Journal articles: 'Carcinoma Endometrio'

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Morán Mejía, Javier Alberto, Rosario Velásquez, Victor Argueta, and Roberto Orozco. "Carcinoma endometriode sincrónico que afecta útero y trompa uterina." Revista médica (Colegio de Médicos y Cirujanos de Guatemala) 159, no. 1 (June 22, 2020): 41–43. http://dx.doi.org/10.36109/rmg.v159i1.173.

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La aparición de tumores sincrónicos en el aparato genital femenino es infrecuente. Se conoce poco sobre la presentación simultánea de carcinomas endometrioides del endometrio y la trompa uterina. Presentamos un caso de una paciente femenina de 38 años, nulípara, con historia de hemorragia vaginal de un mes de evolución, a quien se le realizó histerectomía y salpingooforectomía izquierda, donde el estudio anatomopatológico definitivo fue carcinoma endometriode de endometrio y de trompa uterina sincrónico.

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Cruz Muñóz, Héctor. "Sobre el diagnóstico, pronóstico y tratamiento del carcinoma endometrial." Revista Peruana de Ginecología y Obstetricia 12, no. 3 (June 12, 2015): 324–72. http://dx.doi.org/10.31403/rpgo.v12i884.

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El diagnóstico clínico del carcinoma endometrial en sus estadíos iniciales es muy difícil porque ni la sintomatología ni el examen objetivo proporcionan elementos de juicio lo suficientemente característicos como para poder afirmarlo con alguna certeza. El síntoma que hace pensar siempre en una neoplasia maligna del endometrio es la metrorragia que ocurre en una mujer que está en la época post-menopáusica, pero este síntoma no es de manera alguna propia del carcinoma endometrial desarrollado en este período de la vida. En efecto, en un estudio efectuado en la Clínico Ginecológica Universitaria (23) sobre 488 casos de hemorragia genital post-menopáusica, 265 casos correspondían a una neoplasia maligna (54,5%) de los cuales 55 presentaban un carcinoma endometrial, vale decir, que sólo el 11,2 % de los pacientes que consultaron por una hemorragia genital post-menopáusica tenían un carcinoma del endometrio.

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Aqueche, Gabriela, and Marisol Gramajo. "Carcinoma de células escamosas primario de endometrio." Revista médica (Colegio de Médicos y Cirujanos de Guatemala) 160, no. 3 (December 6, 2021): 298–300. http://dx.doi.org/10.36109/rmg.v160i3.382.

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El carcinoma de células escamosas primario de endometrio, es una entidad poco común, que para ser considerado como primario debe llenar los criterios de Fluhmman, de 1928: 1) ausencia simultánea de adenocarcinoma, 2) que no haya continuidad entre el tumor endometrial y el epitelio que reviste el cuello uterino y 3) comprobar que no exista proliferación de un carcinoma primario de células escamosas del cuello. Se presenta el caso de mujer de 80 años quien consulta a la emergencia de ginecología por hemorragia vaginal de 5 días.

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Díaz, Juan, Marco Martell, Jorge Pomatanta, Luz Cisneros, Guillermo Fonseca, and Rafael Roeder. "Carcinoma de endometrio: cuadro clínico-patológico." Revista Peruana de Ginecología y Obstetricia 43, no. 3 (June 25, 2015): 202–8. http://dx.doi.org/10.31403/rpgo.v43i1072.

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Con la finalidad de identificar el cuadro clínico patológico y determinar el estadío clínico, se analizó retrospectivamente información de 38 pacientes con carcinoma de endometrio admitidas al hospital Belén, Trujillo, Perú, desde 1966 a 1996. La edad promedio en la serie total fue 53,1 ± 11,4 años (rango, 22 a 8,3 años).La edad media de presentación de la menarquía fue 13,4 ± 1,6 años y de la menopausia (n=25) 48,2 ± 3,6 años. Once pacientes, fueron nulíparas (28,9%), cinco (13,2%) presentaron ovario poliquístico, cuatro (10,5%) tuvieron historia previa de hipertensión arterial, dos (5,3%) diabetes mellitus y dos (5,3%) historia personal de otro cáncer primario. El tiempo promedio de enfermedad fue 7,9 meses. Los síntomas más comunes fueron sangrado genital (89,5%) y dolor pélvico (52,6%). El signo más frecuente fue útero aumentado de tamaño (44,7%). El rendimiento diagnóstico de la biopsia de endometrio (n=15) y de la dilatación mas curetaje (n=7) fue 80% y 85,7%, respectivamente. En 12 de 13 pacientes en estadío I, el Papanicolaou fue negativo. De acuerdo a la FIGO, 73,7% de las pacientes estuvo en estadío clínico I, 15,8% en estadío III, 7,9% en estadío IV y 2,6% en estadío II. El adenocarcinoma fue el tipo histológico más frecuente (75,7%) seguido del adenoacantoma (8,1%). En el estadío I, 18 casos fueron carcinomas bien diferenciados y hubo 10 casos entre moderada y pobremente diferenciados. El diagnóstico precoz y el estadiaje adecuado son pasos previos muy importantes al tratamiento definitivo del cáncer endometrial.

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Wood, Juan, Alfredo Durán, Sergio Fuensalida, and Alberto Guzmán. "Relación entre la hiperplasia endometrial y el adenocarcinoma del endometrio." Revista Peruana de Ginecología y Obstetricia 1, no. 2 (June 12, 2015): 1–13. http://dx.doi.org/10.31403/rpgo.v1i896.

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El material histopatológico que se considera en esta ocasión demuestra que la hiperplasia endometrial, como manifestación de un estado estrogénico persistente e incontrarrestado, desempeña un rol importante en la génesis del carcinoma endometria1. Las imágenes histológicas en estas circunstancias pueden corresponder a una hiperplasia glándulo-quística o a una hiperplasia adenomatosa. La hiperplasia endometrial glándulo-quística durante la menacma y el climaterio premenopáusico, reflejo de desequilibrios endocrinos, no tiene mayor importancia en estos períodos, pero cuando se hace presente en la postmenopausia adquiere una significativa influencia en relación con el desarrollo del carcinoma endometrial. La hiperplasia adenomatosa que evoluciona durante el período de madurez sexual reviste mayor importancia que la variedad glándulo-quística, pues si bien traduce al igual que ella la existencia de una disfunción endocrina y como ella constituye también una lesión reversible, su existencia requiere una mayor preocupación aún dentro de este período y en relación directa con la mayor edad de la mujer. Cuando evoluciona en la postmenopausia adquiere mayor significación que la variedad glándulo-quística en la génesis del carcinoma del endometrio. El estudio de 26 casos de coexistencia de hiperplasia y adenocarcinema del endometrio nos permitió establecer en 7 de ellos la concurrencia simultánea de las dos variedades de hiperplasia, glándulo-quística y adenomatosa con adenocarcinoma; en 6 la evolución concomitante de hiperplasia adeno-quística y adenocarcinoma; en otras 6 de hiperplasia adenomatosa y adenocarcinoma y, finalmente, en las 7 restantes se reveló la transformación gradual de una hiperplasia adeno-quística en una hiperplasia adenomatosa y, por dual de una hiperplasia adeno-quística en una hiperplasia adenomatosa y, por último, en un carcinoma, dentro de un plazo variable de 1 a 4 años (Cuadro N°1). Si se analizan las edades de las pacientes que constituyen cada una de estos tres grupos, en el momento en que se estableció el diagnóstico de degeneración maligna, se comprueba que la edad media más baja -48 años- correspondía a la coexistencia de hiperplasia adenomatosa y adenocarcinoma. En cambio, ella era de 52 años para la asociación, hiperplasia glandular quística, hiperplasia adenomatosa y adenocarcinoma y de 58 para la asociación hiperplasia glándulo-quística adenocarcinoma. Sin pretender establecer conclusiones dado su número escaso de observaciones llamamos la atención a que exista una mayor propensión a la degeneración maligna y que ésta se establece más tempranamente, cuando concurre la hiperplasia adenomatosa. Esta afirmación se confirma si establecemos la edad media en los dos grupos de adenocarcinomas en los cuales se hizo presente esta modalidad de hiperplasia en las imágenes histológicas, comprobando que ella es de 50.5 años por 58 en el grupo en que ella no existe. Las comprobaciones anteriores conducen a una conclusión importante en relación con la profilaxia del carcinoma del endometrio en el sentido que la existencia de una hiperplasia endometrial, glándulo-quística o adenomatosa en el período postmenopáusico, haría aconsejable la histerectomia. La radioterapia en general y la curieterapia intrauterina en especial, por constituir el método terapéutico al cual se recurre en las metrorragias disfuncionales del climaterio, sólo podría indicarse cuando existiera una contraindicación quirúrgica absoluta o bien ante la negativa de la paciente para aceptar la intervención. En ambas circunstancias se deberá exigir controles periódicos los que necesariamente deberán comprender exámenes citológicos y nuevos raspados-biópsicos. Las comprobaciones señaladas en la conclusión N° 4 conducirían a aceptar el concepto de carcinoma "in situ" del endometrio, a pesar de algunas autorizadas opiniones en contrario. Se considera que debe mantenérsele vigente para que en la práctica diaria del laboratorio se investiguen las imágenes correspondientes y poder así acumular mayor documentación que permita en el futuro emitir un juicio con mayor fundamento. Convendrá recordar que el Comité de Estocolmo, sin pronunciarse sobre las características propias del carcinoma "in situ" del endometrio ha incluido al igual que en el carcinoma cervical un período 0, definiéndolo así : casos que el patólogo considera que muy probablemente son de naturaleza carcinomatosa aunque no es posible establecer un diagnóstico definitivo en este sentido.

