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1.
Journal of Pathology and Translational Medicine ; : 32-39, 2022.
Article in English | WPRIM | ID: wpr-915805

ABSTRACT

Background@#Primary adrenal (PA) diffuse large B cell lymphoma (DLBCL) was previously reported as an aggressive subset of DLBCL, but its genetic features were not sufficiently characterized. From our previous study of DLBCL with programmed death-ligand 1 (PD-L1) gene alterations, we focused on PD-L1 gene alterations in PA-DLBCL with clinicopathologic implications. @*Methods@#We performed fluorescence in situ hybridization for PD-L1 gene translocation and amplification in PA-DLBCL (n = 18) and comparatively analyzed clinicopathologic characteristics with systemic non-adrenal (NA)-DLBCL (n = 90). @*Results@#PA-DLBCL harbored distinctive features (vs. NADLBCL), including high international prognostic index score (3–5) (72% [13/18] vs. 38% [34/90], p = .007), poor Eastern Cooperative Oncology Group performance score (≥ 2) (47% [7/15] vs. 11% [10/90], p = .003), elevated serum lactate dehydrogenase (LDH) (78% [14/18] vs. 51% [44/87], p = .035) and MUM1 expression (87% [13/15] vs. 60% [54/90], p = .047). Moreover, PA-DLBCL showed frequent PD-L1 gene alterations (vs. NA-DLBCL) (39% [7/18] vs. 6% [5/86], p = .001), including translocation (22% [4/18] vs. 3% [3/87], p = .016) and amplification (17% [3/18] vs. 2% [2/87], p = .034). Within the PA-DLBCL group, PD-L1 gene–altered cases (vs. non-altered cases) tended to have B symptoms (p = .145) and elevated LDH (p = .119) but less frequent bulky disease (≥ 10 cm) (p = .119). In the survival analysis, PA-DLBCL had a poor prognosis for overall survival (OS) and progression-free survival (PFS) (vs. NA-DLBCL; p = .014 and p = .004). Within the PA-DLBCL group, PD-L1 translocation was associated with shorter OS and PFS (p < .001 and p = .012). @*Conclusions@#PA-DLBCL is a clinically aggressive and distinct subset of DLBCL with frequent PD-L1 gene alterations. PD-L1 gene translocation was associated with poor prognosis in PA-DLBCL.

2.
Cancer Research and Treatment ; : 424-433, 2022.
Article in English | WPRIM | ID: wpr-925683

ABSTRACT

Purpose@#Since tumor mutational burden (TMB) and gene expression profiling (GEP) have complementary effects, they may have improved predictive power when used in combination. Here, we investigated the ability of TMB and GEP to predict the immunotherapy response in patients with non–small cell lung cancer (NSCLC) and assessed if this combination can improve predictive power compared to that when used individually. @*Materials and Methods@#This retrospective cohort study included 30 patients with NSCLC who received immune checkpoint inhibitors (ICI) therapy at the Seoul National University Bundang Hospital. programmed cell death-ligand-1 (PD-L1) protein expression was assessed using immunohistochemistry, and TMB was measured by targeted deep sequencing. Gene expression was determined using NanoString nCounter analysis for the PanCancer IO360 panel, and enrichment analysis were performed. @*Results@#Eleven patients (36.7%) showed a durable clinical benefit (DCB), whereas 19 (63.3%) showed no durable benefit (NDB). TMB and enrichment scores (ES) showed significant differences between the DCB and NDB groups (p=0.044 and p=0.017, respectively); however, no significant correlations were observed among TMB, ES, and PD-L1. ES was the best single biomarker for predicting DCB (area under the curve [AUC], 0.794), followed by TMB (AUC, 0.679) and PD-L1 (AUC, 0.622). TMB and ES showed the highest AUC (0.837) among other combinations (AUC [TMB and PD-L1], 0.777; AUC [PD-L1 and ES], 0.763) and was similar to that of all biomarkers used together (0.832). @*Conclusion@#The combination of TMB and ES may be an effective predictive tool to identify patients with NSCLC patients who would possibly benefit from ICI therapies.

