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Primary gastrointestinal (GI) T-cell and natural killer (NK)-cell lymphomas/lymphoproliferative disorders (LPD) are uncommon, and they are usually aggressive in nature. However, T-cell and NK-cell lymphoma/LPD of the GI tract with indolent clinical course has been reported over the past 2 decades. Indolent T-cell LPD was formally proposed a decade ago in 2013 and 4 years later recognized as a provisional entity by the revised fourth edition of WHO Classification of Tumours of Haematopoietic and Lymphoid Tissues in 2017. Indolent T-cell LPD of the GI tract has been changed to indolent T-cell lymphoma of the GI tract as a distinct entity by the fifth edition of WHO Classification of Haematolymphoid Tumours, but the International Consensus Classification of mature lymphoid neoplasms prefers indolent clonal T-cell LPD of the GI tract instead. In the past decade, indolent lymphoma/LPD of the GI tract has been expanded to NK cells, and as such, indolent NK-cell LPD of the GI tract was recognized as an entity by both the fifth edition of WHO Classification of Haematolymphoid Tumours and the International Consensus Classification. The underlying genetic/molecular mechanisms of both indolent T-cell lymphoma/LPD of the GI tract and indolent NK-cell LPD of the GI tract have been recently discovered. In this review, we describe the history; salient clinical, cytohistomorphologic, and immunohistochemical features; and genetic/genomic landscape of both entities. In addition, we also summarize the mimics and differential diagnosis. Finally, we propose future directions with regard to the pathogenesis and clinical management.
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Linfoma de Células T , Linfoma , Transtornos Linfoproliferativos , Humanos , Linfoma/diagnóstico , Linfoma/patologia , Trato Gastrointestinal/patologia , Células Matadoras Naturais , Linfoma de Células T/diagnóstico , Linfócitos T/patologia , Transtornos Linfoproliferativos/diagnóstico , Transtornos Linfoproliferativos/patologiaRESUMO
To characterize the clinicopathologic features of pulmonary sclerosing pneumocytoma (PSP) and compare these features between the tumors with and without metastasis, 68 cases of PSP (1/68 [1.47%] with metastasis) diagnosed from 2009-2022 in our hospital and 15 previously reported metastasizing cases were studied. There were 54 female patients and 14 male patients, with age ranging from 17 to 72 years and tumor size ranging from 0.1 to 5.5 cm (mean, 1.75 cm). In all, 85.4% of the cases presented with ≥2 patterns, including papillary, sclerotic, solid, and hemorrhagic. Thyroid transcription factor 1, epithelial membrane antigen, CKpan, and CK7 were expressed in surface cells in 100% of the cases and napsin A was expressed in 90% of the cases. Stromal cell expression of these markers occurred in 100%, 93.9%, 13.5%, 13.8%, and 0% of the cases, respectively. Of the 16 PSP cases with metastasis, 8 were female patients and 7 were male patients, with age ranging from 14 to 73 years. The tumor size ranged from 2.5 to 12 cm (mean, 4.85 cm). Forty-five of the cases were negative for BRAF V600E immunostaining and 6 were focally weak positive, in which fluorescent PCR tests showed no detectable mutations. There were significant differences in gender, age, and tumor size between PSP cases with and without metastasis. No BRAF V600E mutation was found in patients with PSP. AKT1 p.E17K mutations were detected in both the primary lung tumor and the lymph node metastatic tumor of our PSP case with lymph node metastasis. In conclusion, PSP is an uncommon pulmonary neoplasm with significant female predilection and has distinct morphologic and immunohistochemical characteristics. The BRAFV600E mutation was not detectable in patients with PSP and thus may not involve in its tumorigenesis. Most PSP tumors are benign, with a minority exhibiting potential for metastasis and malignant behavior.