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Aguilar, Ceny. "Carcinoma de Endometrio de Casos." Anales de la Facultad de Medicina 56, no. 1 (April 7, 2014): 17. http://dx.doi.org/10.15381/anales.v56i1.4918.

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El carcinoma de endometrio es un tumor maligno originado a expensas del epitelio, el que resultaría ser consecuencia de un hiperestronismo relativo o absoluto. Según algunos autores, pasaría por una gama de lesiones preliminares como las hiperplasias adenomatosas. En nuestro trabajo, revisamos 62 casos diagnosticados microcóspicamente en el Servicio de Anatomía Patológica del Hospital Daniel A. Carrión en sus 24 años de funcionamiento. El 75% refirió ginecorragia de más de un mes de evolución: el 68% de casos corresponde a mujeres puérperas, nulíparas o con baja paridad. Al examen físico, en la mitad de los casos se reporta útero aumentado de tamaño, y en 30% como de caracteres normales. El diagnóstico clínico presuntivo al que arriba el ginecólogo es de hemorragia uterina disfuncional en 32% y de cáncer en 33%, en este último caso probablemente por contar por un diagnóstico anatomo-patológico previo por legrado biópsico. Al examen microscópico, encontramos que más del 80% de nuestros casos corresponden a adenocarcinoma, sólo 6 son de tipo adenoescamoso. El tipo de adenocarcinoma predominante fue el de aspecto histológico endometrioide, en 32% de los cuales se encontró diferenciación celular. Los carcinomas bien diferenciados fueron frecuentes. En 64% del total no hubo infiltración alguna, llegando el tumor solo al miometrio. Se encontró escasas precursoras.

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Elmore, Lynne W., Kelly Domson, Jonathan R. Moore, Michael Kornstein, and R. Tucker Burks. "Expression of c-Kit (CD117) in Benign and Malignant Human Endometrial Epithelium." Archives of Pathology & Laboratory Medicine 125, no. 1 (January 1, 2001): 146–51. http://dx.doi.org/10.5858/2001-125-0146-eockci.

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Abstract Background.—The proto-oncogene c-kit encodes a tyrosine kinase receptor (CD117) with a molecular weight of 145 kd. Previous studies, predominantly utilizing immunohistochemistry, have led to contradictory findings regarding the expression of CD117 in the endometrium. To help resolve this issue, we analyzed a series of benign and malignant endometrial tissues using both immunohistochemistry and Western blot analysis. Objective.—To examine the expression of CD117 in benign and malignant human endometrial tissues. Methods.—The expression of CD117 in 35 benign endometrial tissues (7 hyperplastic, 14 proliferative, 14 secretory) and 10 endometrioid carcinomas was investigated by immunohistochemistry (clone K45 monoclonal antibody). Immunoprecipitation (clone K69 monoclonal antibody) followed by Western blotting (clone K45 monoclonal antibody and clone 1.D9.3D6 monoclonal antibody) was performed to confirm CD117 expression. Results.—Fifty-seven percent of the hyperplasias, 93% of proliferative endometria, and 79% of secretory endometria immunostained positively for CD117. In benign endometria, epithelial staining tended to be more intense in the hyperplastic and proliferative endometria as compared to the secretory endometria, whereas endometrial stromal cells were not immunoreactive. Of the 10 frozen endometrial tissues analyzed by immunohistochemistry, 4 of 9 endometrioid carcinomas and a single case of an endometrioid polyp developing in association with a carcinoma expressed CD117. Immunoprecipitation followed by Western blot analysis confirmed expression of full-length CD117 in an endometrial polyp and carcinoma, and revealed a correlation between levels of immunoprecipitated CD117 and immunohistochemical staining intensity. Conclusions.—Benign and malignant endometrial tissues express CD117. Our data suggest (a) a possible relationship between estrogen and CD117 expression in benign endometrium and (b) potential involvement of this growth factor receptor in endometrial carcinogenesis.

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Pérez Montiel, Camilo, María Murillo Salas, César Redondo Bermúdez, and Katherine Redondo de Oro. "Endometritis xantogranulomatosa asociada a carcinoma escamocelular de cérvix: presentación de un caso y revisión de la literatura." Revista Ciencias Biomédicas 8, no. 2 (November 7, 2020): 105–10. http://dx.doi.org/10.32997/rcb-2019-2877.

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Introducción: la endometritis xantogranulomatosa es un proceso inflamatorio raro del endometrio, que se caracteriza por la presencia de abundantes histiocitos espumosos asociados a células inflamatorias mixtas. La importancia de este hallazgo histopatológico es su asociación con neoplasias malignas de origen endometrial y cervical, por lo cual el patólogo debe realizar un correcto abordaje morfológico e inmunohistoquímico. Se presenta un caso de endometritis xantogranulomatosa asociado a carcinoma escamocelular mal diferenciado de cérvix.Caso Clínico: paciente femenina de 75 años de edad, con cuadro clínico de seis meses de evolución caracterizado por salida de líquido claro por genitales externos asociado a dolor pélvico intermitente. Ecográficamente se observa aumento de tamaño del útero, a expensas de acumulación de líquido con un volumen de 700 cc y estenosis cervical. Se realiza biopsia endometrial guiada por histeroscopia con reporte histopatológico e inmunohistoquímico de endometritis xantogranulomatosa asociado a carcinoma escamocelular mal diferenciado de cérvix. Conclusión: la endometritis xantogranulomatosa es un hallazgo histopatológico poco frecuente en el endometrio, lo cual es un reto diagnóstico para el patólogo debido a la asociación con neoplasias malignas de origen endometrial y cervical.

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Pérez-Montiel, Camilo Andrés. "Nueva clasificación molecular del carcinoma de endometrio: impacto en el diagnóstico histopatológico, tratamiento y pronóstico." MedUNAB 24, no. 3 (January 5, 2022): 365–74. http://dx.doi.org/10.29375/01237047.4015.

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Introducción. El carcinoma de endometrio es una patología heterogénea a nivel patogénico, histopatológico y molecular. En los últimos años se han sumado esfuerzos para esclarecer y aumentar el conocimiento de las bases moleculares, logrando así dividir las pacientes en cuatro subgrupos descritos por el Atlas del Genoma del Cáncer (TCGA, por sus siglas en inglés), obteniéndose valiosa información que afecta el diagnóstico, tratamiento y pronóstico de las pacientes con esta enfermedad. El objetivo de la siguiente revisión es exponer la nueva clasificación molecular del carcinoma de endometrio, así como discutir las ventajas que esta trae a la hora de estratificar a las pacientes y tomar decisiones terapéuticas. División de los temas tratados. Se realizó una búsqueda bibliográfica no sistemática en las bases de datos PubMed, Cochrane y Medline desde el año 2014 hasta el 2020 sobre el carcinoma de endometrio y su clasificación molecular. Se expone de manera concreta y actualizada el contexto histórico, los diferentes subgrupos moleculares y cómo estos impactan en el manejo de las pacientes. Conclusiones. El carcinoma de endometrio es una enfermedad heterogénea a nivel histopatológico, clínico y molecular. Con la nueva clasificación y los estudios prospectivos se podrán crear nuevas estrategias que permitan brindar mejores protocolos diagnósticos y terapéuticos.

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Ferrero, S., C. Esteve, I. Mora, J. Sabrià, E. González, and J. M. Lailla. "Carcinoma de endometrio y ovario sincrónicos." Clínica e Investigación en Ginecología y Obstetricia 34, no. 2 (April 2007): 77–79. http://dx.doi.org/10.1016/s0210-573x(07)74478-7.

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Soihet, Samoel. "Estrogenoterapia Prolongada en Postmenopausicas y Carcinoma de Endometrio: 20 Años de Seguimiento." Revista Peruana de Ginecología y Obstetricia 28, no. 1 y 2 (May 23, 2015): 33–39. http://dx.doi.org/10.31403/rpgo.v28i664.

