Your browser doesn't support javascript.
Mostrar: 20 | 50 | 100
Resultados 1 - 20 de 7.065
Filtrar
1.
J Nanobiotechnology ; 18(1): 18, 2020 Jan 21.
Artículo en Inglés | MEDLINE | ID: mdl-31964403

RESUMEN

BACKGROUND: Although accumulating evidence suggests that the crosstalk between malignant cells and cancer-associated fibroblasts (CAFs) actively contributes to tumour growth and metastatic dissemination, therapeutic strategies targeting tumour stroma are still not common in the clinical practice. Metal-based nanomaterials have been shown to exert excellent cytotoxic and anti-cancerous activities, however, their effects on the reactive stroma have never been investigated in details. Thus, using feasible in vitro and in vivo systems to model tumour microenvironment, we tested whether the presence of gold, silver or gold-core silver-shell nanoparticles exerts anti-tumour and metastasis suppressing activities by influencing the tumour-supporting activity of stromal fibroblasts. RESULTS: We found that the presence of gold-core silver-shell hybrid nanomaterials in the tumour microenvironment attenuated the tumour cell-promoting behaviour of CAFs, and this phenomenon led to a prominent attenuation of metastatic dissemination in vivo as well. Mechanistically, transcriptome analysis on tumour-promoting CAFs revealed that silver-based nanomaterials trigger expressional changes in genes related to cancer invasion and tumour metastasis. CONCLUSIONS: Here we report that metal nanoparticles can influence the cancer-promoting activity of tumour stroma by affecting the gene expressional and secretory profiles of stromal fibroblasts and thereby altering their intrinsic crosstalk with malignant cells. This potential of metal nanomaterials should be exploited in multimodal treatment approaches and translated into improved therapeutic outcomes.


Asunto(s)
Antineoplásicos/química , Fibroblastos Asociados al Cáncer/efectos de los fármacos , Nanopartículas del Metal/química , Metástasis de la Neoplasia/tratamiento farmacológico , Aleaciones/química , Animales , Antineoplásicos/uso terapéutico , Fibroblastos Asociados al Cáncer/patología , Línea Celular Tumoral , Movimiento Celular , Supervivencia Celular , Progresión de la Enfermedad , Doxorrubicina/química , Doxorrubicina/uso terapéutico , Femenino , Fibroblastos/citología , Fibroblastos/efectos de los fármacos , Regulación Neoplásica de la Expresión Génica , Oro/química , Humanos , Nanopartículas del Metal/uso terapéutico , Ratones Endogámicos BALB C , Metástasis de la Neoplasia/patología , Trasplante de Neoplasias , Plata/química , Microambiente Tumoral/efectos de los fármacos
2.
Cancer Sci ; 111(1): 72-83, 2020 Jan.
Artículo en Inglés | MEDLINE | ID: mdl-31691433

RESUMEN

Capn4, also known as CapnS1, is a member of the calpain family, which plays a crucial role in maintaining the activity and function of calpain. We previously reported that Capn4 also plays an essential role in the migration of nasopharyngeal carcinoma (NPC) cells through regulation of (MMP-2) by nuclear factor-kappa B activation. Epstein-Barr virus latent membrane protein 1 (LMP1) is closely related to the malignant functions of NPC; however, the relationship between LMP1 and Capn4 in NPC remain unclear. Immunohistochemical studies showed that the level of LMP1 and Capn4 expression was high in both primary and metastatic NPC tissues, with a significantly positive correlation. We further found that LMP1 was able to upregulate the Capn4 promoter in a dose-dependent way through the C-terminal activation region (CTAR)1 and CTAR2 domains to activate AP-1. Moreover, we also found that LMP1 activated AP-1 through ERK/JNK phosphorylation. These findings indicate that Capn4 coordination with LMP1 promotes actin rearrangement and, ultimately, cellular migration. These results show that Capn4 coordination with LMP1 enhances NPC migration by increasing actin rearrangement involving ERK/JNK/AP-1 signaling. Therapeutically, additional and more specific LMP1 and Capn4 targeted inhibitors could be exploited to treat NPC.