3.
Biomolecules & Therapeutics ; : 321-330, 2021.
Article in English | WPRIM | ID: wpr-889614

ABSTRACT

Oxidative stress plays a crucial role in the development of neuronal disorders including brain ischemic injury. Thioredoxin 1 (Trx1), a 12 kDa oxidoreductase, has anti-oxidant and anti-apoptotic functions in various cells. It has been highly implicated in brain ischemic injury. However, the protective mechanism of Trx1 against hippocampal neuronal cell death is not identified yet. Using a cell permeable Tat-Trx1 protein, protective mechanism of Trx1 against hydrogen peroxide-induced cell death was examined using HT-22 cells and an ischemic animal model. Transduced Tat-Trx1 markedly inhibited intracellular ROS levels, DNA fragmentation, and cell death in H 2O 2-treatment HT-22 cells. Tat-Trx1 also significantly inhibited phosphorylation of ASK1 and MAPKs in signaling pathways of HT-22 cells. In addition, Tat-Trx1 regulated expression levels of Akt, NF-κB, and apoptosis related proteins. In an ischemia animal model, Tat-Trx1 markedly protected hippocampal neuronal cell death and reduced astrocytes and microglia activation. These findings indicate that transduced Tat-Trx1 might be a potential therapeutic agent for treating ischemic injury.

4.
The Korean Journal of Pain ; : 479-486, 2021.
Article in English | WPRIM | ID: wpr-903826

ABSTRACT

Background@#Prior studies have reported that 40%-90% of the patients with celiac plexus-mediated visceral pain benefit from the neurolytic celiac plexus block (NCPB), but the predictive factors of response to NCPB have not been evaluated extensively. This study aimed to identify the factors associated with the immediate analgesic effectiveness of NCPB in patients with intractable upper abdominal cancer-related pain. @*Methods@#A retrospective review was performed of 513 patients who underwent NCPB for upper abdominal cancer-related pain. Response to the procedure was defined as (1) a decrease of ≥ 50% or ≥ 4 points on the numerical rating scale (NRS) in pain intensity from the baseline without an increase in opioid requirement, or (2) a decrease of ≥ 30% or ≥ 2 points on the NRS from the baseline with simultaneously reduced opioid consumption after NCPB. Logistic regression analysis was performed to determine the factors associated with successful responses to NCPB. @*Results@#Among the 513 patients included in the analysis, 255 (49.8%) and 258 (50.2%) patients were in the non-responder and responder group after NCPB, respectively. Multivariable logistic regression analysis showed that diabetes (odds ratio [OR] = 0.644, P = 0.035), history of upper abdominal surgery (OR = 0.691, P = 0.040), and celiac metastasis (OR = 1.496, P = 0.039) were the independent factors associated with response to NCPB. @*Conclusions@#Celiac plexus metastases, absence of diabetes, and absence of prior upper abdominal surgery may be independently associated with better response to NCPB for upper abdominal cancer-related pain.

5.
Biomolecules & Therapeutics ; : 321-330, 2021.
Article in English | WPRIM | ID: wpr-897318

ABSTRACT

Oxidative stress plays a crucial role in the development of neuronal disorders including brain ischemic injury. Thioredoxin 1 (Trx1), a 12 kDa oxidoreductase, has anti-oxidant and anti-apoptotic functions in various cells. It has been highly implicated in brain ischemic injury. However, the protective mechanism of Trx1 against hippocampal neuronal cell death is not identified yet. Using a cell permeable Tat-Trx1 protein, protective mechanism of Trx1 against hydrogen peroxide-induced cell death was examined using HT-22 cells and an ischemic animal model. Transduced Tat-Trx1 markedly inhibited intracellular ROS levels, DNA fragmentation, and cell death in H 2O 2-treatment HT-22 cells. Tat-Trx1 also significantly inhibited phosphorylation of ASK1 and MAPKs in signaling pathways of HT-22 cells. In addition, Tat-Trx1 regulated expression levels of Akt, NF-κB, and apoptosis related proteins. In an ischemia animal model, Tat-Trx1 markedly protected hippocampal neuronal cell death and reduced astrocytes and microglia activation. These findings indicate that transduced Tat-Trx1 might be a potential therapeutic agent for treating ischemic injury.

