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1.
Cir. Esp. (Ed. impr.) ; 96(5): 276-282, mayo 2018. ilus, tab, graf
Artigo em Espanhol | IBECS | ID: ibc-176336

RESUMO

Introducción: La mutación BRAF V600E en el cáncer papilar de tiroides (CPT) parece asociarse a una resistencia al 131I. Nuestro principal objetivo fue cuantificar la respuesta al 131I tras la cirugía tanto en pacientes que presentaban la mutación (BRAF+) como en los que no presentaban el gen mutado (BRAF-). Método: Estudio prospectivo de los CPT intervenidos y tratados con 131I desde septiembre de 2015 hasta enero de 2017. Variables: edad, género, estadio tumoral, histológicas, tiroglobulina antes de 131I, a las 48h y a los 6 meses; dosis absorbida y % de actividad a los 2 y a los 7días y tiempo de eliminación. Resultados: Cuarenta y un pacientes y 67 restos tiroideos. El 61% eran BRAF+. En los estadios iii y iv, el 80% eran BRAF+. En el vaciamiento ganglionar terapéutico, el 100% eran BRAF+. El número de ganglios fue superior en BRAF+: 3,4 vs 1,2 (p = 0,01). La variante clásica fue predominante en BRAF+ (91,7% vs 8,3%; p=0,03). El 85,7% vs 14,3% de los BRAF+ tuvieron reacción desmoplásica (p = 0,02). Los BRAF+ presentaban menor dosis absorbida respecto a la actividad administrada (5,4 vs 20Gy/MBq; p = 0,02); menor % de actividad respecto a la unidad de masa a los 2 (0,046 vs 0,103%/g; p = 0,02) y a los 7 días (0,006 vs 0,034%/g, p = 0,04). Conclusiones: La mutación del gen BRAF V600E se relaciona con una mayor resistencia al tratamiento posquirúrgico con 131I desde el inicio de la enfermedad


Introduction: The BRAF V600E mutation in papillary thyroid cancer (PTC) has been associated with resistance to 131I. Our aim was to quantify the response to 131I after surgery in patients who had the mutation (BRAF+) and those who did not have the mutated gene (BRAF-). Method: A prospective cohort study was designed, from September 2015 to February 2016, which included patients with PTC receiving therapy after surgical treatment. Variables were described for age, gender, histology, tumor stage, thyroglobulin values before, 48 h after and 6months after 131I; absorbed dose and % activity on days 2 and 7 and elimination time. Results: 41 patients giving in total 67 thyroid remnants were included. 61% were BRAF+. In stagesiii and iv, 80% were BRAF+. In lateral resection, 100% were BRAF+. The number of nodes was higher in BRAF+: 3.4 vs 1.2 (P = .01). The classic variant was predominant in BRAF+ (91.7% vs 8.3%, P = .03). 85.7% vs 14.3% of BRAF+ had desmoplastic reaction (P = .02). The BRAF+ had a lower absorbed dose than the administered activity (5.4Gy/MBq vs 20Gy/MBq, P = .02); lower% activity with respect to the unit of mass at 2 (0.046%/g vs 0.103%/g, P = .02) and at 7days (0.006%/gr vs 0.034%/gr, P = .04) Conclusions: The mutation of the BRAF V600E gene is related with greater resistance to postoperative treatment with 131I since the onset of the disease


Assuntos
Humanos , Masculino , Feminino , Pessoa de Meia-Idade , Radioisótopos do Iodo/uso terapêutico , Mutação , Proteínas Proto-Oncogênicas B-raf/genética , Prognóstico , Estudos Observacionais como Assunto , Estudos de Coortes , Terapia Combinada , Cuidados Pós-Operatórios , Estudos Prospectivos , Proto-Oncogenes , Adenocarcinoma Papilar/cirurgia
2.
Clin. transl. oncol. (Print) ; 19(5): 562-570, mayo 2017. graf
Artigo em Inglês | IBECS | ID: ibc-162189

