Sun-Jae Lee

A 66-year-old woman was referred for evaluation of a large pelvic mass suspected to be ovarian cancer. Contrast-enhanced computed tomography (CECT) revealed a giant multiseptated cystic pelvic mass with enhancing solid components; although its superior aspect closely abutted the gastric serosa, its predominant pelvic location raised concern for an adnexal malignancy. Subsequent [¹⁸F]fluorodeoxyglucose positron emission tomography/computed tomography ([¹⁸F]FDG PET/CT) demonstrated mild uptake confined to the viable solid portion (SUVmax 2.72) without hypermetabolic nodal or distant metastases. Exploratory laparotomy revealed a giant pedunculated tumor arising from the gastric antrum and descending into the pelvis. Histopathology confirmed an epithelioid gastrointestinal stromal tumor positive for CD117, DOG1, and CD34. This case highlights an important diagnostic pitfall in which a giant exophytic gastric GIST may mimic ovarian cancer because of its pelvic location and cystic-solid appearance. Careful correlation of CECT, fused [¹⁸F]FDG PET/CT, and pathologic findings is essential for accurate assessment of the organ of origin in large abdominopelvic masses.

Background/Objectives: Minimally invasive surgery (MIS) is widely used for gynecologic malignancies, but the LACC trial reported significantly worse survival in early-stage cervical cancer compared with open surgery, raising concerns about its oncologic safety. Tumor cell spillage during intracorporeal colpotomy in the Trendelenburg position has been proposed as a potential mechanism underlying these findings. This study aimed to assess the presence of tumor cells exfoliated into the vaginal cavity in cervical and endometrial cancers using vaginal washing cytology. Methods: We retrospectively analyzed patients newly diagnosed with cervical or endometrial cancer between June 2021 and February 2025. Vaginal washing cytology was performed before treatment and interpreted. Chi-square or Fisher’s exact tests and multivariate logistic regression were used to identify factors associated with positive cytology. Results: Positive cytology detected more often in cervical than in endometrial cancer (all stages: 33.3% [12/36] vs. 6.5% [3/46], p = 0.002; early stage: 24.0% [6/25] vs. 0% [0/38], p = 0.003). Multivariate analysis confirmed cervical cancer (OR 14.24, 95% CI 1.83–110.89, p = 0.011) and FIGO stage III–IV (OR 9.53, 95% CI 2.08–43.61, p = 0.004) as independent predictors. Conclusions: Tumor cells exfoliated into the vagina were significantly more frequent in cervical cancer, supporting a mechanism by which intracorporeal colpotomy may allow peritoneal entry. Further studies should reassess MIS for early-stage cervical cancer, considering transvaginal colpotomy in the horizontal position.

This study investigated whether combining niraparib and trabectedin in BRCA-proficient epithelial ovarian cancer induces deficiencies in ssDNA break repair and dsDNA homologous recombination, leading to synthetic lethality. A2780 and SKOV3 ovarian cancer cell lines were treated with niraparib and trabectedin. Cell viability was assessed using CCK-8 assays, while RT-qPCR and Western blot analyzed the expression of DNA repair and apoptosis-related genes. Apoptosis was evaluated via Annexin V/PI assays. The combination therapy exhibited a synergistic effect on A2780 cells but not on SKOV3 cells. Treatment reduced BRCA1, BRCA2, RAD51, PARP1, and PARP2 expression, indicating impaired DNA repair. γ-H2AX levels increased, suggesting DNA damage. The therapy also upregulated p53, PUMA, NOXA, BAX, BAK, and p21, promoting p53-mediated apoptosis and cell cycle arrest. Apoptosis induction was confirmed via Annexin V/PI assays. Silencing p53 with siRNA abolished all synergistic effects in A2780 cells. Niraparib and trabectedin combination therapy impairs DNA repair in BRCA-proficient ovarian cancer, leading to synthetic lethality through p53-dependent apoptosis.

