Chonnam National University Hwasun Hospital

Rationale:Extramedullary relapse of acute lymphoblastic leukemia (ALL) involving the orbit is uncommon, and lacrimal gland infiltration is particularly rare in adults. Bilateral lacrimal gland enlargement can be clinically nonspecific and may be misinterpreted as inflammatory or autoimmune disease, potentially delaying diagnosis. This case report describes a rare adult case of extramedullary relapse of B-cell ALL presenting as bilateral lacrimal gland enlargement following allogeneic hematopoietic stem cell transplantation (HSCT).Patient concerns:A 55-year-old woman presented with a 4-day history of a painless, palpable mass in the right upper eyelid. The patient had a history of Philadelphia chromosome-negative B-cell ALL and had previously undergone chemotherapy followed by allogeneic HSCT.Diagnoses:Orbital computed tomography demonstrated diffuse, heterogeneous enlargement of both lacrimal glands, more prominent on the right side. Incisional biopsy of the right lacrimal gland with immunohistochemical staining (terminal deoxynucleotidyl transferase positive and B-lineage markers positive) confirmed extramedullary relapse of B-cell ALL.Interventions:The patient received salvage chemotherapy followed by a 2nd allogeneic HSCT.Outcomes:Follow-up orbital computed tomography performed 6 months after treatment showed complete resolution of bilateral lacrimal gland enlargement without evidence of local progression.Lessons:Bilateral lacrimal gland enlargement in patients with a history of ALL may represent isolated extramedullary relapse, even in the absence of hematologic abnormalities. Early histopathologic confirmation is essential to prevent diagnostic delay and to enable timely systemic management in ALL patients.

Chronic lymphocytic leukemia (CLL) is uncommon in Asia, and longitudinal genomic data from Asian cohorts are limited. We conducted serial whole-exome sequencing (WES) in a multicenter Korean cohort of newly diagnosed, elderly CLL treated with chlorambucil-obinutuzumab to evaluate mutational heterogeneity and clonal hematopoiesis of indeterminate potential (CHIP) during treatment and follow-up. Tumor-only variants were filtered, restricted to nonsynonymous or loss-of-function coding/splice-site mutations, and summarized as a binary patient-by-gene matrix for principal component analysis (PCA), trajectory analysis, and k-means clustering. CHIP was defined as ≥1 qualifying mutation in a prespecified CHIP gene set. Baseline PCA was more compact in patients with complete response at end of treatment, whereas partial response or progressive disease cases were more dispersed. PCA trajectories were compact and directionally consistent in complete responders, more dispersed in partial responders, and highly heterogeneous without a dominant direction in progressive disease. Clustering identified dispersed and compact clusters, and CHIP-associated mutations were enriched in the dispersed cluster (55.6% vs. 8.3%, Fisher's exact p = 0.0086). In paired samples collected 3-5 months after end of treatment, CHIP status changed in some patients. Serial WES may provide complementary information to treatment response, although these observations require confirmation in larger cohorts.

Extracorporeal membrane oxygenation (ECMO) in pediatric oncology patients remains controversial because of historically poor outcomes and persistent concerns regarding severe infection, bleeding, and immune suppression.We describe a 2-year-old boy with relapsed acute myeloid leukemia who developed profound septic shock and acute respiratory distress syndrome following surgical debridement of a necrotizing perineal infection.The patient had previously experienced tumor lysis syndrome requiring continuous renal replacement therapy, which resulted in complete superior vena cava obstruction.This anatomic limitation precluded conventional internal jugular venous cannulation, and appropriately sized peripheral femoral venous cannulas were not available at the time ECMO was required.Venoarterial ECMO was therefore initiated using direct inferior vena cava cannulation.Hemodynamic stabilization and pulmonary improvement occurred promptly, allowing ECMO decannulation after 8 days and extubation on the following day.The patient ultimately achieved full clinical recovery, with complete wound healing, and remained in complete remission at 9.4 years of follow-up.This case illustrates that ECMO may be lifesaving in carefully selected pediatric oncology patients when the acute illness is reversible and the underlying malignancy is controlled.It further emphasizes the importance of individualized cannulation strategies in the setting of central venous obstruction.

KMT2A (MLL1) is an epigenetic enzyme that activates genes via the addition of histone H3 at lysine 4 (H3K4). As a principal component of the COMPASS (complex of proteins associated with Set1), KMT2A coordinates the transcription of key developmental and lineage-specific genes, thereby shaping cellular plasticity, differentiation, and self-renewal. It is critical for regulating the balance between stem cell renewal and differentiation in both physiological and pathological aspects. Abnormal regulation or chromosomal translocations involving KMT2A are frequently implicated in hematologic malignancies and developmental disorders. In leukemias and other cancers, KMT2A fusion proteins disrupt regular transcriptional programs, creating a tumor-permissive epigenetic environment that supports stem-like properties, therapy resistance, and relapse. In addition to its canonical catalytic role, KMT2A influences chromatin remodeling, enhancer-promoter communication, and transcriptional memory, all of which are crucial for maintaining stemness and enabling cancer cell reprogramming. Given its multifaceted role in cancer and stem cell biology, KMT2A is a promising therapeutic target, and inhibitors that disrupt its interactions, enzymatic activity, or fusion pathways are showing encouraging results. Moreover, current clinical trials investigating venetoclax and menin inhibitors offer renewed hope for curative therapies. This review summarizes the current understanding of the transcriptional mechanisms and noncatalytic roles of KMT2A and the translational implications of targeting KMT2A-driven pathways in stemness and cancer, paving the way for advanced therapeutic intervention.

