 included patients, pretreatment testing was performed in 439 (86.9%), although only 197 of 439 (44.9%) had results available before cycle 1 chemotherapy. Twenty-two (4.4%) patients were heterozygous for a DPYD variant: c.1236G > A in 11, c.2846A > T in 5, c.1905 + 1G > A in 4, and c.557A > G in 2. In the pretreatment cohort, 10 of 21 (47.6%) patients heterozygous for a DPYD variant underwent dose reduction at cycle 1, and 9 of these reductions were documented as genotype guided. Severe treatment-related adverse events requiring urgent evaluation or hospitalization occurred in 5 of 505 (1.0%) patients, including 1 patient heterozygous for a c.1236G > A variant whose result returned after treatment initiation.

In-house DPYD genotyping with integrated clinical reporting was feasible in routine practice and identified actionable variants in a clinically meaningful proportion of patients. The principal implementation limitation was not assay turnaround time itself but rather failure to return results before the first treatment decision in pretreatment-ordered cases. These findings support the value of laboratory-led pharmacogenomic programs that combine rapid testing, structured interpretation, and direct electronic reporting.

Neuroblastoma is the most common extracranial solid tumor in children, predominantly affecting patients under 10 years. Due to therapeutic challenges, most patients are treated in specialized pediatric oncology centers. [¹²³I/¹³¹I]I-mIBG scintigraphy plays a crucial role in the diagnosis, staging, assessment of treatment response and long-term follow-up of patients with neuroblastoma. This study is part of the TEMICARE 2.0 project, which aims to improve the health and psychosocial well-being of patients with neuroblastoma in the Pomerania Euroregion. The aim of this study was to retrospectively analyze the use of [¹²³I/¹³¹I]I-mIBG imaging in the diagnosis of neuroblastoma in children and to compare clinical practice at participating centers.

Patients with suspected or confirmed neuroblastoma who underwent [¹²³I] or [¹³¹I]I-mIBG scintigraphy at two pediatric oncology centers in Poland and Germany from 2019-2024 were retrospectively included. Acquisition parameters were collected in a standardized manner.

A total of 320 examinations were performed in 88 patients. At Site 1, 190 studies were performed using [¹³¹I]I-mIBG, whereas 130 studies using [¹²³I]I-mIBG were conducted at Site 2. The mean age of the patients was 3 years (range: 1 month-14 years). The average number of examinations per patient was four. The mean cumulative effective dose delivered to patients during all examinations with [¹²³I]I-mIBG was 123 mSv, compared with 207 mSv for [¹³¹I]I-mIBG, representing an approximately 40% lower dose with [¹²³I]I-mIBG.

[¹²³I]I-mIBG imaging is an essential tool for disease staging and monitoring treatment response in patients with neuroblastoma. Current guidelines recommend the use of [¹²³I]I-mIBG because of its superior diagnostic performance and more favorable radiation dosimetry profile. However, the availability of this radiopharmaceutical remains limited due to higher costs and the logistical challenges associated with transportation to centers located far from production facilities.

Approximately 5%-10% of colorectal cancer (CRC) cases are due to known Mendelian syndromes. This study aimed to report the diagnostic yield of constitutional genetic testing, alongside clinicopathological factors for hereditary CRC, within a specialised National Bowel Hospital, and outside traditional genetics referral pathways.

This study retrospectively reviewed clinical, pathological and genetic factors using prospectively collected data from the St Mark's Hospital Centre for Familial Intestinal Cancer registry. Between December 2021 and June 2023, consecutive patients at risk of hereditary CRC were selected for genetic testing according to UK National Genomic Testing criteria. The diagnostic yield of genetic testing was calculated by indication. Statistical analysis for clinicopathological data was performed using the Mann-Whitney U test, chi-square test and logistic regression.

A total of 283 consecutive patients underwent genetic testing, 100 (35.3%) mainstreamed with CRC, 95 (33.6%) with multiple polyps, 74 (26.6%) had cascade testing (within families where the probands were known to the registry) and other testing including 'unaffected' patients with a relevant family history. Variants were detected in 85 of 283 (30%) patients with known CRC predisposition genes. Diagnostic yields were high for deficient mismatch repair (dMMR) cancer with Lynch syndrome (LS) at 45%, and also for multiple adenoma cohorts at 16%; and in CRC patients under 40 years (irrespective of tumour MMR status) at 16%.