6.
The Korean Journal of Pain ; : 479-486, 2021.
Article in English | WPRIM | ID: wpr-896122

ABSTRACT

Background@#Prior studies have reported that 40%-90% of the patients with celiac plexus-mediated visceral pain benefit from the neurolytic celiac plexus block (NCPB), but the predictive factors of response to NCPB have not been evaluated extensively. This study aimed to identify the factors associated with the immediate analgesic effectiveness of NCPB in patients with intractable upper abdominal cancer-related pain. @*Methods@#A retrospective review was performed of 513 patients who underwent NCPB for upper abdominal cancer-related pain. Response to the procedure was defined as (1) a decrease of ≥ 50% or ≥ 4 points on the numerical rating scale (NRS) in pain intensity from the baseline without an increase in opioid requirement, or (2) a decrease of ≥ 30% or ≥ 2 points on the NRS from the baseline with simultaneously reduced opioid consumption after NCPB. Logistic regression analysis was performed to determine the factors associated with successful responses to NCPB. @*Results@#Among the 513 patients included in the analysis, 255 (49.8%) and 258 (50.2%) patients were in the non-responder and responder group after NCPB, respectively. Multivariable logistic regression analysis showed that diabetes (odds ratio [OR] = 0.644, P = 0.035), history of upper abdominal surgery (OR = 0.691, P = 0.040), and celiac metastasis (OR = 1.496, P = 0.039) were the independent factors associated with response to NCPB. @*Conclusions@#Celiac plexus metastases, absence of diabetes, and absence of prior upper abdominal surgery may be independently associated with better response to NCPB for upper abdominal cancer-related pain.

7.
Laboratory Animal Research ; : 158-166, 2020.
Article | WPRIM | ID: wpr-836913

ABSTRACT

Fat-mass and obesity-associated protein (Fto) is highly expressed in the brain including, the hippocampus, and its expression is significantly decreased in the brain of Alzheimer’s disease patients. In the present study, we measured Fto immunoreactivity and protein levels in the hippocampus of obese and aged mice, which were induced by high-fat diet for 12 weeks and D-galactose treatment for 10 weeks, respectively. The obesity and aging phenotypes were assessed by physiological parameters and Morris water maze test, respectively. High fat diet fed mice showed significant increases in body weight and blood glucose levels compared to that in the control or D-galactose-induced aged mice. In addition, treatment with D-galactose significantly decreased the spatial memory. Fto immunoreactivity in the control group was mainly detected in the pyramidal cells of the CA1 and CA3 regions and in the granule cells of the dentate gyrus. In the hippocampus of high-fat diet-fed mice, Fto immunoreactive structures were similarly found in the hippocampus compared to that in the control group, but Fto immunoreactivity in high-fat diet-fed mice was also found in the stratum oriens and radiatum of the CA1 and CA3 regions and the polymorphic layer of the dentate gyrus. In the hippocampus of D-galactose-induced aged mice, fewer Fto immunoreactive structures were detected in the granule cell layer of the dentate gyrus compared to the control group. Fto mRNA and protein levels based on quantitative real-time polymerase chain reaction and western blot assays were slightly increased in the hippocampus of high-fat diet-fed mice compared to that in control mice. In addition, Fto mRNA and protein levels were significantly decreased in the aged hippocampus compared to that in the control group. Fto protein levels are susceptible to the aging process, but not in the hippocampus of high-fat diet-induced obesity. The reduction of Fto in aged mice may be associated with reduced memory impairment in mice.

8.
Cancer Research and Treatment ; : 1120-1134, 2020.
Article | WPRIM | ID: wpr-831140

ABSTRACT

Purpose@#Despite advances in treatment, lung cancer remains the leading cause of cancer mortality. This study aimed to characterise genome-wide tumorigenesis events and to understand the hypothesis of the multistep carcinogenesis of lung adenocarcinoma (LUAD) @*Materials and Methods@#We conducted multiregion whole-exome sequencing of LUAD with synchronous atypical adenomatous hyperplasia (AAH), adenocarcinoma in situ, or minimally invasive adenocarcinoma of 19 samples from three patients to characterize genome-wide tumorigenesis events and validate the hypothesis of the multistep carcinogenesis of LUAD. We identified potential pathogenic mutations preserved in preinvasive lesions and supplemented the finding by allelic variant level from RNA sequencing. @*Results@#Overall, independent mutational profiles were observed per patient and between patients. Some shared mutations including epidermal growth factor receptor (EGFR , p.L858R) were present across synchronous lesions. @*Conclusion@#Here, we show that there are driver gene mutations in AAH, and they may exacerbate as a sequence in a histological continuum, supporting the Darwinian evolution model of cancer genome. The intertumoral and intratumoral heterogeneity of synchronous LUAD implies that multi-biomarker strategies might be necessary for appropriate treatment.