RESUMO

Objective. Recent studies have identified Engrailed-2 (EN-2), a homeobox-containing transcription factor, as a candidate oncogene in prostate cancer (PC). Therapeutic targeting on EN-2, however, is limited because the mechanism underlying EN-2 overexpression in prostatic cancer cells is unknown. This study was to investigate the potential regulatory role of miR-33a on EN-2 expression and explore this signaling axis in ability of prostate cancer survival and metastasis. Methods. The relative expression of miR-33a and EN-2 in paired prostate cancer tissue and adjacent normal tissue as well as in prostate cancer cell lines, PC3 and DU145, was determined using quantitative real-time PCR or western blot, respectively. Cells survival, migration and invasion were evaluated by assays of MTT, TUNEL and Boyden chamber assays, respectively. Direct regulation of EN-2 by miR-33a was examined by luciferase reporter assay. Results. The data showed that miR-33a was upregulated and EN-2 was downregulated in both prostate cancer tissue and prostate cancer cells. miR-33a overexpression suppresses prostate cancer cell survival and metastasis. miR-33a can directly act on EN-2 expression by binding to 3′UTR of its mRNA. Also, miR-33a negatively regulated EN-2 mRNA and protein expression. In pcDNA-EN-2 and miR-33a mimic co-transfected PC3 and DU145 cells, EN-2 overexpression reverses the anti-cell survival and metastasis actions of miR-33a overexpression. The pivotal role of miR-33a in inhibiting prostate tumor growth was confirmed in xenograft models of prostate cancer. Conclusion. Our data suggest that the functional interaction of miR-33a and EN-2 is involved in tumorigenesis of prostate cancer. Also in this process EN-2 serves as a negative responder for miR-33a (AU)


No disponible


Assuntos
Humanos , Masculino , Neoplasias da Próstata/complicações , Neoplasias da Próstata/patologia , Metástase Neoplásica/fisiopatologia , RNA Mensageiro/genética , Proteína de Suscetibilidade a Apoptose Celular/genética , Movimento Celular/genética , Biomarcadores Tumorais/genética , Neoplasias da Próstata/genética , Reação em Cadeia da Polimerase/tendências , RNA Mensageiro/metabolismo , Western Blotting , Luciferases/análise , Análise de Variância , Repressão Epigenética/genética , Proto-Oncogenes/genética , Proteínas Oncogênicas/genética
4.
Actas dermo-sifiliogr. (Ed. impr.) ; 107(1): 5-14, ene.-feb. 2016. ilus, tab
Artigo em Espanhol | IBECS | ID: ibc-147456

RESUMO

Las mastocitosis constituyen un grupo heterogéneo de enfermedades caracterizadas por la proliferación clonal de mastocitos en distintos órganos, siendo la localización cutánea la más frecuente. Es «una enfermedad rara o poco frecuente», y afecta a todos los grupos de edad, si bien suele aparecer en la primera década de la vida o entre la segunda y la quinta década de la vida, con una distribución similar por sexos. En los últimos años se han realizado grandes avances en el conocimiento fisiopatogénico del trastorno: las mutaciones somáticas del gen c-kit y la presencia de alteraciones inmunofenotípicas en los mastocitos son elementos importantes en la fisiopatogenia de las mastocitosis. Las manifestaciones clínicas son variadas y las lesiones cutáneas son la clave diagnóstica en la mayoría de los pacientes (AU)


Mastocytosis is a term used to describe a heterogeneous group of disorders characterized by clonal proliferation of mast cells in various organs. The organ most often affected is the skin. Mastocytosis is a relatively rare disorder that affects both sexes equally. It can occur at any age, although it tends to appear in the first decade of life, or later, between the second and fifth decades. Our understanding of the pathophysiology of mastocytosis has improved greatly in recent years, with the discovery that somatic c-kit mutations and aberrant immunophenotypic features have an important role. The clinical manifestations of mastocytosis are diverse, and skin lesions are the key to diagnosis in most patient (AU)


