1.Primary Merkel cell carcinoma of the salivary gland: a clinicopathologic study of four cases with a review of literature
Gyuheon CHOI ; Joon Seon SONG ; Hee Jin LEE ; Gi Hwan KIM ; Young Ho JUNG ; Yoon Se LEE ; Kyung-Ja CHO
Journal of Pathology and Translational Medicine 2025;59(3):171-179
Background:
Primary Merkel cell carcinoma of the salivary gland is currently not listed in the World Health Organization classification. However, cases of Merkel cell type neuroendocrine carcinomas of the salivary gland with perinuclear cytokeratin 20 positivity have been intermittently reported. We here investigated the clinicopathologic features of additional cases.
Methods:
Data of four cases of Merkel cell type small cell neuroendocrine carcinoma of the salivary gland were retrieved. To confirm the tumors’ primary nature, clinical records and pathologic materials were reviewed. Optimal immunohistochemical staining was performed to support the diagnosis.
Results:
All tumors were located in the parotid gland. Possibilities of metastasis were excluded in all cases through a meticulous clinicopathological review. Tumor histology was consistent with the diagnosis of small cell neuroendocrine carcinoma. Tumors’ immunohistochemical phenotypes were consistent with Merkel cell carcinoma, including Merkel cell polyomavirus large T antigen positivity in two of the four cases.
Conclusions
Merkel cell carcinomas can originate in salivary glands and are partly associated with Merkel cell polyomavirus infection as in cutaneous Merkel cell carcinomas.
2.Erratum to "Suppression of Lipopolysaccharide-induced Inflammatory and Oxidative Response by 5-Aminolevulinic Acid in RAW 264.7 Macrophages and Zebrafish Larvae" Biomol Ther 29(6), 685-696 (2021)
Seon Yeong JI ; Hee-Jae CHA ; Ilandarage Menu Neelaka MOLAGODA ; Min Yeong KIM ; So Young KIM ; Hyun HWANGBO ; Hyesook LEE ; Gi-Young KIM ; Do-Hyung KIM ; Jin Won HYUN ; Heui-Soo KIM ; Suhkmann KIM ; Cheng-Yun JIN ; Yung Hyun CHOI
Biomolecules & Therapeutics 2025;33(3):554-554
3.Erratum to "Suppression of Lipopolysaccharide-induced Inflammatory and Oxidative Response by 5-Aminolevulinic Acid in RAW 264.7 Macrophages and Zebrafish Larvae" Biomol Ther 29(6), 685-696 (2021)
Seon Yeong JI ; Hee-Jae CHA ; Ilandarage Menu Neelaka MOLAGODA ; Min Yeong KIM ; So Young KIM ; Hyun HWANGBO ; Hyesook LEE ; Gi-Young KIM ; Do-Hyung KIM ; Jin Won HYUN ; Heui-Soo KIM ; Suhkmann KIM ; Cheng-Yun JIN ; Yung Hyun CHOI
Biomolecules & Therapeutics 2025;33(3):554-554
4.Primary Merkel cell carcinoma of the salivary gland: a clinicopathologic study of four cases with a review of literature
Gyuheon CHOI ; Joon Seon SONG ; Hee Jin LEE ; Gi Hwan KIM ; Young Ho JUNG ; Yoon Se LEE ; Kyung-Ja CHO
Journal of Pathology and Translational Medicine 2025;59(3):171-179
Background:
Primary Merkel cell carcinoma of the salivary gland is currently not listed in the World Health Organization classification. However, cases of Merkel cell type neuroendocrine carcinomas of the salivary gland with perinuclear cytokeratin 20 positivity have been intermittently reported. We here investigated the clinicopathologic features of additional cases.
Methods:
Data of four cases of Merkel cell type small cell neuroendocrine carcinoma of the salivary gland were retrieved. To confirm the tumors’ primary nature, clinical records and pathologic materials were reviewed. Optimal immunohistochemical staining was performed to support the diagnosis.
Results:
All tumors were located in the parotid gland. Possibilities of metastasis were excluded in all cases through a meticulous clinicopathological review. Tumor histology was consistent with the diagnosis of small cell neuroendocrine carcinoma. Tumors’ immunohistochemical phenotypes were consistent with Merkel cell carcinoma, including Merkel cell polyomavirus large T antigen positivity in two of the four cases.
Conclusions
Merkel cell carcinomas can originate in salivary glands and are partly associated with Merkel cell polyomavirus infection as in cutaneous Merkel cell carcinomas.