Asunto(s)
Calpaína/genética , Sistema de Señalización de MAP Quinasas/genética , Carcinoma Nasofaríngeo/genética , Neoplasias Nasofaríngeas/genética , Metástasis de la Neoplasia/genética , Factor de Transcripción AP-1/genética , Proteínas de la Matriz Viral/genética , Línea Celular Tumoral , Infecciones por Virus de Epstein-Barr/genética , Infecciones por Virus de Epstein-Barr/virología , Regulación Neoplásica de la Expresión Génica/genética , Herpesvirus Humano 4/patogenicidad , Humanos , FN-kappa B/genética , Carcinoma Nasofaríngeo/patología , Carcinoma Nasofaríngeo/virología , Neoplasias Nasofaríngeas/patología , Neoplasias Nasofaríngeas/virología , Metástasis de la Neoplasia/patología , Fosforilación/genética , Regiones Promotoras Genéticas/genética , Transducción de Señal/genética , Regulación hacia Arriba/genética
3.
Gene ; 726: 144194, 2020 Feb 05.
Artículo en Inglés | MEDLINE | ID: mdl-31669650

RESUMEN

Increasing evidence indicates that long non-coding RNA (lncRNA) may play important roles in tumorigenesis. Increased lncRNA CASC9 occurs in laryngeal carcinoma, which accounts for 20% of all head and neck cancers, but its role in this disease remains unknown. Using quantitative reverse transcriptase PCR, we found higher expression of CASC9 and GLUT-1 in laryngeal carcinoma tissues and cells, compared to adjacent tissues and cells. A correlation analysis showed a positive relationship between CASC9 and GLUT-1 expression in laryngeal carcinoma tissues. An MTT assay of TU212 and Hep-2 cells showed increased cell proliferation after transfection with overexpressed CASC9 and decreased cell proliferation after transfection with silenced CASC9. A Transwell assay showed that overexpressing CASC9 increased and silencing CASC9 decreased cell migration of TU212 and Hep-2 cells. A flow cytometry assay showed that overexpressing CASC9 reduced and silencing CASC9 increased cell apoptosis. In other words, we found that overexpressing CASC9 increased cell proliferation and cell migration and decreased apoptosis both in TU212 and Hep-2 cells, whereas silencing CASC9 had the opposite effects. Moreover, overexpression vector of GLUT-1 was used to investigate the molecular mechanism of CASC9 in laryngeal carcinoma. The results showed that transfection with an overexpressed GLUT-1vector reversed the effects of silencing CASC9 on proliferation, migration, and apoptosis in TU212 and Hep-2 cells. In conclusion, our study of laryngeal carcinoma found that CASC9 was positively correlated with GLUT-1 expression and that CASC9 may promote proliferation and metastasis of laryngeal carcinoma cells by regulating GLUT-1.


Asunto(s)
Carcinoma/genética , Proliferación Celular/genética , Transportador de Glucosa de Tipo 1/genética , Neoplasias Laríngeas/genética , Metástasis de la Neoplasia/genética , ARN Largo no Codificante/genética , Apoptosis/genética , Línea Celular , Línea Celular Tumoral , Movimiento Celular/genética , Regulación Neoplásica de la Expresión Génica/genética , Humanos , Neoplasias Laríngeas/patología , Metástasis de la Neoplasia/patología , Transfección/métodos
4.
Cell Mol Life Sci ; 77(2): 305-321, 2020 Jan.
Artículo en Inglés | MEDLINE | ID: mdl-31432232

RESUMEN

Pancreatic ductal adenocarcinoma is prone to distant metastasis and is expected to become the second leading cause of cancer-related death. In an extremely nutrient-deficient and hypoxic environment resulting from uncontrolled growth, vascular disturbances and desmoplastic reactions, pancreatic cancer cells utilize "metabolic reprogramming" to satisfy their energy demand and support malignant behaviors such as metastasis. Notably, pancreatic cancer cells show extensive enhancement of glycolysis, including glycolytic enzyme overexpression and increased lactate production, and this is caused by mitochondrial dysfunction, cancer driver genes, specific transcription factors, a hypoxic tumor microenvironment and stromal cells, such as cancer-associated fibroblasts and tumor-associated macrophages. The metabolic switch from oxidative phosphorylation to glycolysis in pancreatic cancer cells regulates the invasion-metastasis cascade by promoting epithelial-mesenchymal transition, tumor angiogenesis and the metastatic colonization of distant organs. In addition to aerobic glycolysis, oxidative phosphorylation also plays a critical role in pancreatic cancer metastasis in ways that remain unclear. In this review, we expound on the intracellular and extracellular causes of the enhancement of glycolysis in pancreatic cancer and the strong association between glycolysis and cancer metastasis, which we expect will yield new therapeutic approaches targeting cancer metabolism.