Assuntos
Humanos , Masculino , Feminino , Mastocitose/complicações , Mastocitose/diagnóstico , Mastocitose/fisiopatologia , Mastocitose Sistêmica/diagnóstico , Mastocitose Sistêmica/fisiopatologia , Mastocitose Cutânea/diagnóstico , Mastocitose Cutânea/fisiopatologia , Urticaria Pigmentosa/complicações , Triptases , Urticaria Pigmentosa/diagnóstico , Urticaria Pigmentosa/fisiopatologia , Mastócitos/citologia , Mastócitos/patologia , Proto-Oncogenes/genética , Valor Preditivo dos Testes , Imuno-Histoquímica/métodos
5.
Clin. transl. oncol. (Print) ; 17(11): 841-846, nov. 2015. tab
Artigo em Inglês | IBECS | ID: ibc-143453

RESUMO

MicroRNA (miRNA), a class of non-proteincoding RNAs, plays a critical role in many cellular processes, such as invasion, proliferation and migration, and also function in disease pathology. The transcription factor and proto-oncogene B cell CLL/lymphoma 6 (BCL6) is aberrantly expressed in various cancers. An increasing body of evidence has demonstrated that miRNAs and BCL6 can target one another and mutually adjust their expression which are of great importance in the pathogenesis of various cancers. In this report, we summarize the mutual interaction between miRNAs and BCL6, which have been studied in cancers, highlighting their mechanisms and potential therapeutic targets in cancers (AU)


No disponible


Assuntos
Feminino , Humanos , Masculino , MicroRNAs , Neoplasias/diagnóstico , Linfócitos B/patologia , Proteínas Proto-Oncogênicas c-bcl-6/administração & dosagem , Proteínas Proto-Oncogênicas c-bcl-6/análise , Proteínas Proto-Oncogênicas c-bcl-6 , Neoplasias da Mama/diagnóstico , Linfoma não Hodgkin/diagnóstico , Carcinoma Hepatocelular/diagnóstico , Proto-Oncogenes/fisiologia , Proteínas Proto-Oncogênicas , Proteínas Oncogênicas , Linfoma Difuso de Grandes Células B/diagnóstico
6.
Endocrinol. nutr. (Ed. impr.) ; 61(8): 398-403, oct. 2014. tab
Artigo em Espanhol | IBECS | ID: ibc-127581

RESUMO

OBJETIVO: El carcinoma medular de tiroides es un tumor de baja prevalencia cuyo pronóstico es peor que el del cáncer diferenciado de tiroides debido su mayor agresividad. El objetivo de este trabajo es describir las características demográficas, clínicas y genéticas de los pacientes atendidos en el área sanitaria de la Comunidad de Castilla-La Mancha durante 16 años. PACIENTES Y MÉTODOS: Los datos se recogieron mediante revisión de historias clínicas. RESULTADOS: Se revisaron las historias clínicas de 58 pacientes con una edad media al diagnóstico de 51 años (intervalo de 6 a 82 años) y un 63,8% de mujeres. La prevalencia fue de 2,84 casos por 100.000 habitantes, con una gran variabilidad entre áreas (de 0 a 5,4 casos por 100.000 habitantes). Los casos familiares representaron el 34,5% del total, siendo la mutación más frecuente la C634Y. El motivo más frecuente de diagnóstico fue la palpación de un bultoma cervical (70,6%); se solicitó ecografía al diagnóstico en 56 de 58 casos, y la calcitonina en 8 de 58 casos. La multicentricidad del tumor fue descrita en el 59 y 50% de los casos de síndrome de neoplasia endocrina múltiple tipo 2A y 2B, respectivamente, y en ningún caso esporádico. El 52% de los pacientes presentaba un estadio avanzado al diagnóstico (III o IV). La mediana de seguimiento fue de 36 meses (rango intercuartílico 14-210), con la pérdida de 11 pacientes durante el seguimiento. CONCLUSIONES: El diagnóstico de carcinoma medular de tiroides en Castilla-La Mancha se basa en la ecografía cervical, pero no en la calcitonina. Existe una alta prevalencia de este carcinoma, tanto familiar como esporádico, y una importante variabilidad en el tipo de mutación del protooncogén rearranged during transfection comparadas con las del resto de la población española