5.Erratum to "Suppression of Lipopolysaccharide-induced Inflammatory and Oxidative Response by 5-Aminolevulinic Acid in RAW 264.7 Macrophages and Zebrafish Larvae" Biomol Ther 29(6), 685-696 (2021)
Seon Yeong JI ; Hee-Jae CHA ; Ilandarage Menu Neelaka MOLAGODA ; Min Yeong KIM ; So Young KIM ; Hyun HWANGBO ; Hyesook LEE ; Gi-Young KIM ; Do-Hyung KIM ; Jin Won HYUN ; Heui-Soo KIM ; Suhkmann KIM ; Cheng-Yun JIN ; Yung Hyun CHOI
Biomolecules & Therapeutics 2025;33(3):554-554
6.Primary Merkel cell carcinoma of the salivary gland: a clinicopathologic study of four cases with a review of literature
Gyuheon CHOI ; Joon Seon SONG ; Hee Jin LEE ; Gi Hwan KIM ; Young Ho JUNG ; Yoon Se LEE ; Kyung-Ja CHO
Journal of Pathology and Translational Medicine 2025;59(3):171-179
Background:
Primary Merkel cell carcinoma of the salivary gland is currently not listed in the World Health Organization classification. However, cases of Merkel cell type neuroendocrine carcinomas of the salivary gland with perinuclear cytokeratin 20 positivity have been intermittently reported. We here investigated the clinicopathologic features of additional cases.
Methods:
Data of four cases of Merkel cell type small cell neuroendocrine carcinoma of the salivary gland were retrieved. To confirm the tumors’ primary nature, clinical records and pathologic materials were reviewed. Optimal immunohistochemical staining was performed to support the diagnosis.
Results:
All tumors were located in the parotid gland. Possibilities of metastasis were excluded in all cases through a meticulous clinicopathological review. Tumor histology was consistent with the diagnosis of small cell neuroendocrine carcinoma. Tumors’ immunohistochemical phenotypes were consistent with Merkel cell carcinoma, including Merkel cell polyomavirus large T antigen positivity in two of the four cases.
Conclusions
Merkel cell carcinomas can originate in salivary glands and are partly associated with Merkel cell polyomavirus infection as in cutaneous Merkel cell carcinomas.
7.Capsosiphon fulvescens suppresses LPS-stimulated inflammatory responses by suppressing TLR4/NF-κB activation in RAW264.7 murine macrophages
Seon Yeong Ji ; EunJin Bang ; Hyun Hwangbo ; Min Yeong Kim ; Da Hye Kim ; Su Hyun Hong ; Shin- Hyung Park ; Chang-Young Kwon ; Gi-Young Kim ; You-Jin Jeon ; Suengmok Cho ; Yung Hyun Choi
Asian Pacific Journal of Tropical Biomedicine 2024;14(3):115-126
Objective: To evaluate the effects of Capsosiphon fulvescens (C. fulvescens) ethanolic extract on inflammation in lipopolysaccharide (LPS)-induced RAW296.7 macrophages. Methods: The protective effects of C. fulvescens ethanolic extract on LPS-induced inflammation in RAW264.7 macrophages were assessed using biochemical analysis, including enzyme-linked immunosorbent assay, quantitative reverse transcription-polymerase chain reaction, and Western blot analysis. To examine reactive oxygen species (ROS) production, flow cytometry analysis, and immunofluorescence staining were used. Furthermore, the modulatory effect of C. fulvescens ethanolic extract on NF-κB activation was investigated. Results: C. fulvescens ethanolic extract significantly attenuated LPS-induced levels of pro-inflammatory cytokines and notably reduced the secretion and mRNA levels of LPS-mediated matrix metalloproteinases. In addition, C. fulvescens ethanolic extract decreased ROS production and suppressed the TLR4/NF-κB signaling pathway. Conclusions: C. fulvescens ethanolic extract alleviates inflammation as well as oxidative stress by modulating the TLR4/NF-κB signaling in LPS-induced RAW264.7 macrophages. C. fulvescens can be used as a potential therapeutic agent to suppress inflammation and oxidative stress-associated diseases.
8.Asparagi radix alleviates testosterone-induced benign prostatic hyperplasia by inhibiting5α-reductase activity and androgenreceptor signaling pathway
Hyun HWANGBO ; Hee-Jae CHA ; Min Yeong KIM ; Seon Yeong JI ; Da Hye KIM ; Jeong Sook NOH ; Tae Hee KIM ; Heui-Soo KIM ; Sung-Kwon MOON ; Gi-Young KIM ; Yung Hyun CHOI
Nutrition Research and Practice 2024;18(6):793-805
BACKGROUND/OBJECTIVES:
Recently, herbal medicines have gained attention for the treatment of benign prostatic hyperplasia (BPH), a common disease in elderly men. In this study, we aimed to determine the effect of ethanol extract of Asparagi radix (EAR), which is traditionally used to treat various diseases, on BPH development using a testosteroneinduced BPH model.MATERIALS/METHODS: Testosterone propionate (TP)-treated Sprague–Dawley rats were used to establish a BPH model in vivo. EAR was orally administered along with TP, and finasteride was used as a positive control. All rats were sacrificed at the end of the experiment, and pathological changes in the prostate tissue and levels of key biomarkers associated with BPH pathogenesis were assessed.