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Con el fin de mejorar los síntomas climatéricos, desde 1960 se comenzó a administrar de 6 -7.5 mg diarios de estrógenos, con la consecuente hemorragia. Algunos legrados mostraron hiperplasia endometrial quística. Luego, se realizaron estudios del endometrio, previos al tratamiento de las candidatas. Durante 20 años fueron seleccionadas 2814 mujeres. Fueron separadas del estudio aquellas con patología cervical, endometrial o mamaria; se les administró estradiol sintético y/o estrógenos conjugados: 0,265-1,25 mg en forma interdiaria. A pesar de los estudios clínicos y epidemiológicos retrospectivos publicados, en favor de que el estrógeno exógeno de reemplazo estaría asociado al cáncer endometrial, en este estudio prospectivo y prolongado se demuestra que no hay relación alguna. Este riesgo ha sido señalado de manera exagerada, porque dichos estudios incluían los casos de hiperplasia endometrial atípica, dentro de los casos de portadoras de cáncer endometrial. Muchas formas de estas han sido criticadas por la manera en que fueron analizadas ya que, confundieron y mal interpretaron la histopatología. Las dosis pequeñas, para satisfacer las necesidades climatéricas, pueden ser un indicador de patología endometrial subclínica, desde los primeros meses de su administración. Los que se apoyan en la evidencia epidemiológica de riesgo, debieran incluir esta información en sus estudios analíticos.

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Serteva, D., E. Poryazova, and Ts Velikova. "Endometriosis Locations and Coexistence with other Uterine Conditions in a Bulgarian Sample of Patients." American International Journal of Multidisciplinary Scientific Research 5, no. 2 (May 14, 2019): 5–9. http://dx.doi.org/10.46281/aijmsr.v5i2.255.

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Endometriosis is a non-tumor, estrogen-dependent, chronic gynecological disease, which is characterized by the presence of endometrial glands and stroma outside the endometrium of the uterus. Endometriosis affects between 10% and 15% of women in reproductive age. It is often associated with chronic pelvic pain and reproductive difficulties. Endometriosis can be classified as ovarian, extra-ovarian or mixed. Adenomyosis is considered, by some authors, as a separate variant of endometriosis. It is diagnosed as the presence of ectopic benign endometrial glands and stroma in the myometrium, where the minimal distance from the endometrio-myometrial junction is 2-4 mm. Our study includes 224 cases of women with endometriosis with different locations - in the myometrium (adenomyosis), in the ovaries, fallopian tubes, soft tissues and appendix as well as in combination with other conditions of the uterine body, such as endometrial carcinoma, leiomyomas, endometrial hyperplasia, polyps and atrophy and cervical cancer. There are cases of coexistence of several conditions in the same patient, and we are trying to find the reason behind this.

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Elhafey, Ahmed S., John C. Papadimitriou, Mohamed S. El-Hakim, Ahmed I. El-Said, Bahaa B. Ghannam, and Steven G. Silverberg. "Computerized Image Analysis of p53 and Proliferating Cell Nuclear Antigen Expression in Benign, Hyperplastic, and Malignant Endometrium." Archives of Pathology & Laboratory Medicine 125, no. 7 (July 1, 2001): 872–79. http://dx.doi.org/10.5858/2001-125-0872-ciaopa.

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Abstract Context.—The endometrium is an intrinsically dynamic tissue with great capability for regeneration and proliferation; consequently, there is some overlap between features seen in benign, premalignant, and malignant lesions. This leads to marked intrabiopsy, interbiopsy, and interobserver variability. Objective.—We studied the specificity and sensitivity of computerized image analysis of molecular markers to evaluate its potential use as a diagnostic tool. Design.—Specimens from 100 patients were examined and the following histologic diagnoses were assigned: proliferative endometrium (n = 10), secretory endometrium (n = 10), endometrial hyperplasia (n = 40; 30 with no atypia, 10 with atypia), and carcinoma (n = 40; 20 endometrioid, 10 serous, and 10 clear cell). All cases were evaluated immunohistochemically for p53 and proliferating cell nuclear antigen (PCNA) expression. Computerized image analysis was performed with a CAS 200 digital analyzer. Results.—Expression of p53 was found only in carcinomas (65%) and endometrial hyperplasia with atypia (30%). Expression of p53 was higher in the poor prognostic categories (serous carcinoma and clear cell carcinoma) than in endometrioid carcinoma. In endometrioid carcinoma, p53 expression correlated with grade. Proliferating cell nuclear antigen showed a similar pattern of results to p53 in the various carcinoma subtypes and endometrioid carcinoma grades. Endometrial hyperplasia PCNA values were the lowest among all the groups. Both carcinomas and proliferative endometrium showed higher glandular and stromal PCNA values, significantly different from endometrial hyperplasia with atypia. In proliferative endometrium, stromal PCNA was the highest among all of the groups. The p53 and PCNA results correlated with each other for carcinoma. Conclusions.—Computerized image analysis correlates well with the established morphologic groups of endometrial pathology and yields results consistent with previous studies. Owing to its higher degree of sensitivity, computerized image analysis is of potential use in cases of diagnostic dilemmas and can help objectively allocate the case in the correct category (eg, proliferative endometrium vs endometrial hyperplasia, endometrial hyperplasia with atypia vs endometrioid carcinoma). It is particularly useful in the evaluation of stromal changes.

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Lara, Ernesto. "Neoplasia intraepitelial endometrial: una lesión precursora de cáncer de endometrio." Revista de Obstetricia y Ginecología de Venezuela 81, no. 01 (March 23, 2021): 75–85. http://dx.doi.org/10.51288/00810111.

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Endometrial cancer represents worldwide the sixth most common malignant pathology in the female population, the endometroid type constitutes the most common form, usually developed from a typical sequence of endometrial hyperplasia secondary to sustained exposure to unopposed estrogens balanced by progestogens. Different classification systems for endometrial hyperplasia have been described, the most recent, published by the World Health Organization in 2014, proposes two categories: 1) hyperplasia without atypia, and 2) atypical hyperplasia or endometrial intraepithelial neoplasia. This classification avoids confusion due to the different terms in use and reflects a better understanding of the pathology behavior. Atypical hyperplasia or endometrial intraepithelial neoplasia is considered a precursor lesion to endometrial carcinoma type I. Health professionals must handle standardized terminology, accurately diagnose this entity, and ensure proper treatment of it. Keywords: Endometrial intraepithelial neoplasia, Endometrial hyperplasia, Atypical hyperplasia, Endometrial cancer.

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Quddus, M. Ruhul, Predrag Latkovich, William J. Castellani, C. James Sung, Margaret M. Steinhoff, Robert C. Briggs, and Roberto N. Miranda. "Expression of Cyclin D1 in Normal, Metaplastic, Hyperplastic Endometrium and Endometrioid Carcinoma Suggests a Role in Endometrial Carcinogenesis." Archives of Pathology & Laboratory Medicine 126, no. 4 (April 1, 2002): 459–63. http://dx.doi.org/10.5858/2002-126-0459-eocdin.

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Abstract Context.—Endometrioid carcinoma is often preceded by characteristic histopathologic lesions known as endometrial hyperplasia. Estrogen appears to be involved in the development of endometrioid carcinoma. Other mechanisms of endometrial carcinogenesis include mutations in p53 and PTEN tumor suppressor genes and overexpression of cyclin D1. However, the pattern of cyclin D1 expression is not well defined in normal, hyperplastic, neoplastic, and metaplastic endometrium. Design.—Cyclin D1 immunohistochemical analysis was used to evaluate 108 fixed, paraffin-embedded endometrial biopsy specimens and uterine resections obtained from 108 patients. Specimens included proliferative and secretory endometria, simple and complex hyperplastic lesions, and endometrioid adenocarcinoma. Normal and metaplastic surface epithelia were also evaluated independently of glandular morphologic features. Results.—Cyclin D1 was significantly overexpressed in glands with complex hyperplasia and endometrioid adenocarcinoma compared with proliferative or secretory endometrium and simple hyperplasia. Significant overexpression was also noted in papillary, syncytial, and squamous metaplasias compared with normal surface epithelium or epithelium with tubal metaplasia. Conclusion.—Overexpression of cyclin D1 increases from normal endometrium to hyperplasia and carcinoma, suggesting that it may play a role in endometrial carcinogenesis. Overexpression of cyclin D1 in endometrial glands was independent from overexpression of cyclin D1 in surface metaplastic epithelium.

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Laguna Olmos, Mariano, Ana Cristina Ruiz Peña, María José Puente Martínez, M. Encarnación Lag Asturiano, Cristina Fernández García, Laura San Juan Sáenz, and Marta Giménez Campos. "Carcinoma endometrioide sincrónico de ovario y endometrio." Revista chilena de obstetricia y ginecología 85, no. 3 (June 2020): 263–69. http://dx.doi.org/10.4067/s0717-75262020000300263.