OBJECTIVE: Medullary thyroid cancer is a rare tumor that is more aggressive and has a worse prognosis than differentiated thyroid cancer. The purpose of this study was to report the demographic, clinical, and genetic characteristics of patients seen in the health care system of the community of Castilla-La Mancha over a 16-year period. PATIENTS AND METHODS: Data were collected through a review of patients' medical records. RESULTS: The medical records of 58 patients (mean age at diagnosis, 51 years; range, 6-82 years; 63.8% women) were reviewed. Prevalence rate was 2.84 cases per 100,000 inhabitants, with a high variability between areas (range, 0-5.4 cases per 100,000 inhabitants). Familial cases accounted for 34.5% of all medullary thyroid cancers, and the most common mutation was C634Y. The condition was most commonly diagnosed following palpation of a cervical lump (70.6%). At diagnosis, 56 of 58 patients underwent ultrasound and 8 of 58 patients were tested for serum calcitonin. Tumor multicentricity was reported in 59 and 50% of patients with multiple endocrine neoplasia syndrome type 2A and 2B, respectively, and in no sporadic cases. Fifty-two percent of patients had an advanced stage (III or IV) at diagnosis. Median follow-up was 36 months (interquartile range, 14-210); 11 patients were lost to follow-up. CONCLUSIONS: In Castilla-La Mancha, medullary thyroid cancer is diagnosed by cervical ultrasound, rather than calcitonin assay. There is a high prevalence of both familial and sporadic medullary thyroid cancer, and a significant variability in the type of proto-oncogen rearranged during transfection mutation as compared to the rest of the Spanish population


Assuntos
Humanos , Carcinoma Medular/epidemiologia , Neoplasias da Glândula Tireoide/epidemiologia , Tireoidectomia/estatística & dados numéricos , Neoplasia Endócrina Múltipla Tipo 2a/epidemiologia , Transfecção , Proto-Oncogenes/genética , Marcadores Genéticos , Estudos Retrospectivos , Nódulo da Glândula Tireoide/patologia
7.
Clin. transl. oncol. (Print) ; 13(11): 787-792, nov. 2011. ilus
Artigo em Inglês | IBECS | ID: ibc-125938

RESUMO

Melanoma is the deadliest cutaneous malignancy and its incidence continues to grow. Until 2011, the treatment options for metastatic melanoma were scarce and without any overall survival benefit. The emergence of new targeted therapies for BRAF mutant melanoma (vemurafenib) and immunotherapy (ipilimumab) has changed the standard of care for this disease. The objective of the present review is to summarise the biological background of the new therapeutic approaches in melanoma, focusing on apoptosis resistance, immune modulation and angiogenesis, and the direct translation into clinical practice (AU)


Assuntos
Humanos , Masculino , Feminino , Antineoplásicos/uso terapêutico , Imunoterapia/métodos , Imunoterapia , Melanoma/terapia , Neoplasias Cutâneas/terapia , Proteínas Proto-Oncogênicas B-raf , Proteínas Proto-Oncogênicas B-raf/genética , Inibidores da Angiogênese/uso terapêutico , Apoptose , Melanoma/imunologia , Melanoma/metabolismo , Neoplasias Cutâneas/imunologia , Neoplasias Cutâneas/metabolismo , Biomarcadores Tumorais/metabolismo , Proto-Oncogenes/genética
9.
Endocrinol. nutr. (Ed. impr.) ; 54(7): 371-378, ago. 2007. ilus, tab
Artigo em Espanhol | IBECS | ID: ibc-056831