9.
Korean Journal of Dermatology ; : 40-41, 2019.
Article in Korean | WPRIM | ID: wpr-719703

ABSTRACT

No abstract available.


Subject(s)
Cellulitis , Klebsiella pneumoniae , Klebsiella , Leg
10.
Annals of Dermatology ; : S64-S65, 2019.
Article in English | WPRIM | ID: wpr-762399

ABSTRACT

No abstract available.


Subject(s)
Giant Cells , Granuloma, Giant Cell , Hot Temperature
11.
Experimental Neurobiology ; : 612-627, 2019.
Article in English | WPRIM | ID: wpr-763785

ABSTRACT

Aldose reductase (AR) protein, a member of the NADPH-dependent aldo-keto reductase family, reduces a wide range of aldehydes and enhances cell survival by inhibition of oxidative stress. Oxidative stress is known as one of the major pathological factor in ischemia. Since the precise function of AR protein in ischemic injury is fully unclear, we examined the function of AR protein in hippocampal neuronal (HT-22) cells and in an animal model of ischemia in this study. Cell permeable Tat-AR protein was produced by fusion of protein transduction domain in Tat for delivery into the cells. Tat-AR protein transduced into HT-22 cells and significantly inhibited cell death and regulated the mitogen-activate protein kinases (MAPKs), Bcl-2, Bax, and Caspase-3 under oxidative stress condition. In an ischemic animal model, Tat-AR protein transduced into the brain tissues through the blood-brain barrier (BBB) and drastically decreased neuronal cell death in hippocampal CA1 region. These results indicate that transduced Tat-AR protein has protective effects against oxidative stress-induced neuronal cell death in vitro and in vivo, suggesting that Tat-AR protein could be used as potential therapeutic agent in ischemic injury.


Subject(s)
Humans , Aldehyde Reductase , Aldehydes , Blood-Brain Barrier , Brain , CA1 Region, Hippocampal , Caspase 3 , Cell Death , Cell Survival , In Vitro Techniques , Ischemia , Models, Animal , Neurons , Oxidative Stress , Oxidoreductases , Protein Kinases
12.
Journal of Pathology and Translational Medicine ; : 86-93, 2019.
Article in English | WPRIM | ID: wpr-766014

ABSTRACT

BACKGROUND: Both human leukocyte antigen (HLA) class I and programmed death-ligand 1 (PD-L1) molecules are known to play important roles in cancer immunity. In this study, we evaluated HLA class I expression in resected adenocarcinoma of the lung, and investigated its prognostic impact in correlation with PD-L1 expression. METHODS: HLA class I and PD-L1 expression was evaluated by immunohistochemistry in a total of 403 resected lung adenocarcinomas using tissue microarray. Correlations between the expression of HLA class I/PD-L1 and clinicopathologic features and prognostic significance were analyzed. RESULTS: HLA class I expression was reduced in 91.6% of adenocarcinoma, and more frequently reduced in patients with younger age, absence of vascular invasion, and low pathologic stage (p = .033, p = .007, and p = .012, respectively). Positive PD-L1 expression in tumor cells was 16.1% (1% cut-off), and associated with poor differentiation, presence of vascular invasion and nodal metastasis (p < .001, p = .002, and p = .032, respectively). On survival analysis, HLA class I or PD-L1 expression alone did not show any statistical significance. On the integrated analysis, HLA class I (+)/PD-L1 (+) subgroup showed a significantly shorter overall survival than other groups (p = .001). Multivariate analysis revealed that coexpression of HLA class I and PD-L1 was an independent poor prognostic factor of lung adenocarcinoma. (p < .001; hazard ratio, 6.106; 95% confidence interval, 2.260 to 16.501). CONCLUSIONS: Lung adenocarcinoma with coexpression of HLA class I and PD-L1 was associated with poor prognosis. This subgroup may evade immune attack by expressing PD-L1 protein despite HLA expression.