Asunto(s)
Glucólisis/fisiología , Metástasis de la Neoplasia/patología , Neoplasias Pancreáticas/patología , Animales , Transición Epitelial-Mesenquimal/fisiología , Humanos , Neovascularización Patológica , Microambiente Tumoral/fisiología
5.
Recent Results Cancer Res ; 215: 147-160, 2020.
Artículo en Inglés | MEDLINE | ID: mdl-31605228

RESUMEN

The development of metastatic disease accounts for the vast majority of cancer-related deaths in solid tumor malignancies. Distant metastases primarily develop as a result of tumor cell dissemination through the circulatory system.


Asunto(s)
Neoplasias de la Mama/patología , Metástasis de la Neoplasia/patología , Células Neoplásicas Circulantes/patología , Humanos
6.
Recent Results Cancer Res ; 215: 231-252, 2020.
Artículo en Inglés | MEDLINE | ID: mdl-31605232

RESUMEN

In only few years, circulating tumor DNA (ctDNA) in breast cancer has moved from purely fundamental research to nearby daily use for treatment selection and drug-resistance assessment. Indeed, technical advances and widespread use of next-generation sequencing or digital PCR allowed for detection of very low amount of tumor DNA in bloodstream. The use of ctDNA as liquid biopsy able either to monitor tumor burden under treatment or to overcome tumor heterogeneity and identify potential targetable drivers. Time has come to define how ctDNA can be implemented for early or metastatic breast cancer management. Data from retrospective analyses of prospective trials have recently highlighted the potential advantages but also the limitations of ctDNA, in particular for patients under endocrine therapy.


Asunto(s)
Neoplasias de la Mama , ADN Tumoral Circulante , Biomarcadores de Tumor/sangre , Biomarcadores de Tumor/genética , Neoplasias de la Mama/diagnóstico , Neoplasias de la Mama/genética , Neoplasias de la Mama/patología , Neoplasias de la Mama/terapia , ADN Tumoral Circulante/sangre , ADN Tumoral Circulante/genética , Resistencia a Antineoplásicos/efectos de los fármacos , Resistencia a Antineoplásicos/genética , Humanos , Metástasis de la Neoplasia/patología , Metástasis de la Neoplasia/terapia
7.
Tumour Biol ; 41(12): 1010428319892790, 2019 Dec.
Artículo en Inglés | MEDLINE | ID: mdl-31815594

RESUMEN

In the last few decades, there has been notable progress in understanding the molecular and cellular basis of the complex process involved in cancer. In this context, tumor-promoting inflammation, dysregulation of apoptotic signaling, tissue invasion and metastasis, and cancer microenvironment have recently attracted interest from researchers. Irisin is a hormone released by muscles during exercise and it directly acts on key functional cells involving energy metabolism and homeostasis. Recently, many studies have reported the anticancer effect of irisin against different types of cancer. Translation of these findings to clinical practice for the diagnosis and treatment of several types of cancer is urgently required. In this review, we summarized preclinical and clinical studies on the anticancer effects of irisin in various types of cancer, and also discussed the mechanisms activated by irisin to suppress cancer pathogenesis. We further discussed the serum level of irisin related to different types of cancer to understand more clearly the association between irisin concentration and tumor burden. This review may serve as a solid foundation for researchers and physicians to support basic and clinical studies on irisin as a promising strategy for early diagnosis and treatment of a various types of cancers.


Asunto(s)
Biomarcadores de Tumor/genética , Carcinogénesis/genética , Fibronectinas/genética , Metástasis de la Neoplasia/genética , Metástasis de la Neoplasia/patología , Neoplasias/genética , Neoplasias/patología , Animales , Humanos , Microambiente Tumoral/genética
8.
Nat Rev Cancer ; 19(12): 716-732, 2019 12.
Artículo en Inglés | MEDLINE | ID: mdl-31666716