RESUMO

El carcinoma medular de tiroides (CMT) puede presentarse en forma esporádica o familiar, en cuyo caso se integra en la neoplasia endocrina múltiple tipo 2 (NEM 2). La NEM 2 se origina como consecuencia de mutaciones germinales en el gen RET. Este gen incluye 21 exones y codifica el receptor RET, un receptor de membrana citoplasmática con actividad tirosinacinasa. La peculiaridad de esta alteración reside en la posibilidad de establecer una relación genotipo-fenotipo. Las distintas mutaciones en los codones del gen RET dan lugar a diversos cuadros clínicos, etiquetados clásicamente como NEM 2A, NEM 2B y CMTF (CMT familiar). En los últimos años se ha añadido una nueva clasificación en función de la agresividad del comportamiento tumoral, en la que se distinguen 3 niveles de riesgo. En la presente revisión exponemos las características fisiológicas y patológicas del gen RET, la relación genotipo-fenotipo tanto clásica como por grados de agresividad, los elementos posiblemente modificadores en esa relación (polimorfismos de un único nucleótido), la actitud a adoptar ante el CMT y el tratamiento recomendado según las características genéticas (AU)


Medullary thyroid carcinoma (MTC) can be sporadic or hereditary. The hereditary form of MTC is classified as multiple endocrine neoplasia type 2 (MEN 2). MEN 2 syndromes are caused by germinal mutations in the RET proto-oncogene. The RET gene includes 21 exons and encodes a plasma membrane-bound tyrosine kinase enzyme, the RET receptor. The peculiarity of this disease lies in the possibility of establishing genotype-phenotype correlations. Distinct RET codon mutations give rise to the different MEN 2 syndromes, traditionally classified as MEN 2A, MEN 2B and familial MTC. In the last few years, a new classification has been suggested, based on biologic tumoral aggressiveness, in which RET mutations are stratified into three levels of risk. In this review, we explain the physiological and pathological features of the RET gene, genotype-phenotype correlations (both traditional and the new risk classification), the elements that may modify this relationship (such as single nucleotide polymorphisms), suggested clinical decision-making in MTC and genetically-based treatment (AU)


Assuntos
Humanos , Carcinoma Medular/genética , Neoplasias da Glândula Tireoide/genética , Neoplasia Endócrina Múltipla/genética , Genótipo , Fenótipo , Proto-Oncogenes/genética
10.
Clin. transl. oncol. (Print) ; 9(4): 208-215, abr. 2007. tab, ilus
Artigo em Inglês | IBECS | ID: ibc-123294

RESUMO

Despite its decreasing incidence overall, gastric cancer is still a challenging disease. Therapy is based mainly upon surgical resection when the tumour remains localised in the stomach. Conventional chemotherapy may play a role in treating micrometastatic disease and is effective as palliative therapy for recurrent or advanced disease. However, the knowledge of molecular pathways implicated in gastric cancer pathogenesis is still in its infancy and the contribution of molecular biology to the development of new targeted therapies in gastric cancer is far behind other more common cancers such as breast, colon or lung. This review will focus first on the difference of two well defined types of gastric cancer: intestinal and diffuse. A discussion of the cell of origin of gastric cancer with some intriguing data implicating bone marrow derived cells will follow, and a comprehensive review of different genetic alterations detected in gastric cancer, underlining those that may have clinical, therapeutic or prognostic implications (AU)