Background/Objectives: This study aimed to evaluate the association between intravascular platelet aggregation in tumors and ovarian carcinoma prognosis and investigate underlying mechanisms. Methods: A retrospective analysis was conducted on 144 patients with ovarian carcinoma. Immunohistochemical staining for CD42b, hypoxia-inducible factor-1α (HIF-1α), platelet-derived growth factor (PDGF), and vascular endothelial growth factor (VEGF) was performed using tissue microarrays to assess intravascular platelet aggregation. Staining grades ranged from 1 to 3 for CD42b (platelet aggregation or microthrombus) and 0 to 3 for HIF-1α, PDGF, and VEGF. Results: Among the patients, 25 (17.4%) had grade 1 (no platelet aggregation), 85 (59.0%) had grade 2 (platelet aggregation), and 34 (23.6%) had grade 3 (microthrombus). The grade of intravascular platelet aggregation in ovarian carcinoma was statistically significantly associated with a poor prognosis (p = 0.037). In addition, in patients with more advanced stages of ovarian cancer, higher levels of intravascular platelet aggregation were observed. Additional analysis revealed a correlation between platelet aggregation and HIF-1α expression (correlation coefficient = 0.226, p= 0.006), while PDGF and VEGF showed no significant correlations. Conclusions: Intravascular platelet aggregation in tumors is associated with advanced stages and poor prognosis in ovarian carcinoma. The results of our study suggest a potential association with hypoxia induced by intravascular platelet aggregation in ovarian carcinoma.

Although frequently prescribed for frozen shoulder, it is not known if corticosteroid injections improve the course of frozen shoulder. This study aimed to assess the disease-modifying effects of an intra-articular corticosteroid administration at the freezing phase of frozen shoulder. Twenty-four Sprague-Dawley rats were divided into four groups. Their unilateral shoulders were immobilized for the first 3 days in all groups, followed by an intra-articular corticosteroid injection in Group A, an injection and the cessation of immobilization in Group B, no further intervention in Group C, and the cessation of immobilization in Group D. All rats were sacrificed in Week 3 of study, at which point the passive shoulder abduction angles were measured and the axillary recess tissues were retrieved for histological and Western blot analyses. The passive shoulder abduction angles at the time of sacrifice were 138° ± 8° (Group A), 146° ± 5° (Group B), 95° ± 11° (Group C), 132° ± 8° (Group D), and 158° ± 2° (Control). The histological assessments and Western blots showed greater fibrosis and inflammation in the groups that did not receive the corticosteroid injection (Groups C and D) compared to the corticosteroid-injected groups (Groups A and B). These findings demonstrate the anti-inflammatory and disease-modifying effects of corticosteroid injections during the freezing phase of frozen shoulder in an animal model.

Liver damage caused by various factors results in fibrosis and inflammation, leading to cirrhosis and cancer. Fibrosis results in the accumulation of extracellular matrix components. The role of STAT proteins in mediating liver inflammation and fibrosis has been well documented; however, approved therapies targeting STAT3 inhibition against liver disease are lacking. This study investigated the anti-fibrotic and anti-inflammatory effects of STAT3 decoy oligodeoxynucleotides (ODN) in hepatocytes and liver fibrosis mouse models. STAT3 decoy ODN were delivered into cells using liposomes and hydrodynamic tail vein injection into 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC)-fed mice in which liver injury was induced. STAT3 target gene expression changes were verified using qPCR and Western blotting. Liver tissue fibrosis and bile duct proliferation were assessed in animal experiments using staining techniques, and macrophage and inflammatory cytokine distribution was verified using immunohistochemistry. STAT3 decoy ODN reduced fibrosis and inflammatory factors in liver cancer cell lines and DDC-induced liver injury mouse model. These results suggest that STAT3 decoy ODN may effectively treat liver fibrosis and must be clinically investigated.

This study investigated the association between maximum standardized uptake values (SUVmax) on preoperative 18-FDG PET-CT and next-generation sequencing (NGS) results in post-surgical ovarian malignant tissue in patients with advanced ovarian cancer. Twenty-five patients with stage IIIC or IV ovarian cancer who underwent both preoperative 18-FDG PET-CT and postoperative NGS for ovarian malignancies were retrospectively enrolled. Two patients had no detected variants, 21 of the 23 patients with any somatic variant had at least one single nucleotide variant (SNV) or insertion/deletion (indel), 10 patients showed copy number variation (CNV), and two patients had a fusion variant. SUVmax differed according to the presence of SNVs/indels, with an SUVmax of 13.06 for patients with ≥ 1 SNV/indel and 6.28 for patients without (p = 0.003). Seventeen of 20 patients with Tier 2 variants had TP53 variants, and there was a statistically significant association between SUVmax and the presence of TP53 variants (13.21 vs. 9.35, p = 0.041). Analysis of the correlation between the sum of the Tier 1 and Tier 2 numbers and SUVmax showed a statistically significant correlation (p = 0.002; Pearson’s r = 0.588). In conclusion, patients with advanced ovarian cancer with SNVs/indels on NGS, especially those with TP53 Tier 2 variants, showed a proportional association with tumor SUVmax on preoperative PET-CT.