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Gallego Noreña, Gildardo, Jaime Uribe Duque, and Juan Luis Londoño. "Carcinoma de endometrio. Quince años de experiencia." Revista Colombiana de Obstetricia y Ginecología 37, no. 4 (August 29, 1986): 299–307. http://dx.doi.org/10.18597/rcog.1932.

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El Cáncer Endometrial ocupa el tercer lugar en frecuencia entre las neoplasias genitales malignas de la mujer. Las publicaciones a nivel mundial indican un incremento en la frecuencia, en oposición al cáncer cérvico uterino que muestra una franca disminución.

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Alcaide, Noelia, Benito Velayos, Guillermo González Redondo, Edel Berroa de la Rosa, Ana Macho Conesa, Luis Fernández Salazar, Isabel Jiménez, and José Manuel González. "Fístulas ileocólicas tras radioterapia por carcinoma de endometrio." Gastroenterología y Hepatología 39, no. 1 (January 2016): 23–24. http://dx.doi.org/10.1016/j.gastrohep.2014.12.009.

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Arai, Y., and M. Nishida. "Differential diagnosis between normal endometrium and endometrial hyperplasia with immunostaining cytology using anti-LeY monoclonal antibody." International Journal of Gynecologic Cancer 13, no. 1 (2003): 42–46. http://dx.doi.org/10.1136/ijgc-00009577-200301000-00008.

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We have previously reported that both endometrial cancer and endometrial hyperplasia stain positively for the anti-LeY monoclonal antibody, whereas normal endometrium does not. Endometrial hyperplasia is a premalignant change associated with the eventual development of endometrial carcinoma. However, it can be difficult to differentiate hyperplasia from normal endometrium in cytology. This study illustrates the use of immunocytochemical cytology using anti-LeY monoclonal antibody to differentiate between endometrial hyperplasia and normal endometrium. Immunostaining using anti-LeY monoclonal antibody was performed on cytologic specimens obtained from 17 normal endometria, 25 endometria with endometrial hyperplasia, and 13 endometria with endometrial carcinoma. All normal endometria displayed negative staining for anti-LeY monoclonal antibody, whereas all endometria with endometrial carcinoma displayed positive staining. Of the endometrial hyperplasia cases, 21 displayed positive staining. However, four displayed negative staining due to the small number of cells available for diagnosis. We believe that immunostaining cytology using anti-LeY monoclonal antibody is a useful method for differentiating between normal endometrium and endometrial hyperplasia.

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Bedoya Hevia, Mariano. "Lesiones pre-malignas del endometrio." Revista Peruana de Ginecología y Obstetricia 18, no. 1-2-3 (July 23, 2015): 225–27. http://dx.doi.org/10.31403/rpgo.v18i1488.

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La hiperplasia genuina, macroscópicamente puede confundirse con el cáncer; pero se le distingue porque el último presenta necrosis y friabilidad. La hiperplasia adenomatosa puede confundirse con el cáncer; en opinión de varios autores (Gundberg, Kaplan), los cambios atípicos están relacionados con una prolongada estimulación estrogénica. Novack reconoce la existencia de cierta correlación entre hiperplasia post-menopáusica y adenocarcinoma. Wilson y Beecham y Carrington, expresan que la hiperplasia adenomatosa exhibe evidencias suficientes para ser consideradas como lesiones pre cancerosas o como carcinoma in-situ. La estimulación estrogénica prolongada en mujeres predispuestas genéticamente al cáncer, puede iniciar la carcinogénesis. Es posible que la metaplasia y los pólipos endometriales puedan ser considerados como lesiones pre-malignas en la mujer añosa.

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Okuda, Tsuyoshi, Akihiko Sekizawa, Yuditiya Purwosunu, Masaaki Nagatsuka, Miki Morioka, Masaki Hayashi, and Takashi Okai. "Genetics of Endometrial Cancers." Obstetrics and Gynecology International 2010 (2010): 1–8. http://dx.doi.org/10.1155/2010/984013.

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Endometrial cancers exhibit a different mechanism of tumorigenesis and progression depending on histopathological and clinical types. The most frequently altered gene in estrogen-dependent endometrioid endometrial carcinoma tumors isPTEN. Microsatellite instability is another important genetic event in this type of tumor. In contrast,p53mutations or Her2/neu overexpression are more frequent in non-endometrioid tumors. On the other hand, it is possible that the clear cell type may arise from a unique pathway which appears similar to the ovarian clear cell carcinoma.K-rasmutations are detected in approximately 15%–30% of endometrioid carcinomas, are unrelated to the existence of endometrial hyperplasia. Aβ-cateninmutation was detected in about 20% of endometrioid carcinomas, but is rare in serous carcinoma. Telomere shortening is another important type of genomic instability observed in endometrial cancer. Only non-endometrioid endometrial carcinoma tumors were significantly associated with critical telomere shortening in the adjacent morphologically normal epithelium. Lynch syndrome, which is an autosomal dominantly inherited disorder of cancer susceptibility and is characterized by a MSH2/MSH6 protein complex deficiency, is associated with the development of non-endometrioid carcinomas.

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Sangwan, Karuna, Monika Garg, Nayana Pathak, and Lavleen Bharti. "Expression of Cyclin D1 in Hyperplasia and Carcinoma of Endometrium and Its Correlation with Histologic Grade, Tumor Type, and Clinicopathological Features." Journal of Laboratory Physicians 12, no. 03 (November 23, 2020): 165–70. http://dx.doi.org/10.1055/s-0040-1721150.

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Abstract Background Endometrial carcinoma is often preceded by characteristic histopathologic lesions known as endometrial hyperplasia. Estrogen, p53, PTEN, and overexpression of cyclin D1 appear to be involved in the development of endometrial carcinogenesis. Design We evaluated and compared the expression profile of cyclin D1 expressions in 50 endometrial samples submitted as either endometrial curetting (n = 34) or hysterectomy (n = 16) specimens, which were diagnosed as simple hyperplasia (n = 10), complex hyperplasia (n = 06), atypical hyperplasia (n = 04), and endometrial carcinoma (n = 20). Ten cases of normal proliferative and secretory endometrium were selected as controls. Breast cancer with known cyclin D1 expression was selected as a positive control in each immunohistochemistry run. Results Cyclin D1 was significantly overexpressed in glands with complex hyperplasia and endometrial adenocarcinoma compared with proliferative or secretory endometrium and simple hyperplasia. A statistical difference was found in the extent of cyclin D1 positivity of simple hyperplasia and carcinoma of the endometrium (p < 0.005). No statistical difference was seen between complex hyperplasia and carcinoma and clinicopathologic parameters in endometrioid carcinomas. All cases of clear cell carcinoma and serous carcinoma showed cyclin D1 immunoreactivity. Significant statistical difference was seen between cyclin D1 expression and only one clinicopathologic parameter, i.e., menopausal status in endometrial carcinomas Conclusion Cyclin D1 over expression may be an early event in endometrial carcinogenesis and cyclin D1 over expression may be an informative biomarker to recognize subsets of endometrial lesions that may be precancerous and therefore amenable to surgical therapy.

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Álvarez, Guillermo, Pedro Salazar, and Silvio Alvarado. "Sonohisterografía en el estudio de la infertilidad." Revista Peruana de Ginecología y Obstetricia 42, no. 3 (August 4, 2015): 23–26. http://dx.doi.org/10.31403/rpgo.v42i1800.

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OBJETIVO: La sonohisterografía en el estudio de la infertilidad. MATERIAL: Quince pacientes infértiles estudiadas con histerosalpingografía y sonohisterografía. MÉTODO: Relleno de la cavidad uterina con solución salina estéril, a través de un catéter y bajo control sonográfico, RESULTADOS: La sonohisterografía nos permite una mejor diferenciación de las capas entre el endometrio y miometrio durante el ciclo menstrual. En alteraciones uterinas, visualiza lesiones intracavitarias con mayor precisión que la endosonografía habitual; pólipos y sinequias endometriales, miomas submucosos o carcinoma endometrial. CONCLUSIÓN: La sonohisterografía constituye un procedimiento valioso en la diferenciación de alteraciones intravicarias, endometriales y submucosas, es una exploración rápida y de bajo costo y no requiere de medios de contraste ni de radiaciones ionizantes.

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Amalinei, Cornelia, Raluca Balan, Luminita Ivan, Razvan Socolov, Demetra Socolov, and Coriolan Cotutiu. "Multiple primary malignant neoplasms — case report." Open Medicine 1, no. 1 (March 1, 2006): 87–98. http://dx.doi.org/10.2478/s11536-006-0004-0.