RESULTS:
Oral administration of EAR significantly inhibited TP-induced BPH by reducing the prostate weight, lumen size, and epithelial thickness in a concentration-dependent manner. EAR also significantly abrogated the expression of 5α-reductase type 2 (SRD5A2), proliferating cell nuclear antigen, and prostate-specific antigen (PSA) induced by TP.Additionally, serum levels of testosterone, dihydrotestosterone, and PSA were elevated in the TP-induced group but decreased in the EAR-treated group. EAR also decreased the expression levels of the androgen receptor (AR) and its coactivators in TP-induced BPH model rats.
CONCLUSION
Our findings revealed that EAR protected against BPH by inhibiting 5α-reductase activity and AR signaling pathway, suggesting its potential for BPH treatment.
9.Asparagi radix alleviates testosterone-induced benign prostatic hyperplasia by inhibiting5α-reductase activity and androgenreceptor signaling pathway
Hyun HWANGBO ; Hee-Jae CHA ; Min Yeong KIM ; Seon Yeong JI ; Da Hye KIM ; Jeong Sook NOH ; Tae Hee KIM ; Heui-Soo KIM ; Sung-Kwon MOON ; Gi-Young KIM ; Yung Hyun CHOI
Nutrition Research and Practice 2024;18(6):793-805
BACKGROUND/OBJECTIVES:
Recently, herbal medicines have gained attention for the treatment of benign prostatic hyperplasia (BPH), a common disease in elderly men. In this study, we aimed to determine the effect of ethanol extract of Asparagi radix (EAR), which is traditionally used to treat various diseases, on BPH development using a testosteroneinduced BPH model.MATERIALS/METHODS: Testosterone propionate (TP)-treated Sprague–Dawley rats were used to establish a BPH model in vivo. EAR was orally administered along with TP, and finasteride was used as a positive control. All rats were sacrificed at the end of the experiment, and pathological changes in the prostate tissue and levels of key biomarkers associated with BPH pathogenesis were assessed.
RESULTS:
Oral administration of EAR significantly inhibited TP-induced BPH by reducing the prostate weight, lumen size, and epithelial thickness in a concentration-dependent manner. EAR also significantly abrogated the expression of 5α-reductase type 2 (SRD5A2), proliferating cell nuclear antigen, and prostate-specific antigen (PSA) induced by TP.Additionally, serum levels of testosterone, dihydrotestosterone, and PSA were elevated in the TP-induced group but decreased in the EAR-treated group. EAR also decreased the expression levels of the androgen receptor (AR) and its coactivators in TP-induced BPH model rats.
CONCLUSION
Our findings revealed that EAR protected against BPH by inhibiting 5α-reductase activity and AR signaling pathway, suggesting its potential for BPH treatment.
10.Asparagi radix alleviates testosterone-induced benign prostatic hyperplasia by inhibiting5α-reductase activity and androgenreceptor signaling pathway
Hyun HWANGBO ; Hee-Jae CHA ; Min Yeong KIM ; Seon Yeong JI ; Da Hye KIM ; Jeong Sook NOH ; Tae Hee KIM ; Heui-Soo KIM ; Sung-Kwon MOON ; Gi-Young KIM ; Yung Hyun CHOI
Nutrition Research and Practice 2024;18(6):793-805
BACKGROUND/OBJECTIVES:
Recently, herbal medicines have gained attention for the treatment of benign prostatic hyperplasia (BPH), a common disease in elderly men. In this study, we aimed to determine the effect of ethanol extract of Asparagi radix (EAR), which is traditionally used to treat various diseases, on BPH development using a testosteroneinduced BPH model.MATERIALS/METHODS: Testosterone propionate (TP)-treated Sprague–Dawley rats were used to establish a BPH model in vivo. EAR was orally administered along with TP, and finasteride was used as a positive control. All rats were sacrificed at the end of the experiment, and pathological changes in the prostate tissue and levels of key biomarkers associated with BPH pathogenesis were assessed.
RESULTS:
Oral administration of EAR significantly inhibited TP-induced BPH by reducing the prostate weight, lumen size, and epithelial thickness in a concentration-dependent manner. EAR also significantly abrogated the expression of 5α-reductase type 2 (SRD5A2), proliferating cell nuclear antigen, and prostate-specific antigen (PSA) induced by TP.Additionally, serum levels of testosterone, dihydrotestosterone, and PSA were elevated in the TP-induced group but decreased in the EAR-treated group. EAR also decreased the expression levels of the androgen receptor (AR) and its coactivators in TP-induced BPH model rats.
CONCLUSION
Our findings revealed that EAR protected against BPH by inhibiting 5α-reductase activity and AR signaling pathway, suggesting its potential for BPH treatment.


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