Genetic testing performed by our specialist unit provides patients with a high-yield, and effective genetic diagnosis, directly indicating comprehensive lifelong care, outside the context of a traditional genetics service.

Pathologic fracture is a complication of bone cancer with probable increased risk following radiation therapy (RT). Low-dose-rate (LDR) RT can spare late-responding normal tissues by allowing intrafraction DNA repair, which could also impact tumor response. This retrospective cohort study evaluated efficacy and fracture rate in canine patients (n = 184) with confirmed or suspected appendicular osteosarcoma that received 10 Gy × 2 palliative RT on consecutive days with LDR (cobalt-60) or standard-dose-rate (SDR, linear accelerator). The overall fracture rate was 21.7%. Patients treated with SDR (600 cGy/min, n = 46) and LDR (range 21.9-83.29 cGy/min, n = 152) did not differ in pathologic fracture rates (22.4% vs. 17.4%, respectively, p = 0.54) or median survival times (231 vs. 248.5 days, respectively, p = 0.448). Pathologic fracture rates did not differ on the basis of weight (<35, 35-50, and >50 kg) or location (24% forelegs, 18% hindlegs, p = 0.44). However, no dog (n = 7) weighing less than 20 kg developed a fracture. Radiographs prior to RT were subjectively assessed for bone integrity. Dogs with predominantly lytic lesions did not have a significantly higher pathologic fracture rate (21.2%-31.69% lytic/mixed vs. 10%-12.5% proliferative, p = 0.054), suggesting that pretreatment radiographic appearance does not reflect fracture risk. Additionally, the presence of a pretreatment cortical bone defect was not associated with eventual fracture (p = 0.7). Adjunctive chemotherapy improved survival time significantly (p = 0.01). On the basis of our data, it is reasonable to compare response rates and survival outcomes in published studies using cobalt irradiation with reports using linear accelerators.

Epithelioid trophoblastic tumour (ETT) is a rare form of gestational trophoblastic disease (GTD). We report a case of a 28-year-old woman presenting with abnormal uterine bleeding and mildly elevated serum beta human chorionic gonadotropin (β-hCG) levels. Imaging revealed a heterogeneous uterine mass with lymphadenopathy and pulmonary metastases. Core biopsy histology suggested ETT, but definitive subclassification was limited by small sample size and an ambiguous immunohistochemical profile, which is itself a recognised source of diagnostic uncertainty in this entity. The patient received neoadjuvant platinum-based chemotherapy, followed by total hysterectomy with bilateral salpingo-oophorectomy and lymphadenectomy. At 10 months postoperatively, the patient remains disease-free with normalisation of β-hCG levels. This case illustrates the diagnostic challenges inherent to GTD, particularly the overlap between ETT, placental site trophoblastic tumour (PSTT) and choriocarcinoma; emphasises the importance of integrating multimodal imaging with histopathology within a multidisciplinary team; and demonstrates that a combined approach of chemotherapy and surgical resection can lead to favourable outcomes in this rare entity.

Carotid body tumors or carotid body paragangliomas, are rare, highly vascular neuroendocrine neoplasms originating from the paraganglionic cells of the carotid body situated near the adventitial layer of the carotid bifurcation. Although they typically exhibit slow growth and benign behavior, their close proximity to the neurovascular structures of the neck poses diagnostic and therapeutic challenges. Timely recognition through clinical examination and imaging studies is crucial for establishing the diagnosis and improving the prognosis. We present the case of an 84-year-old male with a progressively enlarging mass in the right parotid region, present for one month, without associated neurological symptoms. Carotid body tumors should be considered in the differential diagnosis of neck masses. Correlating clinical findings with imaging studies enables a timely diagnosis and appropriate treatment planning, thereby fostering a favorable clinical outcome.