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AbstractThe synchronous occurence of primary carcinomas of endometrium and ovary is well recognized. Malignant peripheral nerve sheath tumours (MPNSTs) may also rarely occur in patients diagnosed with malignancies of the female genital tract. We report a rare case of synchronous primary carcinomas of endometrium and ovary, followed by a metachronous retroperitoneal MPNST. Ascites cytology and endometrial biopsy, followed by hysterectomy and bilateral adnexectomy, were performed to remove the synchronous tumors. Histology was suggestive of synchronous endometrial endometrioid carcinoma and ovarian mucinous adenocarcinoma. After the removal of the retroperitoneal tumor, a MPNST was diagnosed by immunohistochemistry. The patient developed two consecutive vaginal tumors diagnosed as metastases of the previously diagnosed endometrial carcinoma. Although synchronous tumors of endometrium and ovary were relatively early staged and consequently had a favorable prognosis, subsequently occuring implants along the lower genital tract and the metachronous MPNST added up to a poor prognosis.

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Abu-Rustum, Nadeem, Catheryn Yashar, Rebecca Arend, Emma Barber, Kristin Bradley, Rebecca Brooks, Susana M. Campos, et al. "Uterine Neoplasms, Version 1.2023, NCCN Clinical Practice Guidelines in Oncology." Journal of the National Comprehensive Cancer Network 21, no. 2 (February 2023): 181–209. http://dx.doi.org/10.6004/jnccn.2023.0006.

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Adenocarcinoma of the endometrium (also known as endometrial cancer, or more broadly as uterine cancer or carcinoma of the uterine corpus) is the most common malignancy of the female genital tract in the United States. It is estimated that 65,950 new uterine cancer cases will have occurred in 2022, with 12,550 deaths resulting from the disease. Endometrial carcinoma includes pure endometrioid cancer and carcinomas with high-risk endometrial histology (including uterine serous carcinoma, clear cell carcinoma, carcinosarcoma [also known as malignant mixed Müllerian tumor], and undifferentiated/dedifferentiated carcinoma). Stromal or mesenchymal sarcomas are uncommon subtypes accounting for approximately 3% of all uterine cancers. This selection from the NCCN Guidelines for Uterine Neoplasms focuses on the diagnosis, staging, and management of pure endometrioid carcinoma. The complete version of the NCCN Guidelines for Uterine Neoplasms is available online at NCCN.org.

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SAVCI, Gamze, and Kadir BAKAY. "A rare case of synchronous genital carcinoma involving endometrium and unilateral fallopian tube in a 24 years old patient." Journal of Experimental and Clinical Medicine 39, no. 1 (January 1, 2022): 308–9. http://dx.doi.org/10.52142/omujecm.39.1.62.

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Multifocal synchronous development of malignancies of the female genital tract is a rare occurrence and less than 3% of primary malignancies of this region is synchronous. Although the simultaneous presentation of endometrial and ovarian carcinoma of the endometrioid type is well described little is known about a similar phenomenon involving the endometrium and fallopian tube. The relationship between the synchronous tumours is uncertain. More illuminating studies are being conducted on the relationship between synchronized endometrial and ovarian carcinomas in recent studies.This case is about synchronous genital carcinoma involving endometrium and unilateral fallopian tube in a 24 years old patient.

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Lahori, M., and N. Borazan. "Concurrently Presenting Endometrial And Ovarian Endometrioid Adenocarcinomas- A Clinicopathologic Study Of 52 Cases." American Journal of Clinical Pathology 154, Supplement_1 (October 2020): S48. http://dx.doi.org/10.1093/ajcp/aqaa161.102.

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Abstract Introduction/Objective Concurrent presentation of endometrioid adenocarcinomas in endometrium and ovary is uncommon, but oft-noted. They may arise from ovarian metastasis of endometrial carcinoma, endometrial metastasis of ovarian carcinoma, or synchronous development of independent primary lesions. Scully and Young criteria have been widely used to differentiate the site of origin.1 Role of a field effect in the genesis of synchronous carcinomas is supported by increasing evidence that endometrioid ovarian carcinomas arise from endometriosis. 2–5 Methods All cases of concurrent endometrioid adenocarcinomas of the endometrium and ovary between 2002 and 2019 in the Mount Sinai health system New York were included, using pathology database (Powerpath) and EMR database (Epic). Results 52 cases of concurrent endometrioid adenocarcinomas of endometrium and ovary were identified between 2002 and 2019. Mean age at presentation was 54.07 years (24–80). 69.2% had synchronous origin, 21.15% had endometrial primary and 3.8% had an ovarian primary. Ovarian endometriosis was identified in 51.9% and complex atypical hyperplasia in 26.9%. Lower uterine segment involvement was seen in 26.9%, bilateral ovarian involvement in 40.3%, fallopian tube involvement in 23% and lymphovascular space invasion in 25%. Different histologic grade of ovarian and endometrial counterparts was noted in 25% cases. Synchronous endometrioid carcinomas had the following characteristics: mean age at presentation 50.6 years, associated with CAH in 33.3% and endometriosis in 66.6%, presentation at stage 1 in 63.8% and lower grade of differentiation (grade 1/2) in 80.5% cases. Conclusion In majority of cases, synchronous endometrioid carcinomas have a younger mean age at presentation, are lower grade tumors, present at stage 1 and have associated endometriosis. It can be inferred that the percentage of synchronous tumors with endometriotic foci would be even higher (with extensive sampling & assuming that the neoplastic process has replaced native benign endometriotic foci) – pointing towards the likely role of endometriosis in the genesis of these tumors.

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Munakata, Satoru, Hanae Kushibiki, Taishi Akimoto, Tsuyoshi Yamashita, and Norihiko Shimoyama. "A Case of Endometrial Carcinosarcoma Containing Sertoliform Endometrioid Carcinoma Component." Case Reports in Pathology 2021 (September 20, 2021): 1–9. http://dx.doi.org/10.1155/2021/5868818.

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Carcinosarcomas (CSs) of the endometrium have admixture of malignant epithelial and mesenchymal components. The carcinomatous component exhibit endometrioid, serous, or clear cell differentiation, or are undifferentiated. CSs are considered homologous or heterologous according to the type of sarcomatous component. Sertoliform endometrioid carcinomas (SECs) of the endometrium which comprise a rare subtype of endometrial cancer, typically occur in the ovary. SECs as a carcinomatous component of CS of the endometrium have not been reported. Here, we report an endometrial carcinosarcoma that contains an SEC component. An 88-year-old female presented to a clinic with atypical genital bleeding. She was referred to our hospital and underwent total hysterectomy, bilateral adnexectomy and partial omentectomy due to endometrial carcinoma. Gross examination revealed a polypoid mass in the uterine cavity with massive myometrial invasion. Histologically, the tumor was a high-grade endometrioid carcinoma. In addition to an ordinary conventional endometrioid carcinoma, approximately 30% of the area exhibited sex cord-like pattern and contained small hollow tubules, anastomosing cords and trabeculae, and tightly packed nests. Immunohistochemically, the SEC component showed diffuse p53 staining. Sex cord-like area, especially the solid area, showed positive staining for EMA, vimentin, α-inhibin, CD99, calretinin, p53, CD56, synaptophysin, and chromogranin A, which is a staining pattern similar to that previously reported SEC of the endometrium. Diminished membranous and positive cytoplasmic staining for β-catenin was observed. This is the first case report of an endometrial carcinosarcoma containing an SEC component. SECs of the endometrium might exhibit sex cord-like differentiation in contrast to SECs of the ovary, which do not exhibit sex cord differentiation.

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Horrée, Nicole, Paul J. van Diest, Petra van der Groep, Daisy M. D. S. Sie-Go, and A. Peter M. Heintz. "Hypoxia and Angiogenesis in Endometrioid Endometrial Carcinogenesis." Analytical Cellular Pathology 29, no. 3 (January 1, 2007): 219–27. http://dx.doi.org/10.1155/2007/434731.

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Background: Hypoxia-inducible factor 1α (HIF-1α) plays an essential role in the adaptive response of cells to hypoxia, triggering biologic events associated with aggressive tumor behavior. Methods: Expression of HIF-1α and proteins in the HIF-1α pathway (Glut-1, CAIX, VEGF) in paraffin-embedded specimens of normal (n = 17), premalignant (n = 17) and endometrioid endometrial carcinoma (n = 39) was explored by immunohistochemistry, in relation to microvessel density (MVD). Results: HIF-1α overexpression was absent in inactive endometrium but present in hyperplasia (61%) and carcinoma (87%), with increasing expression in a perinecrotic fashion pointing to underlying hypoxia. No membranous expression of Glut-1 and CAIX was noticed in inactive endometrium, in contrast with expression in hyperplasia (Glut-1 0%, CAIX 61%, only focal and diffuse) and carcinoma (Glut-1 94.6%, CAIX 92%, both mostly perinecrotically). Diffuse HIF-1α was accompanied by activation of downstream targets. VEGF was significantly higher expressed in hyperplasias and carcinomas compared to inactive endometrium. MVD was higher in hyperplasias and carcinomas than in normal endometrium (p < 0.001). Conclusion: HIF-1α and its downstream genes are increasingly expressed from normal through premalignant to endometrioid adenocarcinoma of the endometrium, paralleled by activation of its downstream genes and increased angiogenesis. This underlines the potential importance of hypoxia and its key regulator HIF-1α in endometrial carcinogenesis.