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Neoplasias Pulmonares , Hemangioma Esclerosante Pulmonar , Neoplasias da Glândula Tireoide , Humanos , Masculino , Feminino , Adolescente , Adulto Jovem , Adulto , Pessoa de Meia-Idade , Idoso , Pulmão/patologia , Hemangioma Esclerosante Pulmonar/genética , Hemangioma Esclerosante Pulmonar/diagnóstico , Hemangioma Esclerosante Pulmonar/patologia , Neoplasias Pulmonares/genética , Neoplasias Pulmonares/patologia , Metástase Linfática/patologia , Proteínas Proto-Oncogênicas B-raf/genética , Neoplasias da Glândula Tireoide/patologiaRESUMO
AIMS: To compare the fibroinflammatory diseases Kimura's disease (KD) and immunoglobulin (Ig)G4-related disease (IgG4RD) and to explore their possible relationship. METHODS AND RESULTS: Forty-six cases of KD and 29 IgG4RD from our institution diagnosed from 2011 to 2020 were studied. They were compared with each other on clinical, pathological and immunohistological features. There were similar clinical features, except that IgG4RD affected an older patient population, with more frequent salivary gland involvement and KD affected head and neck lymph nodes, and showed blood eosinophilia more frequently than IgG4RD. IgG4RD exhibited frequent storiform fibrosis and obliterative phlebitis, while KD showed more frequent tissue eosinophilia, eosinophilic abscess, germinal centre eosinophilic deposit and vascularisation. Twenty to 30% of KD had more than 50 IgG4+ plasma cells (PC) per high-power field (HPF) and IgG4/IgG+ PC ratio exceeding 40%. These parameters, however, occurred in 100% of IgG4RD. Significantly more KD had >10 IgE+ PC/HPF and lymphoid germinal centre IgE reticular staining compared to IgG4RD. All these histological and immunohistological features are overlapping in the two diseases, although they differed with statistical significance. CONCLUSION: Our study confirmed that there is significant overlap in clinical, pathological and immunohistological features between KD and IgG4RD. It is important to recognise these overlapping features, and correlation with a clinicopathological picture is required in differential diagnoses. The overlapping features also suggest a possible close relationship between KD and IgG4RD, which could represent different facets of a continuous fibroinflammatory disease spectrum.
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Doença Relacionada a Imunoglobulina G4 , Doença de Kimura , Diagnóstico Diferencial , Eosinofilia/patologia , Eosinófilos/patologia , Feminino , Humanos , Imunoglobulina E/metabolismo , Imunoglobulina G/metabolismo , Doença Relacionada a Imunoglobulina G4/diagnóstico , Doença Relacionada a Imunoglobulina G4/patologia , Doença de Kimura/diagnóstico , Doença de Kimura/patologia , MasculinoRESUMO
C3N4 is widely applied in the synthesis of single-atom catalysts. However, understanding on the active site and the reaction mechanism is not fully in consensus. Especially, bare studies have considered the coordination environment of the single-atomic dopant and the effect of nitrogen vacancy on C3N4. In this study, we found that the presence of nitrogen vacancies promotes the activation of water and reduces the activation energy barrier for hydrogen generation. The results show that a synergistic effect between single-atom Pt and nitrogen vacancies enables the catalyst to achieve a superior hydrogen production rate of 3,890 µmol/g/h, which is 16.8 times higher than that of pristine C3N4. Moreover, the catalyst is also applicable for photocatalytic hydrogen production from seawater without significantly decreased hydrogen production rate. This study paves the way for the rational design and optimization of next-generation photocatalysts for sustainable energy applications, particularly in solar-driven hydrogen production.
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BACKGROUND & AIMS: Largazole is a novel histone deacetylase (HDAC) inhibitor. This study investigated the effects of largazole against liver fibrosis. METHODS: The in vitro effects of largazole were examined using hepatic stellate cells (HSCs). In vivo effects of largazole were studied using a mouse liver fibrotic model induced by CCl4 . RESULTS: Largazole augmented acetylation of histone H3 (H3) and histone H4 (H4) in HSCs. It directly inhibited the activation of HSCs owing to HDAC inhibitory activity as the antifibrotic effect of largazole was significantly decreased in cells with HDAC1, HDAC2 and HDAC3 knockdown. Largazole also induced apoptosis of HSCs. Largazole not only inhibited the expression of TGFßR2, but also reduced phosphorylation of Smad2 and Akt induced by TGF-ß1. Largazole also inhibited the expression of vascular endothelial growth factor (VEGF) and its receptor. VEGF-induced proliferation of HSCs and activation of Akt and p38MAPK were also suppressed by largazole. In vivo, largazole reduced the expression of collagen I, α-smooth muscle actin and tissue inhibitor of metalloproteinase-1 in CCl4 -induced fibrosis, and these antifibrotic effects were associated with increased acetylation of H3 and H4. Largazole also induced HSCs to undergo apoptosis in vivo, which was correlated with downregulation of bcl-2 and bcl-xL. Furthermore, largazole inhibited angiogenesis in vivo as evidenced by reduced expression of CD34, VEGF and VEGFR. In addition to its antifibrotic activity, the drug reduced inflammatory activity in CCl4 -induced liver fibrosis. CONCLUSIONS: Our findings revealed a novel role of largazole in the treatment of liver fibrosis. Through multiple mechanisms, largazole could be a potentially effective antifibrotic agent.