Renal fibrosis is a common feature of chronic kidney disease and is a promising therapeutic target. However, there is still limited treatment for renal fibrosis, so the development of new anti-fibrotic agents is urgently needed. Accumulating evidence suggest that oxidative stress and endoplasmic reticulum (ER) stress play a critical role in renal fibrosis. Carnosol (CS) is a bioactive diterpene compound present in rosemary plants and has potent antioxidant and anti-inflammatory properties. In this study, we investigated the potential effects of CS on renal injury and fibrosis in a murine model of unilateral ureteral obstruction (UUO). Male C57BL/6J mice underwent sham or UUO surgery and received intraperitoneal injections of CS (50 mg/kg) daily for 8 consecutive days. CS improved renal function and ameliorated renal tubular injury and interstitial fibrosis in UUO mice. It suppressed oxidative injury by inhibiting pro-oxidant enzymes and activating antioxidant enzymes. Activation of ER stress was also attenuated by CS. In addition, CS inhibited apoptotic and necroptotic cell death in kidneys of UUO mice. Furthermore, cytokine production and immune cell infiltration were alleviated by CS. Taken together, these findings indicate that CS can attenuate renal injury and fibrosis in the UUO model.

The global burden of chronic kidney disease is increasing, and the majority of these diseases are progressive. Special site-targeted drugs are emerging as alternatives to traditional drugs. Oligonucleotides (ODNs) have been proposed as effective therapeutic tools in specific molecular target therapies for several diseases. We designed ring-type non-coding RNAs (ncRNAs), also called mTOR ODNs to suppress mammalian target rapamycin (mTOR) translation. mTOR signaling is associated with excessive cell proliferation and fibrogenesis. In this study, we examined the effects of mTOR suppression on chronic renal injury. To explore the regulation of fibrosis and inflammation in unilateral ureteral obstruction (UUO)-induced injury, we injected synthesized ODNs via the tail vein of mice. The expression of inflammatory-related markers (interleukin-1β, tumor necrosis factor-α), and that of fibrosis (α-smooth muscle actin, fibronectin), was decreased by synthetic ODNs. Additionally, ODN administration inhibited the expression of autophagy-related markers, microtubule-associated protein light chain 3, Beclin1, and autophagy-related gene 5-12. We confirmed that ring-type ODNs inhibited fibrosis, inflammation, and autophagy in a UUO mouse model. These results suggest that mTOR may be involved in the regulation of autophagy and fibrosis and that regulating mTOR signaling may be a therapeutic strategy against chronic renal injury.

Streptococcus pyogenes (S. pyogenes) bacteria cause almost all primary skin infections in humans. Bee venom (BV) and melittin (Mel) have multiple effects, including antibacterial and anti-inflammatory activities. This study aims to demonstrate their effects on bacterial mouse skin infection using S. pyogenes. The dorsal skin was tape-stripped, then S. pyogenes was topically applied. BV or Mel were topically applied to the lesion. The tissues were stained with hematoxylin and eosin, while immunohistochemical staining was performed with anti-neutrophil. S. pyogenes-infected skin revealed increased epidermal and dermal layers, but it was reduced in the BV and Mel groups. Finding increased neutrophils in the mice infected with S. pyogenes, but the BV and Mel mice showed decreased expression. These results suggest that BV and Mel treatments could reduce the inflammatory reactions and help improve lesions induced by S. pyogenes skin infection. This study provides additional assessment of the potential therapeutic effects of BV and Mel in managing skin infection caused by S. pyogenes, further suggesting that it could be a candidate for developing novel treatment alternative for streptococcal skin infections.