RESUMEN

Experimental evidence accumulated over decades has implicated epithelial-mesenchymal plasticity (EMP), which collectively encompasses epithelial-mesenchymal transition and the reverse process of mesenchymal-epithelial transition, in tumour metastasis, cancer stem cell generation and maintenance, and therapeutic resistance. However, the dynamic nature of EMP processes, the apparent need to reverse mesenchymal changes for the development of macrometastases and the likelihood that only minor cancer cell subpopulations exhibit EMP at any one time have made such evidence difficult to accrue in the clinical setting. In this Perspectives article, we outline the existing preclinical and clinical evidence for EMP and reflect on recent controversies, including the failure of initial lineage-tracing experiments to confirm a major role for EMP in dissemination, and discuss accumulating data suggesting that epithelial features and/or a hybrid epithelial-mesenchymal phenotype are important in metastasis. We also highlight strategies to address the complexities of therapeutically targeting the EMP process that give consideration to its spatially and temporally divergent roles in metastasis, with the view that this will yield a potent and broad class of therapeutic agents.


Asunto(s)
Plasticidad de la Célula , Transición Epitelial-Mesenquimal , Metástasis de la Neoplasia/patología , Neoplasias/metabolismo , Neoplasias/patología , Células Madre Neoplásicas/patología , Animales , Línea Celular Tumoral , Progresión de la Enfermedad , Resistencia a Antineoplásicos , Humanos , Inmunoterapia , Ratones , Invasividad Neoplásica , Células Madre Neoplásicas/metabolismo , Fenotipo , Ratas
9.
Expert Rev Clin Pharmacol ; 12(12): 1107-1119, 2019 Dec.
Artículo en Inglés | MEDLINE | ID: mdl-31687857

RESUMEN

Introduction: Melanoma in-transit metastases (ITMs) occur between the primary tumor site and the regional node field. Most patients with ITMs have a poor prognosis. The treatment of ITMs can be simple if surgical excision is possible, but challenging when ITMs are advanced, multiple or recurrent and impacting quality of life.Areas covered: The management of ITM is still evolving. Patients who are disease-free after surgical excision of ITMs are today candidates for adjuvant systemic treatment to reduce recurrence risk. Some who have multiple or advanced ITMs may achieve long-term survival or disease control with systemic therapies alone. Those who do not remain candidates for the numerous locoregional therapies used to treat ITMs, including electrocautery, intralesional injection, topical therapy, electrochemotherapy, isolated limb infusion, isolated limb perfusion, radiation therapy and, rarely, amputation. Relevant publications identified in Pubmed and MEDLINE databases are reviewed.Expert opinion: Patients with multiple ITMs can benefit from use of systemic therapies as primary treatment, in the adjuvant setting and in neoadjuvant trials. Multiple alternative treatment modalities exist for patients unsuitable for systemic therapies or in whom systemic therapies have failed. Trials assessing combined systemic and locoregional therapies for ITMs are in progress.


Asunto(s)
Melanoma/patología , Metástasis de la Neoplasia/terapia , Neoplasias Cutáneas/patología , Terapia Combinada , Supervivencia sin Enfermedad , Humanos , Terapia Neoadyuvante/métodos , Metástasis de la Neoplasia/patología , Pronóstico , Calidad de Vida
14.
J Cancer Res Clin Oncol ; 145(12): 2969-2982, 2019 Dec.
Artículo en Inglés | MEDLINE | ID: mdl-31612319

RESUMEN

PURPOSE: Non-canonical NFκB (NC-NFκB) pathway plays an influential role in metastasis, which promotes cancer proliferation and progression. The aim of the study was to examine the expression of NC-NFκB proteins and their correlation with clinicopathological factors associated with metastatic cases of uveal melanoma (UM) and with the patient outcome. METHOD: Expression of NC-NFκB proteins (p52, RelB, and co-expression of p52/RelB) was evaluated in 75 formalin-fixed cases of uveal melanoma by immunohistochemistry. Validation of nuclear immunoreactivity was done by western blotting. Transcriptional status of NC-NFκB genes was assessed in 60 fresh tumor tissues by quantitative real-time PCR. Co-immunoprecipitation was performed to determine the presence of native p52/RelB heterodimer in UM. Prognostic relevance was determined using Cox proportional hazard and Kaplan-Meier methods. RESULTS: Immunohistochemical expression of p52, RelB, and their co-expression was observed in 81%, 68.7%, 56.2% of metastatic cases, respectively, while their expression was seen only in 38%, 33% and 30% of non-metastatic cases. Loss of BAP-1 was correlated with expression of p52 and RelB proteins. Co-immunoprecipitation assay confirmed the putative interaction of p52 with RelB protein in metastatic cases of uveal melanoma. Co-expression of p52/RelB and expression of p52 protein was significantly correlated with decreased metastasis-free survival (MFS) (p = 0.004; p = 0.002) and overall survival (OS) (p = 0.004; p = 0.032), while the RelB expression only correlated with reduced MFS (p = 0.003). CONCLUSION: Our data showed that non-canonical NFκB proteins were significantly higher in metastatic cases and associated with poor outcome of the patients. Furthermore, the p52 protein could be used as a potential therapeutic biomarker for metastatic cases in uveal melanoma.