Subject(s)
Humans , Adenocarcinoma , Carcinoma, Non-Small-Cell Lung , Immunohistochemistry , Leukocytes , Lung , Multivariate Analysis , Neoplasm Metastasis , Prognosis
13.
Laboratory Animal Research ; : 154-164, 2019.
Article in English | WPRIM | ID: wpr-786408

ABSTRACT

In the present study, we investigated the effects of heat shock protein 70 (HSP70) on novel object recognition, cell proliferation, and neuroblast differentiation in the hippocampus. To facilitate penetration into the blood–brain barrier and neuronal plasma membrane, we created a Tat-HSP70 fusion protein. Eight-week-old mice received intraperitoneal injections of vehicle (10% glycerol), control-HSP70, or Tat-HSP70 protein once a day for 21 days. To elucidate the delivery efficiency of HSP70 into the hippocampus, western blot analysis for polyhistidine was conducted. Polyhistidine protein levels were significantly increased in control-HSP70- and Tat-HSP70-treated groups compared to the control or vehicle-treated group. However, polyhistidine protein levels were significantly higher in the Tat-HSP70-treated group compared to that in the control-HSP70-treated group. In addition, immunohistochemical study for HSP70 showed direct evidences for induction of HSP70 immunoreactivity in the control-HSP70- and Tat-HSP70-treated groups. Administration of Tat-HSP70 increased the novel object recognition memory compared to untreated mice or mice treated with the vehicle. In addition, the administration of Tat-HSP70 significantly increased the populations of proliferating cells and differentiated neuroblasts in the dentate gyrus compared to those in the control or vehicle-treated group based on the Ki67 and doublecortin (DCX) immunostaining. Furthermore, the phosphorylation of cAMP response element-binding protein (pCREB) was significantly enhanced in the dentate gyrus of the Tat-HSP70-treated group compared to that in the control or vehicle-treated group. Western blot study also demonstrated the increases of DCX and pCREB protein levels in the Tat-HSP70-treated group compared to that in the control or vehicle-treated group. In contrast, administration of control-HSP70 moderately increased the novel object recognition memory, cell proliferation, and neuroblast differentiation in the dentate gyrus compared to that in the control or vehicle-treated group. These results suggest that Tat-HSP70 promoted hippocampal functions by increasing the pCREB in the hippocampus.


Subject(s)
Animals , Mice , Blotting, Western , Cell Membrane , Cell Proliferation , Cyclic AMP Response Element-Binding Protein , Dentate Gyrus , Heat-Shock Proteins , Hippocampus , Hot Temperature , HSP70 Heat-Shock Proteins , Injections, Intraperitoneal , Memory , Neurons , Phosphorylation
14.
Korean Journal of Dermatology ; : 406-407, 2018.
Article in English | WPRIM | ID: wpr-715722

ABSTRACT

No abstract available.


Subject(s)
Dextrans , Giant Cells , Granuloma, Foreign-Body
15.
Annals of Dermatology ; : 688-693, 2018.
Article in English | WPRIM | ID: wpr-719023

ABSTRACT

BACKGROUND: There are few pharmacologic options to reduce erythema and flushing in patients with recalcitrant erythematotelangiectatic rosacea (ETR). We previously reported two cases of refractory flushing and erythema of rosacea that were successfully treated with intradermal botulinum toxin injection, and additional research is needed to prove the efficacy and safety of this treatment. OBJECTIVE: To report the efficacy and safety of botulinum toxin injection as an aid in persistent erythema of rosacea patients. METHODS: A total of 20 Korean patients with recalcitrant ETR were enrolled to receive treatment by injection of botulinum toxin. Patients received one treatment of intradermal botulinum toxin injection and were assessed 1, 2, 4, and 8 weeks after treatment. The severity of erythema and telangiectasia was investigated by a non-treating physician, and the Erythema Index (EI) was assessed by mexameter at each visit. Patient satisfaction and any adverse events were also assessed at each visit. RESULTS: 17 patients completed all follow-up visits and were included in the analysis. Intradermal injection of botulinum toxin significantly reduced erythema severity and EI in ETR patients. Patients reported a satisfaction score of 2.94±0.56 at 8 weeks after treatment. Except for three patients who discontinued the study early due to inconvenience of facial muscle paralysis, 17 patients participating in the final analysis did not report side effects except injection pain at the time of the procedure. CONCLUSION: Intradermal injection of botulinum toxin can be used as an effective and relatively safe adjuvant agent for recalcitrant and persistent erythema of ETR patients.