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Inibidores da Angiogênese/farmacologia , Depsipeptídeos/farmacologia , Inibidores de Histona Desacetilases/farmacologia , Histona Desacetilases/metabolismo , Cirrose Hepática Experimental/prevenção & controle , Fígado/efeitos dos fármacos , Neovascularização Fisiológica/efeitos dos fármacos , Transdução de Sinais/efeitos dos fármacos , Tiazóis/farmacologia , Fator de Crescimento Transformador beta/metabolismo , Fator A de Crescimento do Endotélio Vascular/metabolismo , Acetilação , Animais , Apoptose/efeitos dos fármacos , Tetracloreto de Carbono , Linhagem Celular , Relação Dose-Resposta a Droga , Células Estreladas do Fígado/efeitos dos fármacos , Células Estreladas do Fígado/enzimologia , Células Estreladas do Fígado/patologia , Histona Desacetilases/genética , Histonas/metabolismo , Humanos , Fígado/irrigação sanguínea , Fígado/enzimologia , Fígado/patologia , Cirrose Hepática Experimental/induzido quimicamente , Cirrose Hepática Experimental/enzimologia , Cirrose Hepática Experimental/patologia , Masculino , Camundongos , Camundongos Endogâmicos BALB C , Interferência de RNA , Ratos , Fatores de Tempo , TransfecçãoRESUMO
We explored the application of TFE3 immunostaining and TFE3 mRNA expression in the differential diagnosis and prognostication of adrenal cortical tumors and distinction of the latter from clear cell renal cell carcinoma (ccRCC) which show significant morphologic overlap. TFE3 immunostaining was performed on a large cohort of samples including 40 adrenal cortex tissues, 95 adrenocortical adenoma (ACA), 11 adrenocortical carcinoma (ACC), 53 ccRCC, and 18 pheochromocytomas. TFE3 was compared with other immunomarkers melan-A, inhibin-α, synaptophysin, chromogranin A, CAIX and CD10. One hundred percent normal adrenal cortices and 94% ACA were strongly and diffusely stained for TFE3 while no ACC showed diffuse staining. TFE3 is thus useful in distinguishing ACA from ACC. TFE3 is also useful in separating ACC from ccRCC as 64% ACC showed partial, while only 7% of ccRCC showed partial TFE3 staining. Only 1 pheochromocytoma showed focal weak TFE3 staining. Results also demonstrated superiority of TFE3 over other commonly used immunomarkers. TFE3 gene rearrangement testing by fluorescence in situ hybridization showed no rearrangement in 6 TFE3 positive adrenal tumors. TFE3 mRNA were analyzed by the Cancer Genome Atlas database and we found TFE3 mRNA expression correlated with overall patient survival in ACC. Our study showed usefulness of TFE3 in distinguishing ACA from ACC, and ACC from ccRCC. TFE3 is superior over other commonly used immunomarkers for adrenal tumors. In addition, decreased TFE3 immunoexpression and TFE3 mRNA expression may carry poor prognostic implication in adrenal tumors.
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Neoplasias das Glândulas Suprarrenais , Neoplasias Renais , Humanos , Hibridização in Situ Fluorescente , Cromogranina A , Neoplasias Renais/diagnóstico , Neoplasias Renais/genética , Fatores de Transcrição de Zíper de Leucina e Hélice-Alça-Hélix Básicos/genéticaRESUMO
Proline, glutamate, and leucine-rich protein 1 (PELP1) are involved in several cancers, but little is known about PELP1 in lung cancer. In this study, PELP1 expression was evaluated in 305 lung cancer (NSCLC) specimens to explore the role of PELP1 in lung cancer. After silencing PELP1, the proliferation, migration, invasion of tumor cells, PELP1 in relation to cell cycle and signaling pathways were evaluated, and whole-genome exons were analyzed. PELP1 is overexpressed in lung cancer, PELP1 expression correlated with squamous carcinoma, smoking, and wild-type EGFR status (all Ps<0.001) but associated with lung cancer-specific survival (P > 0.05). Silencing significantly inhibited lung cancer cell proliferation, migration, and invasion (P < 0.05) and promoted high sensitivity of lung cancer cells to tyrosine kinase inhibitor (TKI) gefitinib. PELP1-silenced cells showed downregulated phosphorylated MAPK, cyclinD1, CDK2, and upregulated RB (P < 0.05) but no change in AKT. In PELP1-silenced lung cancer cells, 140 genes were upregulated, and 143 genes were downregulated. Furthermore, the number of T regulatory cell was higher in lung adenocarcinoma with pelp1 high-expression and pelp1 expression was negatively correlated with CD274 (PDL-1) and CTLA4. Therefore, PELP1 plays an important role in the malignant behavior of NSCLC and could be a potential therapeutic target.