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Posligua, Lorena, Anais Malpica, Jinsong Liu, Jubilee Brown, and Michael T. Deavers. "Combined Large Cell Neuroendocrine Carcinoma and Papillary Serous Carcinoma of the Endometrium With Pagetoid Spread." Archives of Pathology & Laboratory Medicine 132, no. 11 (November 1, 2008): 1821–24. http://dx.doi.org/10.5858/132.11.1821.

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Abstract Neuroendocrine carcinomas of the endometrium are rare tumors that can be pure, combined with endometrioid adenocarcinoma, or a component of malignant mixed müllerian tumor. Recently, a case of combined small cell carcinoma and papillary serous carcinoma of the endometrium was described for the first time. We report the first case, to our knowledge, of combined large cell neuroendocrine carcinoma and papillary serous carcinoma of the endometrium, with an unusual pagetoid spread of the neuroendocrine component into normal endometrial and endocervical glands. The endometrial carcinoma had a small serous component, but most of the tumor was characterized by solid sheets of medium to large cells with abundant mitotic figures, numerous apoptotic bodies, and foci of necrosis. This component was diffusely positive for neuroendocrine markers. Following surgery, the patient was treated with radiation therapy and chemotherapy. She was without evidence of progression at 5 months of follow-up.

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Guzmán G, Pablo, and María José Iriarte C. "Carcinoma epidermoide de cuello uterino con extensión superficial a endometrio." Revista chilena de obstetricia y ginecología 81, no. 2 (April 2016): 122–25. http://dx.doi.org/10.4067/s0717-75262016000200007.

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Reyna-Villasmil, E., D. Torres-Cepeda, M. Colmenares-Vega, O. Delgado-Delgado, and I. Sabatini-Saéz. "Carcinoma neuroendocrino de células pequeñas del endometrio. Reporte de caso." Clínica e Investigación en Ginecología y Obstetricia 36, no. 2 (March 2009): 70–72. http://dx.doi.org/10.1016/j.gine.2007.12.004.

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Baquedano, L., P. J. Coronado, M. A. Martínez-Maestre, Y. José-Gutiérrez, D. Judez, F. Villalobos, and M. A. Ruiz-Conde. "Factores de riesgo para carcinoma de endometrio de alto grado." Clínica e Investigación en Ginecología y Obstetricia 45, no. 2 (April 2018): 64–68. http://dx.doi.org/10.1016/j.gine.2016.07.004.

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Henson, Donald Earl, Arnold M. Schwartz, Amy Tilara, Philip M. Grimley, and William F. Anderson. "Population-Based Analysis of Pathologic Data: A New Approach to the Investigation of Uterine Endometrial and Ovarian Endometrioid Carcinomas." Archives of Pathology & Laboratory Medicine 131, no. 9 (September 1, 2007): 1337–42. http://dx.doi.org/10.5858/2007-131-1337-paopda.

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Abstract Context.—Population-based analysis of the histopathology of endometrioid adenocarcinoma of the endometrium and ovary combined with epidemiologic techniques offer a new approach to exploring the relationship of tumors that share a similar range of morphologic phenotypes. Objective.—To evaluate the contribution of the Surveillance, Epidemiology, and End Results database to our understanding of gynecologic pathology. Specifically, to test and compare whether the etiology/pathogenesis of ovarian endometrioid cancer is as dependent upon the reproductive environment as uterine endometrial carcinoma. Design.—Graphic plots of the epidemiologic patterns were analyzed relating to incidence and age-specific rates of ovarian and uterine endometrioid carcinomas. The graphic analysis included evaluation of age frequency density plots and logarithmic plots (log-log) of age-specific incidence rates. Results.—At all ages, uterine endometrioid carcinomas have higher incidence rates than their ovarian homologues. Up to the age of 50 years, the log-log plots of age-specific incidence rates for each of these tumors remain essentially parallel. In contrast, after age 50 (menopause), the incidence rates begin to diverge: the rates for uterine endometrial carcinomas continue to rise, whereas the rates for ovarian endometrioid carcinomas plateau. This divergence persists even when the age-specific incidence is stratified according to histologic grade. Interestingly, endometrial stromal sarcomas follow an incidence rate pattern nearly identical to that of ovarian endometrioid carcinomas. Conclusions.—The continuum of cellular and molecular events predisposing to gynecologic cancers of endometrioid phenotype apparently cease to operate in the ovary after menopause, but additional cellular and molecular events appear to occur in the ageing uterine endometrium.

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Navarro, M., A. J. Muñoz, and R. Martínez de la Ossa. "Carcinoma escamoso in situ de endometrio y vagina asociado a carcinoma microinvasivo de cérvix." Clínica e Investigación en Ginecología y Obstetricia 35, no. 5 (October 2008): 190–92. http://dx.doi.org/10.1016/s0210-573x(08)73075-2.

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Hachisuga, T., K. Fukuda, M. Uchiyama, N. Matsuo, T. Iwasaka, and H. Sugimori. "Immunohistochemical study of p53 expression in endometrial carcinomas: correlation with markers of proliferating cells and clinicopathologic features." International Journal of Gynecologic Cancer 3, no. 6 (1993): 363–68. http://dx.doi.org/10.1046/j.1525-1438.1993.03060363.x.

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Using anti-p53 (PAb1801 and PAb240), anti-DNA polymerase α and Ki-67 monoclonal antibodies, the expression of p53 was studied in 11 normal endometria, 14 endometrial hyperplasias and 27 endometrial carcinomas and its relationship to the proliferative activity of the tumors was examined. Normal endometria and simple hyperplasias were completely negative for p53. The PAb1801 indices of complex hyperplasias and complex atypical hyperplasias were 2.5±1.8% and 5.0±3.2%, respectively. The PAb1801 indices of grade 1, grade 2 and grade 3 endometrial carcinomas were 10.2±14.2%, 44.4±29/0% and 45.0±32.5%, respectively. These results indicate a progressively enhanced p53 expression in the sequence from normal endometrium, through hyperplasia to carcinoma. A significant correlation between p53 expression and labeling indices of Ki-67 and DNA polymerase α was observed in endometrial carcinomas. The endo-metrial carcinomas with p53 overexpression developed mainly in post-menopausal patients and were frequently high-grade tumors with deep myometrial invasion. These findings may indicate that overexpression of p53 protein contributes to the proliferative activity of the tumor cells.

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Erkanli, S., F. Kayaselcuk, E. Kuscu, T. Bagis, F. Bolat, A. Haberal, and B. Demirhan. "Expression of survivin, PTEN and p27 in normal, hyperplastic, and carcinomatous endometrium." International Journal of Gynecologic Cancer 16, no. 3 (2006): 1412–18. http://dx.doi.org/10.1136/ijgc-00009577-200605000-00071.

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We aimed to investigate if expressions of survivin and p27 proteins are involved in the development of endometrioid carcinoma, along with whether there are any correlations between these proteins and loss of wild-type PTEN that is found in up to 80% of endometrial carcinomas. We also studied their correlations with classical prognostic factors and survival in endometrial carcinoma. To our knowledge, this is the first time survivin expression is investigated in endometrial hyperplasia along with endometrioid adenocarcinoma. For immunohistochemical analysis, 29 endometrioid adenocarcinoma, 38 endometrial hyperplasia, and 10 proliferative endometrium tissue samples were selected in the pathology archives. Staining of cells was scored as +2 if >50%, +1 if <50%, and negative if none were stained positive. Survivin expression increased from proliferative to hyperplasia to carcinoma cases. PTEN and p27 expressions decreased in hyperplasia and carcinoma cases with respect to proliferative endometrium. All these differences were statistically significant (P < 0.05). PTEN positively correlated to p27 (P < 0.05); however, neither was correlated with survivin. None of these genes were correlated with classical prognostic factors such as grade and myometrial invasion in endometrioid adenocarcinoma. However, mean survival was statistically significantly higher in PTEN-positive cases (46.6 vs 16.4 months) (P < 0.05). Survivin overexpression might be one of the important mechanisms in the development of endometrioid adenocarcinoma along with lost or decreased activity of PTEN and p27. However, survivin seems to exert its role in ways different from those of PTEN or p27 in the development of endometrioid adenocarcinoma. These findings on the role of survivin in endometrioid adenocarcinoma should be confirmed and the pathways through which survivin acts in endometrioid adenocarcinoma studied further with a larger sample size.