Subject(s)
Humans , Botulinum Toxins , Erythema , Facial Muscles , Flushing , Follow-Up Studies , Injections, Intradermal , Paralysis , Patient Satisfaction , Pilot Projects , Rosacea , Telangiectasis
16.
Laboratory Animal Research ; : 176-184, 2018.
Article in English | WPRIM | ID: wpr-718851

ABSTRACT

In this study, we observed chronological changes in the immunoreactivity and expression level of myelin basic protein (MBP), one of the most abundant proteins in the central nervous system, in the hippocampus of Zucker diabetic fatty (ZDF) rats and their control littermates (Zucker lean control; ZLC). In the ZLC group, body weight steadily increased with age; the body weight of the ZDF group, however, peaked at 30 weeks of age, and subsequently decreased. Based on the changes of body weight, animals were divided into the following six groups: early (12-week), middle (30-week), and chronic (52-week) diabetic groups and their controls. MBP immunoreactivity was found in the alveus, strata pyramidale, and lacunosum-moleculare of the CA1 region, strata pyramidale and radiatum of the CA3 region, and subgranular zone, polymorphic layer, and molecular layer of the dentate gyrus. MBP immunoreactivity was lowest in the hippocampus of 12-week-old rats in the ZLC group, and highest in 12-week-old rats in the ZDF group. Diabetes increased MBP levels in the 12-week-old group, while MBP immunoreactivity decreased in the 30-week-old group. In the 52-week-old ZLC and ZDF groups, MBP immunoreactivity was detected in the hippocampus, similar to the 30-week-old ZDF group. Western blot results corroborated with immunohistochemical results. These results suggested that changes in the immunoreactivity and expression of MBP in the hippocampus might be a compensatory response to aging, while the sustained levels of MBP in diabetic animals could be attributed to a loss of compensatory responses in oligodendrocytes.


Subject(s)
Animals , Rats , Aging , Blotting, Western , Body Weight , Central Nervous System , Dentate Gyrus , Hippocampus , Models, Animal , Myelin Basic Protein , Myelin Sheath , Oligodendroglia
17.
Laboratory Animal Research ; : 239-247, 2018.
Article in English | WPRIM | ID: wpr-718843

ABSTRACT

Bacopa monnieri is a medicinal plant with a long history of use in Ayurveda, especially in the treatment of poor memory and cognitive deficits. In the present study, we hypothesized that Bacopa monnieri extract (BME) can improve memory via increased cell proliferation and neuroblast differentiation in the dentate gyrus. BME was administered to 7-week-old mice once a day for 4 weeks and a novel object recognition memory test was performed. Thereafter, the mice were euthanized followed by immunohistochemistry analysis for Ki67, doublecortin (DCX), and phosphorylated cAMP response element-binding protein (CREB), and western blot analysis of brain-derived neurotrophic factor (BDNF). BME-treated mice showed moderate increases in the exploration of new objects when compared with that of familiar objects, leading to a significant higher discrimination index compared with vehicle-treated mice. Ki67 and DCX immunohistochemistry showed a facilitation of cell proliferation and neuroblast differentiation following the administration of BME in the dentate gyrus. In addition, administration of BME significantly elevated the BDNF protein expression in the hippocampal dentate gyrus, and increased CREB phosphorylation in the dentate gyrus. These data suggest that BME improves novel object recognition by increasing the cell proliferation and neuroblast differentiation in the dentate gyrus, and this may be closely related to elevated levels of BDNF and CREB phosphorylation in the dentate gyrus.