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Carcinoma Pulmonar de Células não Pequenas , Neoplasias Pulmonares , Humanos , Gefitinibe/farmacologia , Gefitinibe/uso terapêutico , Antígeno CTLA-4 , Proteínas Proto-Oncogênicas c-akt/metabolismo , Proteínas Correpressoras/genética , Leucina/uso terapêutico , Fatores de Transcrição/metabolismo , Neoplasias Pulmonares/tratamento farmacológico , Neoplasias Pulmonares/genética , Neoplasias Pulmonares/patologia , Carcinoma Pulmonar de Células não Pequenas/tratamento farmacológico , Carcinoma Pulmonar de Células não Pequenas/genética , Carcinoma Pulmonar de Células não Pequenas/patologia , Proliferação de Células/genética , Inibidores de Proteínas Quinases/farmacologia , Inibidores de Proteínas Quinases/uso terapêutico , Receptores ErbB/genética , Glutamatos/uso terapêutico , Prolina/uso terapêutico , Linhagem Celular Tumoral , Resistencia a Medicamentos Antineoplásicos/genéticaRESUMO
Researchers of temporal networks (e.g., social networks and transaction networks) have been interested in mining dynamic patterns of nodes from their diverse interactions. Inspired by recently powerful graph mining methods like skip-gram models and graph neural networks (GNNs), existing approaches focus on generating temporal node embeddings sequentially with nodes' sequential interactions. However, the sequential modeling of previous approaches cannot handles the transition structure between nodes' neighbors with limited memorization capacity. In detail, an effective method for the transition structures is required to both model nodes' personalized patterns adaptively and capture node dynamics accordingly. In this article, we propose a method, namely transition propagation graph neural networks (TIP-GNN), to tackle the challenges of encoding nodes' transition structures. The proposed TIP-GNN focuses on the bilevel graph structure in temporal networks: besides the explicit interaction graph, a node's sequential interactions can also be constructed as a transition graph. Based on the bilevel graph, TIP-GNN further encodes transition structures by multistep transition propagation and distills information from neighborhoods by a bilevel graph convolution. Experimental results over various temporal networks reveal the efficiency of our TIP-GNN, with at most 7.2% improvements of accuracy on temporal link prediction. Extensive ablation studies further verify the effectiveness and limitations of the transition propagation module. Our code is available at https://github.com/doujiang-zheng/TIP-GNN.
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BACKGROUND: Malignant gastrointestinal neuroectodermal tumor (GNET) is a rare malignant mesenchymal neoplasm that commonly arises in the small bowel, stomach or colon. Meanwhile, SMARCA4-deficient undifferentiated carcinoma is a rarely reported entity with highly aggressive behavior that may involve the ovary, lung, gastrointestinal (GI) tract, endometrium and other organs. To our knowledge, we describe for the first time, an extremely rare case of synchronous GNET and SMARCA4-deficient undifferentiated carcinoma with independent origins in the small intestine. CASE PRESENTATION: A 46-year-old woman presented with multiple small intestine masses and underwent surgical resection. Two distinct entities, GNET and SMARCA4-deficient undifferentiated carcinoma, were identified. GNET was composed of epithelioid and spindle cells with clear or eosinophilic cytoplasm arranged in sheets, nest, papillary, fascicular, palisade, rosette like or pseudoalveolar pattern. The neoplastic cells were positive for S-100 and SOX-10. Ewing sarcoma breakpoint region 1 gene (EWSR1) rearrangement was confirmed by fluorescence in situ hybridization (FISH), and EWSR1-CREB1 fusion was revealed by next-generation sequencing (NGS). SMARCA4-deficient undifferentiated carcinoma was composed mainly of poorly adhesive rhabdoid cells with eosinophilic cytoplasm arranged in a diffuse pattern. Multifocal necrosis, brisk mitotic figures as well as multinucleated tumor cells were observed. The neoplastic cells diffusely expressed pancytokeratin and vimentin, and was negative for SMARCA4(BRG1). Frame shift mutation of SMARCA4 was detected by NGS. CONCLUSIONS: This is the first report that GNET and SMARCA4-deficient undifferentiated carcinoma occurred simultaneously in the small intestine, with the latter showing multiple involvement of the jejunum and ileum. The potential mechanism underlying co-existence of these two rare malignancies is unknown and need further investigations and concern.