Asunto(s)
Regulación Neoplásica de la Expresión Génica/genética , Melanoma/genética , Subunidad p52 de NF-kappa B/genética , Metástasis de la Neoplasia/genética , Factor de Transcripción ReIB/genética , Neoplasias de la Úvea/genética , Adulto , Supervivencia sin Enfermedad , Femenino , Humanos , Inmunohistoquímica/métodos , Masculino , Melanoma/patología , Metástasis de la Neoplasia/patología , Pronóstico , Estudios Prospectivos , Transcripción Genética/genética , Neoplasias de la Úvea/patología
15.
Anticancer Res ; 39(10): 5653-5662, 2019 Oct.
Artículo en Inglés | MEDLINE | ID: mdl-31570463

RESUMEN

BACKGROUND/AIM: Factors influencing fulvestrant efficacy may be useful in selecting the optimal treatment regimen for postmenopausal Japanese women with metastatic/recurrent HR-positive, HER2-negative breast cancer. PATIENTS AND METHODS: We retrospectively evaluated progression-free and overall survival (PFS and OS) in 100 fulvestrant-treated patients according to metastatic site. RESULTS: Median PFS was significantly better in patients with non-visceral (bone and regional metastases; 22.8 months) vs. visceral metastasis (lung, liver, and other organs; 8.2 months; p=0.024), although median OS did not differ (p=0.922). Median PFS in patients with lung metastasis (20.8 months) and non-visceral metastasis (22.8 months) were comparable; patients with liver metastasis (6.1 months) and other organ metastases (3.7 months) had worse prognoses. CONCLUSION: Patients with non-visceral metastases had a better prognosis than those with visceral metastases. Fulvestrant induced a longer PFS in patients with non-visceral metastasis, and also in those with lung metastasis without liver or other organ involvement.


Asunto(s)
Neoplasias de la Mama/tratamiento farmacológico , Fulvestrant/uso terapéutico , Metástasis de la Neoplasia/prevención & control , Recurrencia Local de Neoplasia/tratamiento farmacológico , Adulto , Anciano , Anciano de 80 o más Años , Neoplasias de la Mama/genética , Neoplasias de la Mama/patología , Femenino , Humanos , Persona de Mediana Edad , Metástasis de la Neoplasia/genética , Metástasis de la Neoplasia/patología , Recurrencia Local de Neoplasia/genética , Recurrencia Local de Neoplasia/patología , Pronóstico , Supervivencia sin Progresión , Receptor ErbB-2/genética , Receptores de Superficie Celular/genética , Estudios Retrospectivos
16.
Cytogenet Genome Res ; 158(4): 205-212, 2019.
Artículo en Inglés | MEDLINE | ID: mdl-31434093

RESUMEN

EHMT2 (euchromatic histone lysine methyltransferase 2), a histone methyltransferase, has been shown to be involved in multiple human cancers. In this study, we determined mRNA and protein expression of EHMT2 in cervical cancer cells and normal cervical epithelial cells. EHMT2 was inhibited with short hairpin RNA (shEHMT2) in cervical cancer cells. Cell viability, colony proliferation, apoptosis, adhesion, and invasion assays and Western blot were performed to assess the function of EHMT2. As a result, EHMT2 was upregulated in human cervical cancer cells compared to normal cervical epithelial cells. Suppression of EHMT2 expression impairs cell proliferation and induces apoptosis. Furthermore, EHMT2 silencing inhibited cell adhesion and invasion. Finally, knockdown of EHMT2 resulted in a reduction of the expression of the tumorigenic proteins Bcl-2, Mcl-1, and Survivin and in an increase in the expression of the anti-malignant protein E-cadherin. In conclusion, our data suggest that EHMT2 plays a key role in cell proliferation and metastatic capacity in cervical cancer cells and could serve as a potential therapeutic target.