Recurrent syncope and behavioral changes in the older population may suggest several disease entities associated with aging. Hypoglycemia is an often-missed potentially correctable underlying cause that should also be considered in the differential diagnosis. We present a case of a 62-year-old Filipino female who presented with recurrent syncopal attacks, behavioral changes and unintentional weight gain, associated with endogenous hyperinsulinemic hypoglycemia with no pancreatic mass seen on abdominal CT scan. A pancreatic head tumor was visualized through endoscopic ultrasound. Surgical removal of the mass resulted in resolution of her symptoms and restoration of her physical and functional wellbeing. This case is being reported to highlight that surgery cured her of the disease and she remains asymptomatic and well 13 years after her surgery.

Cemento-ossifying fibroma (COF) is a benign fibro-osseous neoplasm that most often affects the mandible and occurs predominantly in women during the third and fourth decades of life. Maxillary involvement is less common and may remain minimally symptomatic while expanding into the maxillary sinus. We present a 26-year-old woman with a six-month history of progressive right midface enlargement without pain, nasal obstruction, diplopia, visual symptoms, or dental mobility. Computed tomography demonstrated a well-circumscribed expansile right maxillary lesion measuring 44.9 × 42.5 × 31.9 mm, occupying a substantial portion of the maxillary sinus and extending toward a thinned but radiologically intact orbital floor. A preoperative incisional biopsy showed a fibrocellular spindle-cell stroma with cementum-like mineralized deposits, supporting the diagnosis of conventional COF. Through a Weber-Ferguson approach, the encapsulated lesion demonstrated a favorable cleavage plane and underwent macroscopically complete enucleation with peripheral osteotomy while preserving the orbital floor and residual maxillary bone. Immediate reconstruction was not required. At approximately three months of follow-up, wound healing remained satisfactory without infection, dehiscence, ectropion, alar retraction, visual symptoms, or other functional complications. Infraorbital hypoesthesia persisted as the only postoperative neurologic finding. Follow-up computed tomography was reviewed by the treating surgical team and demonstrated postoperative changes without a discrete residual or recurrent expansile lesion. This case highlights the importance of individualized intraoperative assessment of lesion boundaries and remaining structural support when considering a bone-preserving strategy. Although the early clinical and radiologic outcomes were favorable, the limited follow-up precludes conclusions regarding long-term recurrence, structural stability, or definitive sensory recovery.

Primary cutaneous mucinous carcinoma (PCMC) is a rare malignant cutaneous adnexal neoplasm prone to local recurrence. Neuroendocrine differentiation has been recognized in a subset of these tumors, and emerging evidence suggests that its presence may be associated with differences in clinical behavior and prognosis. Reports characterizing neuroendocrine differentiation in eyelid PCMC remain limited. A 47-year-old man underwent excision of a chalazion-like mass of the right upper eyelid at another clinic, and histopathologic examination revealed mucinous carcinoma. Systemic evaluation found no extracutaneous primary malignancy. Although no residual lesion was clinically apparent at referral, a full-thickness excision approximately 7 mm in total width was performed at the presumed primary site. Histopathologic examination demonstrated residual mucinous carcinoma within the orbicularis muscle, with negative surgical margins. Four months later, firm nodules developed on both sides of the surgical scar, and local recurrence was confirmed. The recurrent lesions were treated with wide full-thickness excision using 7-8 mm clinical margins, and intraoperative frozen-section analysis confirmed negative margins. Staged eyelid reconstruction followed. Immunohistochemistry was negative for synaptophysin and chromogranin A, whereas insulinoma-associated protein 1 (INSM1) showed only focal weak positivity. Gross cystic disease fluid protein-15 (GCDFP-15) was partially positive, while GATA binding protein 3 (GATA3), estrogen receptor, and progesterone receptor were positive. The overall immunophenotype supported apocrine (breast-like) differentiation without significant neuroendocrine differentiation, consistent with non-neuroendocrine PCMC. No recurrence was observed during 36 months of follow-up. This case suggests that histologically negative margins may not exclude occult residual disease when the original tumor site is uncertain. Careful surgical planning, appropriate margin assessment, and long-term surveillance may be warranted because occult residual disease or subclinical tumor spread may contribute to early recurrence.