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While treatment for B-cell malignancies has been revolutionized through the advent of CAR immunotherapy, similar strategies for T-cell malignancies have been limited. Additionally, T-cell leukemias and lymphomas can commonly metastasize to the CNS, where outcomes are poor and treatment options are associated with severe side effects. Consequently, the development of safer and more effective alternatives for targeting malignant T cells that have invaded the CNS remains clinically important. CD5 CAR has previously been shown to effectively target various T-cell cancers in preclinical studies. As IL-15 strengthens the anti-tumor response, we have modified CD5 CAR to secrete an IL-15/IL-15sushi complex. In a Phase I clinical trial, these CD5-IL15/IL15sushi CAR T cells were tested for safety and efficacy in a patient with refractory T-LBL with CNS infiltration. CD5-IL15/IL15sushi CAR T cells were able to rapidly ablate the CNS lymphoblasts within a few weeks, resulting in the remission of the patient's lymphoma. Despite the presence of CD5 on normal T cells, the patient only experienced a brief, transient T-cell aplasia. These results suggest that CD5-IL15/IL15sushi CAR T cells may be a safe and useful treatment of T-cell malignancies and may be particularly beneficial for patients with CNS involvement.Graphical Abstract.
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Imunoterapia Adotiva , Interleucina-15 , Leucemia-Linfoma Linfoblástico de Células Precursoras , Linfócitos T , Humanos , Leucemia-Linfoma Linfoblástico de Células Precursoras/terapiaRESUMO
Dedifferentiated liposarcoma rarely occurs in the esophagus. It always has atypical clinical manifestations and different pathologic features, which usually lead to misdiagnosis and mistreatment. Given its poor prognosis, early and accurate diagnosis is of the utmost importance. The accumulation of similar cases is critical for surgeons and pathologists to raise awareness of such tumors. This report aims to discuss the diagnosis and provide a reference for the clinical diagnosis and treatment for pathologists and clinicians.
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Neoplasias Esofágicas/patologia , Lipossarcoma/patologia , Adulto , Feminino , HumanosRESUMO
PURPOSE: Proline, glutamic acid, and leucine-rich protein 1 (PELP1), a novel nuclear receptor (NR) co-regulator, is highly expressed in breast cancer. We investigated its expression in breast cancer subtypes, in comparison with other breast markers as well as cancers from different sites. Its prognostic relevance with different subtypes and other NR expression was also examined in breast cancers. METHODS: Immunohistochemical analysis was performed on totally 1,944 cancers from six different organs. RESULTS: PELP1 expression rate was the highest in breast cancers (70.5%) among different cancers. Compared to GATA3, mammaglobin and gross cystic disease fluid protein 15, PELP1 was less sensitive than GATA3 for luminal cancers, but was the most sensitive for non-luminal cancers. PELP1 has low expression rate (<20%) in colorectal cancers, gastric cancers and renal cell carcinomas, but higher in lung cancers (49.1%) and ovarian cancers (42.3%). In breast cancer, PELP1 expression was an independent adverse prognostic factor for non-luminal cancers (disease-free survival [DFS]: hazard ratio [HR], 1.403; p=0.012 and breast cancer specific survival [BCSS]: HR, 1.443; p=0.015). Interestingly, its expression affected the prognostication of androgen receptor (AR). ARposPELP1lo luminal cancer showed the best DFS (log-rank=8.563, p=0.036) while ARnegPELP1hi non-luminal cancers showed the worst DFS (log-rank=9.536, p=0.023). CONCLUSION: PELP1 is a sensitive marker for breast cancer, particularly non-luminal cases. However, its considerable expression in lung and ovarian cancers may limit its utility in differential diagnosis in some scenarios. PELP1 expression was associated with poor outcome in non-luminal cancers and modified the prognostic effects of AR, suggesting the potential significance of NR co-regulator in prognostication.