Asunto(s)
Silenciador del Gen , Antígenos de Histocompatibilidad/genética , N-Metiltransferasa de Histona-Lisina/deficiencia , N-Metiltransferasa de Histona-Lisina/genética , Invasividad Neoplásica/genética , Invasividad Neoplásica/prevención & control , Neoplasias del Cuello Uterino/enzimología , Neoplasias del Cuello Uterino/patología , Apoptosis/genética , Cadherinas/biosíntesis , Adhesión Celular/genética , Proliferación Celular/genética , Femenino , Regulación Neoplásica de la Expresión Génica , Técnicas de Silenciamiento del Gen , Antígenos de Histocompatibilidad/metabolismo , N-Metiltransferasa de Histona-Lisina/metabolismo , Humanos , Invasividad Neoplásica/patología , Metástasis de la Neoplasia/genética , Metástasis de la Neoplasia/patología , Metástasis de la Neoplasia/prevención & control , Neoplasias del Cuello Uterino/genética
17.
Biomed Pharmacother ; 117: 109126, 2019 Sep.
Artículo en Inglés | MEDLINE | ID: mdl-31387165

RESUMEN

Approximately 40% of patients with non-small cell lung cancer (NSCLC) develop bone metastasis. The formin protein formin-like 1 (FMNL1) plays a key role in the pathogenic processes of hematopoietic malignancies, and has been reported to be associated with the progression of multiple types of cancer. In the study, we found that FMNL1 expression was markedly up-regulated in primary NSCLC samples, and stronger expression of FNML1 was detected in bone metastasis. Reducing FMNL1 expression significantly suppressed cell proliferation in NSCLC cells. We also investigated the functional effects of FMNL1 knockdown on the inhibition of migration and invasion by meditating the expression of epithelial to mesenchymal transition (EMT)-associated signals in NSCLC cells. The transforming growth factor-ß1 (TGF-ß1)/SMADs signaling pathway was repressed in FMNL1-knockdown NSCLC cells. Further studies indicated that additional treatment with TGF-ß1 could markedly abrogate FMNL1 knockdown-induced suppression of migration and invasion in NSCLC cells. In addition, NSCLC cell-induced osteoclastogenesis was also inhibited by FMNL1 deletion, as evidenced by the down-regulated expression of tartrate-resistant acid phosphatase (TRAP) and NFATc1. In vivo studies confirmed the results that FMNL1 knockdown markedly limited tumor growth. Importantly, decreasing FMNL1 reduced bone metastasis ability in vivo. Therefore, our results demonstrated that suppressing FMNL1 expression could inhibit bone metastasis in NSCLC through blocking TGF-ß1 signaling, and FMNL1 might be a novel target for developing effective therapeutic strategy to limit the bone metastasis of NSCLC.


Asunto(s)
Neoplasias Óseas/genética , Carcinoma de Pulmón de Células no Pequeñas/genética , Regulación hacia Abajo/genética , Neoplasias Pulmonares/genética , Metástasis de la Neoplasia/genética , Factor de Crecimiento Transformador beta1/genética , Células A549 , Animales , Neoplasias Óseas/patología , Carcinoma de Pulmón de Células no Pequeñas/patología , Línea Celular , Línea Celular Tumoral , Movimiento Celular/genética , Proliferación Celular/genética , Transición Epitelial-Mesenquimal/genética , Femenino , Regulación Neoplásica de la Expresión Génica/genética , Humanos , Neoplasias Pulmonares/patología , Masculino , Ratones , Ratones Endogámicos C57BL , Ratones Desnudos , Persona de Mediana Edad , Metástasis de la Neoplasia/patología , Transducción de Señal/genética
18.
Anticancer Res ; 39(8): 4315-4324, 2019 Aug.
Artículo en Inglés | MEDLINE | ID: mdl-31366523

RESUMEN

BACKGROUND/AIM: This study aimed to obtain accurate differential diagnosis (DDx) of multicentric carcinogenesis (MC) and intrahepatic metastasis (IM) in recurrent lesions of hepatocellular carcinoma. MATERIALS AND METHODS: A total of 79 patients who underwent re-hepatectomy (2000-2013) were examined. PCR was used to analyze 13 chromosomal microsatellite loci by PCR. On the basis of this genetic analysis, the recurrent lesions were diagnosed as IM, MC or not determined (ND). Subsequently, DDx was compared with types of resection and outcome. RESULTS: The recurrent lesions were diagnosed as IM in 33 patients, MC in 44, and ND in 2. The anatomical resection group included 14 IM lesions (28%) and 36 MC lesions (72%), while the non-anatomical resection group included 19 IM lesions (70%) and 8 MC lesions (30%) (p<0.001). CONCLUSION: Anatomical resection at initial hepatectomy may reduce the likelihood of IM recurrence, leading to a better outcome for patients with HCC.