Assuntos
Humanos , Masculino , Adulto , Idoso , Adesão Celular/genética , Marcadores Genéticos , Proteínas Tirosina Quinases/genética , Proteínas Tirosina Quinases/metabolismo , Neoplasias Gástricas/genética , Neoplasias Gástricas/cirurgia , Biomarcadores Tumorais/análise , Gastrectomia/métodos , Genes Supressores de Tumor , Instabilidade de Microssatélites , Mutação , Neovascularização Patológica/genética , Prognóstico , Proto-Oncogenes , Transdução de Sinais , Neoplasias Gástricas/mortalidade , Neoplasias Gástricas/patologia
12.
Cir. pediátr ; 18(3): 106-108, jul. 2005. tab
Artigo em Espanhol | IBECS | ID: ibc-040505

RESUMO

El carcinoma medular de tiroides (CMT) es una rara neoplasiaen la infancia. En la actualidad el estudio molecular del proto-oncogén RET, relacionado con los síndromes de neoplasia endocrina múltiple (MEN II) y carcinoma medular familiar de tiroides (CMFT)permiten identificar pacientes con riesgo de padecer carcinoma medularde tiroides en edades precoces, antes de que se manifieste la enfermedad clínicamente. Niños con antecedentes familiares de MEN II o CMFT fueron estudiados bioquímica (test de pentagastrina) y genéticamente con el fin dedeterminar el riesgo de padecer CMT y evaluar la posibilidad de realizar tiroidectomía profiláctica (AU)


The medullary thyroid carcinoma (MTC) is a rare neoplasiaoccurring during childhood. At present time the molecular examinationof the proto-oncogen RET, related to syndromes of multipleendocrine neoplasia (MEN II) and familial medullary thyroid carcinoma(FMTC) to allows identify patients with risk of suffering of medullarythyroid carcinoma in early ages, before the disease becomes clinicallypronunced. Children with familial antecedents of MEN II orFMTC were biochemically (pentagastrin-stimulated) and geneticallystudied with the purpose of determining the risk of developing a MTCand in order to assess the possibilities of making a prophylactic thyroidectomyThe medullary thyroid carcinoma (MTC) is a rare neoplasia occurring during childhood. At present time the molecular examinationof the proto-oncogen RET, related to syndromes of multiple endocrine neoplasia (MEN II) and familial medullary thyroid carcinoma(FMTC) to allows identify patients with risk of suffering of medullary thyroid carcinoma in early ages, before the disease becomes clinically pronunced. Children with familial antecedents of MEN II orFMTC were biochemically (pentagastrin-stimulated) and genetically studied with the purpose of determining the risk of developing a MTCand in order to assess the possibilities of making a prophylactic thyroidectomy (AU)


Assuntos
Masculino , Feminino , Criança , Humanos , Carcinoma Medular/prevenção & controle , Tireoidectomia , Marcadores Genéticos , Neoplasias da Glândula Tireoide/prevenção & controle , Carcinoma Medular/patologia , Neoplasia Endócrina Múltipla/genética , Pentagastrina , Proto-Oncogenes , Neoplasias da Glândula Tireoide/patologia
13.
Endocrinol. nutr. (Ed. impr.) ; 52(5): 199-201, mayo 2005.
Artigo em Espanhol | IBECS | ID: ibc-036283

RESUMO

Las neoplasias endocrinas múltiples (MEN) son síndromes de herencia autosómica dominante caracterizados por la asociación de lesiones en distintas glándulas presentes en varios miembros de una misma familia. Las principales características de MEN tipo 1 incluyen hiperparatiroidismo primario, tumores pancreáticos y adenomas hipofisarios; con menos frecuencia pueden aparecer adenomas suprarrenales, tumores tímicos y bronquiales, lipomas y varias lesiones cutáneas. Los síndromes tipo 2 (MEN 2A y 2B, y carcinoma medular de tiroides familiar) se caracterizan por alta penetrancia de carcinoma medular de tiroides y difieren en su expresión variable de feocromocitoma, hiperparatiroidismo y otros rasgos clínicos. El gen supresor de tumores MEN1 codifica para una proteína nuclear, la menina, que interactúa con diferentes factores de transcripción. Los síndromes MEN 2 se producen por mutaciones en línea germinal en el protooncogén RET, que codifica para un receptor tirosincinasa. El estudio genético de mutaciones en estos 2 genes permite la identificación de individuos con predisposición a la enfermedad, el diagnóstico temprano y el adecuado tratamiento clínico y terapéutico (AU)