Subject(s)
Animals , Mice , Bacopa , Blotting, Western , Brain-Derived Neurotrophic Factor , Cell Proliferation , Cognition Disorders , Cyclic AMP Response Element-Binding Protein , Dentate Gyrus , Discrimination, Psychological , Immunohistochemistry , Memory , Neurogenesis , Phosphorylation , Plants, Medicinal
18.
Journal of Pathology and Translational Medicine ; : 232-237, 2018.
Article in English | WPRIM | ID: wpr-741181

ABSTRACT

Primary combined hepatocellular carcinoma (HCC) and neuroendocrine carcinoma is a rare entity, and so is hypercalcemia due to ectopic parathyroid hormone (PTH) secretion by tumor. A 44-year-old man with hepatitis B virus associated chronic liver disease presented with a hepatic mass. Hemihepatectomy discovered the mass as combined HCC and poorly differentiated cholangiocarcinoma. During adjuvant chemoradiation therapy, he presented with nausea, and multiple systemic metastases were found. Laboratory tests revealed hypercalcemia with markedly elevated PTH and neuron specific enolase. Parathyroid scan showed normal uptake in parathyroid glands, suggestive of ectopic PTH secretion. Subsequently, immunohistochemistry of neuroendocrine marker was performed on the primary lesion, and confirmed the neuroendocrine differentiation in non-HCC component. The patient died 71 days after surgery. This report may suggest the possibility of ectopic PTH secretion by neuroendocrine carcinoma of hepatic origin causing hypercalcemia. Caution for neuroendocrine differentiation should be exercised when diagnosing poorly differentiated HCC.


Subject(s)
Adult , Humans , Carcinoma, Hepatocellular , Carcinoma, Neuroendocrine , Cholangiocarcinoma , Hepatitis B virus , Hypercalcemia , Immunohistochemistry , Liver , Liver Diseases , Nausea , Neoplasm Metastasis , Parathyroid Glands , Parathyroid Hormone , Phosphopyruvate Hydratase
19.
Journal of Pathology and Translational Medicine ; : 130-132, 2018.
Article in English | WPRIM | ID: wpr-741157

ABSTRACT

No abstract available.


Subject(s)
Adenocarcinoma
20.
Laboratory Animal Research ; : 58-64, 2018.
Article in English | WPRIM | ID: wpr-715046

ABSTRACT

In the present study, we compared the cell-specific expression and changes protein levels in the glucose transporters (GLUTs) 1 and 3, the major GLUTs in the mouse and gerbil brains using immunohistochemistry and Western blot analysis. In both mouse and gerbils, GLUT1 immunoreactivity was mainly found in the blood vessels in the dentate gyrus, while GLUT3 immunoreactivity was detected in the subgranular zone and the molecular layer of the dentate gyrus. GLUT1-immunoreactivity in blood vessels and GLUT1 protein levels were significantly decreased with age in the mice and gerbils, respectively. In addition, few GLUT3-immunoreactive cells were found in the subgranular zone in aged mice and gerbils, but GLUT3-immunoreactivity was abundantly found in the polymorphic layer of dentate gyrus in mice and gerbils with a dot-like pattern. Based on the double immunofluorescence study, GLUT3-immunoreactive structures in gerbils were localized in the glial fibrillary acidic protein-immunoreactive astrocytes in the dentate gyrus. Western blot analysis showed that GLUT3 expression in the hippocampal homogenates was slightly, although not significantly, decreased with age in mice and gerbils, respectively. These results indicate that the reduction in GLUT1 in the blood vessels of dentate gyrus and GLUT3 in the subgranular zone of dentate gyrus may be associated with the decrease in uptake of glucose into brain and neuroblasts in the dentate gyrus. In addition, the expression of GLUT3 in the astrocytes in polymorphic layer of dentate gyrus may be associated with metabolic changes in glucose in aged hippocampus.


Subject(s)
Animals , Mice , Aging , Astrocytes , Blood Vessels , Blotting, Western , Brain , Dentate Gyrus , Fluorescent Antibody Technique , Gerbillinae , Glucose Transport Proteins, Facilitative , Glucose Transporter Type 1 , Glucose , Hippocampus , Immunohistochemistry
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