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Biomarcadores Tumorais , Neoplasias da Mama/diagnóstico , Neoplasias da Mama/metabolismo , Proteínas Correpressoras/metabolismo , Fatores de Transcrição/metabolismo , Neoplasias da Mama/mortalidade , Proteínas de Transporte/metabolismo , Feminino , Fator de Transcrição GATA3/metabolismo , Expressão Gênica , Glicoproteínas/metabolismo , Humanos , Imuno-Histoquímica , Estimativa de Kaplan-Meier , Mamoglobina B/metabolismo , Proteínas de Membrana Transportadoras , Gradação de Tumores , PrognósticoRESUMO
BACKGROUND: Indolent T-cell proliferative disorder of the GIT is a rare and provisional entity in the revised WHO 2016 classification. The patients usually have prolonged survival with persistent disease even without any treatment. CASE PRESENTATION: The 46 years old male patient has been followed up for more than 6 years without chemotherapy. Repeated gastrointestinal biopsies showed expansion of the lamina propria extending to the submucosa by small to medium sized lymphocytes with minimal cytologic atypia. The lymphoid cells were positive for CD3, CD43, TIA-1, CD2, CD7 and the B-cell marker CD20; but negative for CD4, CD8, PAX5, CD56, cyclinD1, granzyme (GraB) and Epstein Barr virus-encoded RNA (EBER). Ki-67(MIB1) index was less than 10%. Molecular tests demonstrated a clonal rearrangement for T-cell receptor γ (TCR γ) gene but immunoglobulin chain (IgH, IgK, IgL) gene remained germline. Recognition of possible aberrant CD20 expression in indolent T-cell LPD is important to avoid potential diagnostic pitfall and improper treatment. CONCLUSIONS: We present an unusual case of indolent T-cell lymphoproliferative disorder with aberrant CD20 expression, Recognition of this unusual immunophenotype of indolent T-cell LPD of GI helps to eschew misdiagnosis of B-cell and other high grade lymphomas and inappropriate aggressive treatment.
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Antígenos CD20/análise , Doenças da Medula Óssea/imunologia , Proliferação de Células , Gastroenteropatias/imunologia , Transtornos Linfoproliferativos/imunologia , Linfócitos T/imunologia , Biomarcadores/análise , Biópsia , Doenças da Medula Óssea/genética , Doenças da Medula Óssea/patologia , Diagnóstico Diferencial , Endoscopia Gastrointestinal , Gastroenteropatias/genética , Gastroenteropatias/patologia , Humanos , Imuno-Histoquímica , Transtornos Linfoproliferativos/patologia , Masculino , Pessoa de Meia-Idade , Fenótipo , Valor Preditivo dos Testes , Prognóstico , Linfócitos T/patologia , Fatores de TempoRESUMO
Abdominal leiomyomas are extremely rare intraabdominal tumors, especially in male patient. Here, we report a case of a 22 years-old male with a huge abdominal leiomyoma. The patient presented with a chief complaint of abdominal distension for three months, no others significant symptom were found. CT-scan showed a cystic-solid huge mass in the middle and lower abdominal peritoneal cavity with uneven density. An exploratory laparotomy was performed and the tumor was completely resected. Microscopically, Tumor cells have a spindled shape, eosinophilic cytoplasm, and cigar-like nuclei, arranged in bundles or intersecting fascicles. Immunohistochemistry, the tumor cells were SMA, desmin diffuse positive and CD117, S-100 negative, interestingly, ER, PR were positive. The characteristics of a few of the male abdominal leiomyoma reported in the literature were generalized.
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Neoplasias Abdominais/patologia , Leiomioma/patologia , Neoplasias Abdominais/química , Neoplasias Abdominais/cirurgia , Biomarcadores Tumorais/análise , Humanos , Imuno-Histoquímica , Leiomioma/química , Leiomioma/cirurgia , Masculino , Tomografia Computadorizada Multidetectores , Resultado do Tratamento , Carga Tumoral , Adulto JovemRESUMO
Dendritic fibromyxolipoma is an uncommon benign soft tissue tumor. Here, we report a case in a 53-year-old man presenting a painless mass located deep in the latissimus dorsi of the right back. Microscopically, the tumor was mainly consisted of small spindle and stellate cells, abundant myxoid stroma, collagen bundles and mature adipose tissue. Immunohistochemical study showed the spindle and stellate cells were positive for CD34, Bcl-2 and Vimentim, but not for Keratin, EMA, SMA and Desmin. To date, one year after operation, the patient is well without evidence of recurrence or metastasis. The implication of this report is to provide insights into further understanding of this rare tumor with review of the literature.