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Han, Jiheun, and Hyun-Soo Kim. "Abdominopelvic Metastasis of Endometrial Serous Carcinoma Initially Misdiagnosed as Early-Stage Low-Grade Endometrioid Carcinoma: The Importance of Recognizing Minimal Uterine Serous Carcinoma." Case Reports in Oncology 13, no. 3 (December 23, 2020): 1537–44. http://dx.doi.org/10.1159/000511701.

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Minimal uterine serous carcinomas (MUSCs) include serous carcinomas with invasion confined to the endometrium (superficial serous carcinoma) and those without stromal invasion (serous endometrial intraepithelial carcinoma). Although these tumors are confined to the endometrium proper, they have highly metastatic potential for disseminating to extra-uterine sites. We report here a case of MUSC that was initially misdiagnosed as early-stage low-grade endometrioid carcinoma but later metastasized to the abdominopelvic peritoneum. The patient was a 61-year-old woman who was diagnosed with grade 1 endometrioid carcinoma of the endometrium and underwent total hysterectomy. Because the tumor was confined to the endometrium (International Federation of Gynecology and Obstetrics stage IA), no further treatment was performed. However, several metastatic tumor masses were detected in the vaginal stump and abdominopelvic peritoneum 7 years after the surgery. Histologically, the metastatic tumor tissues showed high-grade carcinoma. A review of previous hysterectomy slides showed multiple separate foci of atypical glandular proliferation measuring up to 0.8 cm in the greatest dimension and consisting of markedly atypical cells involving the surface and atrophic glands. The tumor showed a predominantly glandular architecture without evident papillary growth or stromal invasion. However, it had large, pleomorphic nuclei showing a high nuclear-to-cytoplasmic ratio, conspicuous eosinophilic nucleoli, and numerous mitotic figures. Characteristically, the tumor showed marked nuclear atypia immediately appreciated at low magnification in the background of well-formed glandular structures, indicating a significant discordance between nuclear and architectural features. On immunostaining, both the uterine and metastatic tumor tissues exhibited diffuse and strong p16 expression and mutant pattern of p53 expression, confirming the diagnosis of serous carcinoma. In summary, the case findings support that failure to preoperatively recognize high-risk endometrial carcinoma is associated with worse outcomes. Complete surgical staging and accurate pathological diagnosis are critical for patients with serous carcinoma even at the early clinical stage.

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Zhan, Xiangbo, Lei Li, Ming Wu, and Jinghe Lang. "The prognosis of stage IA synchronous endometrial endometrioid and ovarian carcinomas." Archives of Gynecology and Obstetrics 300, no. 4 (September 14, 2019): 1045–52. http://dx.doi.org/10.1007/s00404-019-05288-5.

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Abstract Introduction Little is known about the prevalence and prognosis of synchronous endometrial and ovarian carcinomas. This report explores the survival outcomes of synchronous stage IA endometrioid endometrial and stage IA ovarian carcinomas in a retrospective cohort study. Methods All cases of pathological confirmed synchronous stage IA endometrial endometrioid and ovarian carcinomas from June 1, 2010, to June 1, 2017, in a teaching hospital were reviewed. Patients were followed up to February 1, 2019. Survival outcomes were compared between patients with and without synchronous carcinomas. Results In total, 841 cases with confirmed FIGO stage IA endometrioid endometrial carcinomas were included in the study; 33 patients (3.9%) had synchronous stage IA ovarian carcinomas, including 27 (81.8%) and 6 (18.2%) cases of endometrioid and mixed endometrioid/clear cell subtypes, respectively. After a median follow-up time of 56.8 months, 829 patients (97.9%) had definitive survival outcomes. Synchronous ovarian carcinomas had no impact on disease-free, overall or cancer-specific overall survival in univariate and multivariate analyses. Conclusion In these patients with stage IA endometrioid endometrial carcinoma, the genuine incidence of synchronous stage IA ovarian carcinoma was very low, and synchronous carcinoma had no significant effects on survival outcomes.

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Cruz Tovar, Diana, and Sandra Liliana Garzón. "Citología endometrial de toma directa. Estudio comparativo." Revista Repertorio de Medicina y Cirugía 12, no. 1 (March 1, 2003): 25–26. http://dx.doi.org/10.31260/repertmedcir.v12.n1.2003.307.

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El carcinoma endometrial se ha convertido en la lesión maligna más frecuente del cuerpo uterino. Se presentan anualmente 34.000 nuevos casos, de los cuales 6.000 ocasionan defunciones, lo que lo convierte en la séptima causa de muerte en mujeres; es más agresivo con el aumento de la edad. Es así como surge la idea de realizar un estudio cuidadoso con la citología endometrial de toma directa, que permita investigar y diagnosticar lesiones hormonales, premalignas y malignas del endometrio, y promueva la citología endometrial de toma directa como un método de tamización para usar con mayor frecuencia en Colombia. También, demostrar que la interpretación de la citología endometrial tiene resultados tan satisfactorios como los de la biopsia y la pueden realizar citohistotecnólogos con un adecuado entrenamiento. Fueron estudiados 133 casos del Instituto Nacional de Cancerología (1999-2000), de los cuales sólo 123 fueron adecuados para lectura. A todos se les realizó un estudio citológico e histológico, con 94% de resultados benignos, 4,9% de resultados premalignos, y 0,8% de malignidad en la citología. De estos casos el 88% se correlacionó con los resultados de la biopsia.

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Baquedano Mainar, Laura, Pilar Del Tiempo Marqués, Ignacio Adiego Calvo, Francisco Villalobos Salguero, Patricia Rubio Cuesta, Esther Gimeno, and Miguel Angel Ruiz Conde. "Acetato de ulipristal en el diagnóstico diferencial de carcinoma de endometrio." Revista chilena de obstetricia y ginecología 81, no. 2 (April 2016): 113–16. http://dx.doi.org/10.4067/s0717-75262016000200005.

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Fernández, Esther, M. Carmen Barrera, Cristina Gervás, Emma Salvador, Melcior Sentís, and Borja Rivero. "Carcinoma de endometrio: valor de la estadificación prequirúrgica por resonancia magnética." Radiología 45, no. 3 (January 2003): 115–23. http://dx.doi.org/10.1016/s0033-8338(03)77873-4.

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Salibay, Christine, and Oluwole Fadare. "High-Grade Endometrioid Carcinoma of the Endometrium With a GATA-3-Positive/PAX8-Negative Immunophenotype Metastatic to the Breast: A Potential Diagnostic Pitfall." International Journal of Surgical Pathology 28, no. 6 (March 19, 2020): 631–36. http://dx.doi.org/10.1177/1066896920913114.

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This report describes clinicopathologic findings from the case of a patient with a breast mass that was ultimately diagnosed as a metastatic high-grade endometrioid carcinoma of endometrial origin. The breast lesion as well as the solid areas of the endometrial lesion displayed a similar immunoprofile: GATA3-positive; synaptophysin positive; negative for mammaglobin, gross cystic disease fluid protein-15, chromogranin, estrogen receptor, progesterone receptor, and HER2/neu; and intact expression of the DNA mismatch repair proteins MLH1, MSH2, MSH6, and PMS2. The breast lesion was negative for PAX-8, whereas the solid areas of the endometrial lesion showed focal weak positivity. A review of the literature on GATA-3 expression in endometrial carcinomas found a reported frequency of expression that ranged from 0% to 13% of cases, typically in a patchy, focal, and generally restricted pattern. However, GATA-3 may be diffusely expressed in high-grade endometrial carcinomas. Since the potential for PAX-8 expression to be lost in high-grade endometrioid carcinomas is well known, a GATA-3-positive/PAX8-negative immunoprofile may be encountered in high-grade endometrioid carcinomas of the endometrium, and this composite immunoprofile is a potential diagnostic pitfall when such a lesion is being evaluated in a breast metastasis.

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Perez-Medina, T., V. Engels, F. Salazar, B. Bueno, L. Sanfrutos, J. de la Fuente, I. Orensanz, and JM Bajo-Arenas. "Anatomopathologic Subtypes of Endometrial Carcinoma: Case-Control Study of 122 Cases. Epidemiology and Ultrasound." Clinical medicine. Oncology 1 (January 2007): CMO.S367. http://dx.doi.org/10.4137/cmo.s367.

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Objective To determine the epidemiological and sonographic characteristics of patients with endometrial carcinoma of endometrioid and non-endometrioid subtype to analyse if any differences can be observed between the groups. Study design A case-control study was performed considering 122 patients with endometrial carcinoma where 96 (78.69%) had endometrioid carcinomas (controls) and 26 (21.31%) had non-endometrioid carcinomas (cases). Epidemiological, clinical, and sonographic variables (endometrial thickness and sonographic suspicion of myometrial invasion of the tumour) were analysed. Qualitative variables were studied with the Chi-square test and the Fisher's exact test and quantitative variables with the t test. A value of p < 0.05 was considered statistically significant. Results Tumours of the non-endometrioid type are observed in older patients (p = 0.003) and frequently show a higher sonographic tumoral invasion (p = 0.0036). Conclusions This study supports previous observations that non-endometrioid endometrial carcinomas present at older ages and provides new data that non-endometrioid carcinoma more frequently show sonographic images compatible with myometrial invasion.