Multiple endocrine neoplasias (MEN) are inherited autosomal dominant syndromes characterized by the association of distinct glandular lesions in several members of the same kindred. The main clinical features of MEN1 include primary hyperparathyroidism, pancreatic islet cell tumors and pituitary adenomas; less common features are adrenal adenomas, thymic and bronchial carcinoid tumors, lipomas and various cutaneous lesions. The MEN2 syndromes (MEN2A, MEN2B and familial medullary thyroid carcinomas) are characterized by a high penetrance of medullary thyroid carcinoma and differ in their variable expression of pheochromocytoma, hyperparathyroidism and other clinical features. The MEN1 tumor suppressor gene encodes a nuclear protein, menin, which interacts with distinct transcription factors. The MEN2 syndromes are caused by germ-line which encodes a tyrosine kinase transmembrane receptor. Genetic testing for mutmutations of the RET proto-oncogene, ations in these two genes allows identification of individuals predisposed to the disease, and their early diagnosis, and appropriate clinical and therapeutic management (AU)


Assuntos
Humanos , Neoplasia Endócrina Múltipla/genética , Suscetibilidade a Doenças , Hiperparatireoidismo/etiologia , Heterozigoto , Proto-Oncogenes
14.
Oncología (Barc.) ; 25(5): 243-257, mayo 2002. tab
Artigo em Espanhol | IBECS | ID: ibc-13815

RESUMO

Los proto-oncogenes desempeñan un papel clave en la regulación de la proliferación y diferenciación celular, junto con genes supresores, genes de reparación del ADN y genes reguladores de la apoptosis, fundamentalmente. La acumulación de sucesivas alteraciones cualitativas y/o cuantitativas de estos genes constituye la base del desarrollo del cáncer. La sobreexpresión de proto-oncogenes constituye un importante mecanismo de activación oncogénica al representar una ganancia de función y, por tanto, la estimulación de la proliferación o la supervivencia celular. La sobreexpresión génica puede estar asociada a cambios genéticos, tales como la translocación cromosómica o la amplificación génica, o a cambios epigenéticos, consistentes principalmente en alteraciones de los patrones de metilación del ADN y acetilación de las histonas. Dicha alteración es frecuente en cáncer de mama y se asocia a factores de mal pronóstico y resistencia al tratamiento. (AU)


Assuntos
Feminino , Humanos , Expressão Gênica , Neoplasias da Mama/genética , Proto-Oncogenes/genética , Prognóstico , Regulação da Expressão Gênica
15.
MAPFRE med ; 12(4): 289-293, oct. 2001.
Artigo em Espanhol | IBECS | ID: ibc-8764

RESUMO

La pleiotrofina (PTN) es un factor de crecimiento perteneciente a una familia de proteínas homólogas a las HBGF. El gen Ptn se expresa ampliamente durante el desarrollo mientras que en la vida adulta su distribución es muy restringida. Pero su expresión aumenta en los procesos tumorales e inflamatorios crónicos. El propósito de este artículo es realizar una revisión y análisis de los conocimientos actuales sobre la PTN, con especial interés en sus propiedades como factor promotor del crecimiento celular y la angiogénesis (AU)


Assuntos
Humanos , Divisão Celular/fisiologia , Fatores de Crescimento de Fibroblastos/fisiologia , Neovascularização Fisiológica/fisiologia , Citocinas/fisiologia , Citocinas/genética , Fatores de Crescimento de Fibroblastos/genética , Fatores de Crescimento de Fibroblastos/química , Neoplasias/genética , Proto-Oncogenes/genética
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