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Fibroma/patologia , Lipoma/patologia , Neoplasias Musculares/patologia , Tumores Fibrosos Solitários/patologia , Músculos Superficiais do Dorso/patologia , Biomarcadores Tumorais/análise , Biópsia , Fibroma/química , Fibroma/cirurgia , Humanos , Imuno-Histoquímica , Lipoma/química , Lipoma/cirurgia , Masculino , Pessoa de Meia-Idade , Neoplasias Musculares/química , Neoplasias Musculares/cirurgia , Tumores Fibrosos Solitários/química , Tumores Fibrosos Solitários/cirurgia , Resultado do TratamentoRESUMO
AIM: To investigate the effect of transplantation of bone marrow-derived mesenchymal stem cells (MSCs), or co-transplantation of islet and MSCs, on maturation and function of bone marrow-derived dendritic cells (DCs) in recipient mice. METHODS: Bone marrow MSCs were isolated from BALB/c mice and co-cultured with bone marrow mononuclear cells (BMCs) from C57BL/6 mice at indicated ratios. The co-cultures were treated with recombinant mice granulocyte-macro-phage colony-stimulating factor (rmGM-CSF) and recombinant mice IL-4 (rmIL-4) for 7 days to induce the differentiation of DCs, with lipopolysaccharide (LPS) favoring the maturation of DCs. The differentiation markers and antigen uptake capability of DCs were analyzed by FCM. Production of Interleukin-12 in the supernatants of the DC cultures was quantified by ELISA. BALB/c-derived MSCs and islet were co-transplanted to the capsule of kidney in allogeneic C57BL/c mice. The recipient mice were assayed for their tissue morphology, blood glucose level, and the in vitro differentiation ability of their BMC into mature and functional DCs. RESULTS: The transplantation of MSCs prevented BMC from differentiating into mature DCs, as shown by down-regulated surface markers of DCs including CD11c, CD83, CD86 and I-Ab; (P<0.05), impaired antigen uptake and decreased IL-12 secretion (P<0.01). Co-transplantation of MSCs and islet inhibited immune rejection in the allogeneic recipient mice. CONCLUSION: Transplantation of MSCs inhibits maturation and function of monocyte-derived dendritic cells in the recipient mice, resulting in immune tolerance for the allogeneic islet.
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Células da Medula Óssea/citologia , Diferenciação Celular , Células Dendríticas/citologia , Diabetes Mellitus/terapia , Transplante das Ilhotas Pancreáticas , Transplante de Células-Tronco Mesenquimais , Animais , Células da Medula Óssea/imunologia , Células Cultivadas , Células Dendríticas/imunologia , Diabetes Mellitus/imunologia , Diabetes Mellitus/fisiopatologia , Modelos Animais de Doenças , Humanos , Tolerância Imunológica , Interleucina-12/imunologia , Transplante das Ilhotas Pancreáticas/imunologia , Camundongos , Camundongos Endogâmicos BALB C , Camundongos Endogâmicos C57BL , TransplanteRESUMO
AIM: To study the effect of murine mesenchymal stem cells (MSCs) on the differentiation, maturation and function of allogenetic bone marrow-derived dendritic cells (DCs) and to investigate the mechanism of MSCs displaying immunoregulatory activity. METHODS: BALB/c mice BMCs were isolated and cultured in vitro and then coclutured with C57BL/6 murine bone marrows cells (BMCs) at different ratios in vitro to induce DCs generation. The phenotype of cells was analyzed by flow cytometry. Endocytosis was measured as the cellular uptake of fluorescein isothiocyanate (FITC)-dextram amd was quantified by flow cytometry. The level of IL-12 secretion in the cell culture supernatants was detected by enzyme-linked immunosorbent assay (ELISA). RESULTS: Decreased expression of CD11c, CD14, CD83, CD86 and I-A(b);, down-regulated endocytosis capacity and interleukin-12 (IL-12) secretion of DCs were all observed when MSCs cocultured with BMCs at a higher ratio (1:10). CONCLUSION: Murine MSCs could supress the differentiation and maturation of DCs derived from allogeneic BMCs in vitro.