This study was aimed to evaluate the impact of multivisceral resection (MVR) on the oncologic outcomes of patients with locally advanced colorectal cancer. We conducted a retrospective review of patients who underwent surgical resection between 2011 and 2020. Patients were divided into two groups: the MVR group and the standard resection group. Prognostic factors were compared, and the effect of MVR on oncologic outcomes was assessed. Among 625 patients, 108 underwent MVR. The MVR group showed a significantly lower rate of lymph node metastasis (51.9% vs. 72.5%, p < 0.001), lymphovascular invasion (25.9% vs. 42.8%, p = 0.001), and perineural invasion (45.4% vs. 73.2%, p < 0.001) compared to the standard resection group. Postoperative complications were more frequent in the MVR group (57.4% vs. 26.9%, p < 0.001). Three-year disease-free survival (68.6% vs. 62.7%, p = 0.743) and overall survival (OS) (80.9% vs. 85.0%, p = 0.290) were comparable between the two groups. Multivariable analysis identified lymph node metastasis, perineural invasion, R2 resection, and absence of adjuvant chemotherapy as independent poor prognostic factors for OS. The MVR group showed a significantly lower rate of lymph node metastasis and comparable oncologic outcomes. Therefore, when adjacent organ invasion is suspected, an aggressive en-bloc MVR should be considered to achieve radical resection.

BackgroundAdvanced metastasis produces cachexia, a complex skeletal muscle wasting syndrome that accounts for one-third of patient deaths. There is currently no approved drug therapy for cancer cachexia. Cancer-associated fibroblasts (CAF) within tumors have been hypothesized to contribute to cachexia, but the detailed mechanism(s) are unknown.MethodsMyotubes were treated with conditioned media (CM) from CAF or CAF activated by cancer cells. Upregulated chemokines in the cancer-activated CAF CM were identified by cytokine array. The effects of chemokine neutralization were investigated using in vitro myotube cultures and in vivo mouse models. The mechanism of action was characterized by in vivo RNA Seq and validated in human muscle cells. Immunostaining delineated the chemokine expression pattern in a patient tumor type highly associated with cachexia.ResultsCancer-activated CAF induced myotube atrophy. CXCL5 was as the major chemokine highly upregulated in the cancer-activated CAF. CXCL5 treatment alone induced myotube atrophy and inhibited myogenic ERK1/2 signaling, similar to cancer-activated CAF treatment. CXCL5 neutralization inhibited cachexia in mice co-injected with HCT 116 colon cancer cells and CAF. RNA Seq showed that CXCL5 neutralization upregulated hypertrophy-related PI3K-AKT-MyoG signaling and remodeled the muscle ECM. CXCL5 neutralization ameliorated muscle wasting induced by CXCL5 and IL-6 co-treatment, and also prevented atrophy in cancer-activated CAF CM-treated human myotubes. CAF were the major detectable source of CXCL5 in a patient tumor highly associated with cachexia.ConclusionCAF contribute to cachexia via cancer cell crosstalk that upregulates CXCL5 secretion. CXCL5 neutralization offers a novel therapeutic approach to maintain muscle mass in cancer patients.Supplementary InformationThe online version contains supplementary material available at 10.1186/s12929-025-01192-0.

Since the onset of the COVID-19 pandemic, concerns regarding airborne viral infections in health care settings have intensified. Following the installation of an air sterilizer in an outpatient clinic at a tertiary university hospital and an initial evaluation of its short-term effects, this study investigated the long-term impact of the air sterilizer on indoor air quality and employee satisfaction over a 1-year period. The ENT outpatient clinic at Chonnam National University Hospital was remodeled, and 15 KOKKOS air sterilizers (Bentech Frontier Co., Ltd., Gwangju, Korea) were installed. To evaluate the effectiveness of the air sterilizers, total culturable microorganisms (TCMs) and volatile organic compounds (VOCs) were measured at four time points: 3 days before installation, 2 weeks postinstallation, 4 weeks postinstallation, and 1 year postinstallation. In addition, a product satisfaction survey was conducted among 11 clinic staff who had used the air sterilizers for 1 year. Survey categories included design, product performance, product service, and overall satisfaction. One year after installation, TCMs and VOCs removal rates improved significantly, with mean reductions of 34.3% and 77.1%, respectively (P<0.05). The satisfaction survey yielded high scores across all categories: 4.4 for design, 4.5 for product performance, 4.6 for product service, and 4.8 for overall satisfaction. The KOKKOS air sterilizer demonstrated sustained efficacy in reducing TCMs and VOCs in ENT outpatient clinics over a 1-year period. Furthermore, clinic staff reported high levels of satisfaction across multiple aspects of the product, supporting its potential utility in health care environments.

Heart failure with preserved ejection fraction (HFpEF), defined by clinical heart failure with left ventricular ejection fraction ≥ 50%, represents more than half of heart failure cases in Asia and carries a one-year composite hospitalization and mortality rate of approximately 12.1%. Recent landmark trials have transformed the therapeutic landscape: Sodium-glucose cotransporter 2 inhibitors emerged as treatment for HFpEF, shown beneficial in EMPEROR-preserved and DELIVER. Empagliflozin significantly reduced the risk of cardiovascular death or heart failure hospitalization and dapagliflozin demonstrated comparable efficacy across regions. Furthermore, glucagon-like peptide-1 receptor agonist such as semaglutide have shown promising improvements in functional capacity and symptom burden in obesity-related HFpEF. Asian HFpEF phenotypes often exhibit high rates of hypertension and diabetes, alongside lower average body mass index compared to Western cohorts. In numerous respects, the clinical and pathophysiological features of HFpEF in Asian populations diverge from those traditionally observed in Western cohorts. In this brief review, we will focus on therapeutics approved for HFpEF and agents currently under clinical trial, as well as the distinctive characteristics of HFpEF patients observed in Asia and the key considerations for future therapeutic development in this region.