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Rodríguez, Alba, Jara Gallardo, Zoraida Frías, Manuel Pantoja, María Aguilar, Inmaculada Rodríguez, Mario Roquette, and Alvaro Gutiérrez. "Tumor sincrónico de endometrio y ovario. Patología infrecuente en ginecología oncológica." Revista de Obstetricia y Ginecología de Venezuela 80, no. 04 (December 7, 2020): 348–55. http://dx.doi.org/10.51288/00800412.

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Endometrial cancer remains the most common gynecological tumor in women in the United States of America. The simultaneous finding of endometrial and ovarian neoplasm, as a synchronous tumor, accounts for about 5 - 10 % of endometrial and ovarian tumors. Therefore, is a rare entity. Consideration as restricted metastases or pseudometastasis to define the spread of this kind of tumor, is becoming more relevant nowadays thanks to the latest advances in the field of immunohistochemistry and molecular biology. In this article we present the case of a 57-year-old patient initially diagnosed with FIGO stage IIIA endometrial carcinoma; subsequently, it was a synchronous endometrial tumor stage IB and IC ovary, despite the presurgical suspicion of a metastatic tumor. Keywords: Endometrial Neoplasm, Ovarian Neoplasm, Synchronous Neoplasm, Multiple Primary Neoplasm, Neoplasm Metastasis.

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López Fernández, J. A., L. Luque Martínez, M. T. Casanova Sanchís, E. M. Moreno Ruiz, J. C. Martínez Escoriza, and F. M. Peiró-Marqués. "Diagnóstico precoz de carcinoma de endometrio en una paciente tratada con tamoxifeno." Progresos de Obstetricia y Ginecología 45, no. 10 (January 2002): 448–52. http://dx.doi.org/10.1016/s0304-5013(02)75819-6.

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Silverberg, Steven G. "The Endometrium." Archives of Pathology & Laboratory Medicine 131, no. 3 (March 1, 2007): 372–82. http://dx.doi.org/10.5858/2007-131-372-te.

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Abstract Context.—Endometrial tissue specimens are commonly encountered in daily practice. It is well known that a number of problematic diagnostic scenarios occur relative to these specimens. Objective.—To emphasize practical aspects of endometrial specimen handling and reporting, with selected comments on common diagnostic pitfalls, including (1) the diagnosis of endometrial intraepithelial carcinoma in atrophic endometrial biopsy specimens, (2) evaluation of adequacy of endometrial sampling specimens, (3) problems in diagnosing and measuring the depth of myometrial invasion in endometrial carcinoma, (4) the question of metastasis versus independent primaries in concurrent carcinomas of endometrium and one or both ovaries, (5) the problematic differential diagnoses between type 1 (primarily endometrioid) and type 2 (primarily serous) adenocarcinomas, and (6) atypical hyperplasia and proposed classification systems for its replacement. Data Sources.—Published literature, consensus statements, and personal experience. Conclusions.—A systematic approach to the handling and reporting of endometrial specimens reduces the potential for omission and error. Recognition of diagnostic pitfalls and practical approaches to their resolution help improve quality.

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Nishimura, N., T. Hachisuga, T. Saito, and T. Kawarabayashi. "Subsequent endometrial carcinoma with adjuvant tamoxifen treatment in Japanese breast cancer patients." International Journal of Gynecologic Cancer 11, no. 4 (2001): 272–76. http://dx.doi.org/10.1136/ijgc-00009577-200107000-00003.

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Abstract.Nishimura N, Hachisuga T, Saito T, Kawarabayashi T. Subsequent endometrial carcinoma with adjuvant tamoxifen treatment in Japanese breast cancer patients.This study aimed to detail the clinicopathologic features of endometrial carcinomas that developed in Japanese patients receiving adjuvant tamoxifen treatment for breast cancer patients. Ten endometrial carcinomas in tamoxifen-treated breast cancer patients were collected from two medical centers. The endometrial carcinomas included two stage Ia, four stage Ib, two stage Ic and two stage IIIc. Three tumors were Grade 1, six were Grade 2, and one was Grade 3. The tumor was limited to the endometrium in two cases. Myometrial invasion was limited to the inner half of the myometrium in five cases and involved the outer half in three. A mild degree of lymphovascular space invasion was identified in five cases. Deep cervical invasion was recognized in one case. The cell types comprised nine endometrioid adenocarcinomas and one serous carcinoma. Five of eight postmenopausal endometrial carcinomas were associated with polypoid endometrial lesions composed of cystically dilated atrophic and proliferative glands widely separated by fibrotic stroma. Two patients with retroperitoneal lymph node metastases died of endometrial cancer. One patient developed a contralateral breast cancer during tamoxifen treatment. No patient died of breast cancer. We did not demonstrate a higher frequency of either high-grade tumors or unfavorable histologic subtypes in tamoxifen-treated Japanese breast cancer patients.

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Opric, Dejan, Amer Suskic, Sanela Halilovic Suskic, Gorana Nikolic, and Isidora Filipovic. "Value of p53 and estrogen receptors immunohistochemical staining in endometrial carcinoma." International Journal of Reproduction, Contraception, Obstetrics and Gynecology 8, no. 12 (November 26, 2019): 4885. http://dx.doi.org/10.18203/2320-1770.ijrcog20195339.

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Background: Since there are many articles dealing with estimating prognostic and diagnostic value of ER and p53, using different, usually complex ICH interpretation methods, we wanted to evaluate significance of p53 and ER ICH positivity in endometrial carcinoma, using easily applicable criteria that would help pathologists and clinicians to be sure in ICH findings noted in the report.Methods: This paper deals with data of the patients treated for endometrial carcinoma in Public Hospitals in Travnik, gynecological department in the period from 1st January 2013 to 1st January 2019. The study included 97 women with endometrial carcinoma, with ages ranging from 42 to 90 years (mean of 64 years). Sample consisted of 72 cases (74.2%) of endometrioid and 25 cases (25.8%) of non-endometrioid carcinoma.Results: p53 expression was observed in 13.8% carcinomas of the endometrioid type and in 68% carcinomas of non-endometrioid type, while estrogen receptors were more frequently observed in tumors of the endometrioid type (61%) in contrast to non-endometrioid type (28%). Among 72 cases, those with grade I expressed estrogen receptors (26 out of 34 cases - 72%) more frequently than those with grades II and III. Frequency of p53 positivity was significantly higher at higher grades (grade I - 5.8%, grade II - 11.5%, grade III - 71.4%). Stage I carcinomas showed p53 staining less frequently (22.2%) that carcinomas diagnosed at later stages (31.5%).Conclusions: Using 80% nuclei stained as threshold for p53 positivity, we concluded that p53 is marker of high-grade endometrial carcinomas: high grade endometrioid and non-endometrioid carcinomas. Using 1% of cells as threshold for ER positivity, we confirmed that ER are common in endometrioid type carcinoma, in contrast to non-endometrioid type. Although observed, higher frequency of ER in tumors with lower grade and stage was not statistically confirmed in our study population.

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Bell, Daphne W., and Lora Hedrick Ellenson. "Molecular Genetics of Endometrial Carcinoma." Annual Review of Pathology: Mechanisms of Disease 14, no. 1 (January 24, 2019): 339–67. http://dx.doi.org/10.1146/annurev-pathol-020117-043609.

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Endometrial cancer is the most commonly diagnosed gynecologic malignancy in the United States. Endometrioid endometrial carcinomas constitute approximately 85% of newly diagnosed cases; serous carcinomas represent approximately 3–10% of diagnoses; clear cell carcinoma accounts for <5% of diagnoses; and uterine carcinosarcomas are rare, biphasic tumors. Longstanding molecular observations implicate PTEN inactivation as a major driver of endometrioid carcinomas; TP53 inactivation as a major driver of most serous carcinomas, some high-grade endometrioid carcinomas, and many uterine carcinosarcomas; and inactivation of either gene as drivers of some clear cell carcinomas. In the past decade, targeted gene and exome sequencing have uncovered additional pathogenic aberrations in each histotype. Moreover, an integrated genomic analysis by The Cancer Genome Atlas (TCGA) resulted in the molecular classification of endometrioid and serous carcinomas into four distinct subgroups, POLE (ultramutated), microsatellite instability (hypermutated), copy number low (endometrioid), and copy number high (serous-like). In this review, we provide an overview of the major molecular features of the aforementioned histopathological subtypes and TCGA subgroups and discuss potential prognostic and therapeutic implications for endometrial carcinoma.

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Journal articles on the topic 'Carcinoma Endometrio'

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