Asunto(s)
Carcinoma Hepatocelular/diagnóstico , Neoplasias Hepáticas/diagnóstico , Metástasis de la Neoplasia/diagnóstico , Recurrencia Local de Neoplasia/diagnóstico , Adulto , Anciano , Carcinogénesis/genética , Carcinoma Hepatocelular/genética , Carcinoma Hepatocelular/patología , Carcinoma Hepatocelular/cirugía , Diagnóstico Diferencial , Femenino , Hepatectomía/métodos , Humanos , Neoplasias Hepáticas/genética , Neoplasias Hepáticas/patología , Neoplasias Hepáticas/secundario , Masculino , Repeticiones de Microsatélite/genética , Persona de Mediana Edad , Metástasis de la Neoplasia/genética , Metástasis de la Neoplasia/patología , Recurrencia Local de Neoplasia/genética , Recurrencia Local de Neoplasia/patología , Recurrencia Local de Neoplasia/cirugía
20.
Radiología (Madr., Ed. impr.) ; 61(4): 324-332, jul.-ago. 2019. ilus, tab
Artículo en Español | IBECS | ID: ibc-185310

RESUMEN

Objetivo: El objetivo de este trabajo es analizar las características radiológicas de lesiones con diagnóstico histológico de metástasis en la mama. Material y métodos: En la Sección de Diagnóstico e Intervencionismo mamario, en el período comprendido entre marzo de 2010 y septiembre de 2018 se seleccionaron 9 pacientes que presentaban diagnóstico anatomopatológico de metástasis en la mama. Resultado: En total se registraron 9 pacientes de sexo femenino con diagnóstico de metástasis en la mama. La media de edad fue de 60 años (rango: 28-89 años). En 1 caso (11,11%), el diagnóstico de la enfermedad primaria se realizó a partir de la lesión mamaria. Se diagnosticaron cinco metástasis de melanoma, dos metástasis de carcinomas neuroendocrinos (uno de origen en intestino delgado y otro de origen en cérvix uterino), una metástasis de adenocarcinoma de pulmón y una metástasis de ovario. Las manifestaciones clínicas y de imagen dependen de la forma de diseminación de la enfermedad y pueden simular lesiones benignas y malignas primarias de la mama. Conclusión: Las metástasis en la mama no presentan un patrón imagenológico específico que nos oriente a este diagnóstico. Es importante pensar en esta posibilidad etiológica si el paciente presenta el antecedente del diagnóstico de un tumor primario en otro órgano


Objective: To analyze the imaging characteristics of histologically diagnosed metastases to the breast. Material and methods: We selected patients histologically diagnosed with metastases to the breast in our diagnostic and interventional breast imaging unit between March 2010 and September 2018. Results: A total of 9 patients (all women; mean age, 60 y; age range, 28-89 y) were diagnosed with metastases to the breast. In 1 (11.11%) case, the primary disease was diagnosed from the breast lesion. The primary tumors were melanoma (n=5), neuroendocrine tumor (n=2, one from the small bowel and one from the cervix), lung adenocarcinoma (n=1), and ovarian cancer (n=1). The clinical and imaging manifestations depend on the type of dissemination of disease and can simulate benign and malignant primary breast lesions. Conclusion: There is no specific imaging pattern for metastases to the breast that would help to orient the diagnosis. It is important to consider this etiological possibility if the patient has a history of a primary tumor in another organ


Asunto(s)
Humanos , Femenino , Adulto , Persona de Mediana Edad , Anciano , Anciano de 80 o más Años , Neoplasias de la Mama/secundario , Metástasis de la Neoplasia/diagnóstico por imagen , Diagnóstico por Imagen/métodos , Neoplasias de la Mama/diagnóstico por imagen , Metástasis de la Neoplasia/patología
SELECCIÓN DE REFERENCIAS
DETALLE DE LA BÚSQUEDA