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2.
Article in English | LILACS-Express | LILACS | ID: biblio-1534157

ABSTRACT

Introduction: Hydatidiform mole is a type of gestational trophoblastic disease that results from the abnormal fertilization of an oocyte and causes nonspecific symptoms such as amenorrhea, metrorrhagia, and enlarged uterus. Although rare, its most characteristic symptoms include hyperemesis, early-onset pre-eclampsia, anemia, and respiratory distress. Case presentation: A 47-year-old Moroccan woman consulted the emergency department of the Hospital Clínico Universitario in Valladolid (Spain) after a month of persistent coughing and emesis. The patient reported epigastralgia and amenorrhoea for two months, as well as scant vaginal bleeding two days prior to consultation. Taking into account that the patient tested positive for pregnancy, that a heterogeneous intrauterine mass measuring 124x120mm was observed on transvaginal ultrasound, that no abnormal findings were reported on Doppler ultrasound, and that her serum ßhCG levels reached a value of 772.110 mIU/mL, a diagnosis of hydatidiform mole was suspected. Once informed about the possible therapeutic options, the patient decided to undergo a total hysterectomy, as she stated that she had already fulfilled her desire to be a mother. After the procedure, the patient's clinical condition improved, and the pathology report of the mass confirmed the diagnosis of partial hydatidiform mole. Conclusion: Early diagnosis of hydatidiform mole is paramount in order to provide adequate treatment and improve the prognosis of these patients. Therefore, despite its low incidence and non-specific clinical manifestations, it should be considered as a differential diagnosis for first-trimester metrorrhagia.


Introducción. La mola hidatiforme es un tipo de enfermedad trofoblástica gestacional que se presenta como resultado de la fertilización anormal de un ovocito y que ocasiona síntomas inespecíficos como amenorrea, metrorragia y aumento del tamaño del útero. Aunque infrecuentes, sus síntomas más característicos incluyen hiperémesis, preeclampsia de inicio temprano, anemia y distrés respiratorio. Presentación del caso. Mujer marroquí de 47 años que consultó al servicio de urgencias del Hospital Clínico Universitario de Valladolid debido a que había presentado tos y vómitos por un mes. La paciente refirió haber sufrido epigastralgia y amenorrea por dos meses, así como escaso sangrado vaginal en los últimos dos días. Teniendo en cuenta que la paciente dio positivo en una prueba de embarazo, que en la ecografía transvaginal se observó una masa intrauterina heterogénea de 124x120mm, que no se reportaron hallazgos anormales en la ecografía Doppler y que sus niveles séricos de ßhCG alcanzaron un valor de 772.110 mUI/mL, se sospechó un diagnóstico de mola hidatiforme. Una vez informada sobre las posibles alternativas terapéuticas, la paciente decidió someterse a una histerectomía total, pues refirió que ya había cumplido su deseo de ser madre. Luego de realizar procedimiento, la condición clínica de la paciente mejoró; además, el informe de patología de la masa permitió confirmar el diagnóstico de mola hidatiforme parcial. Conclusiones. El diagnóstico temprano de la mola hidatiforme es de gran importancia para ofrecer un tratamiento adecuado y, de esta forma, mejorar el pronóstico de estas pacientes. Por tanto, a pesar de su baja incidencia y sus manifestaciones clínicas inespecíficas, se debe considerar como diagnóstico diferencial de las metrorragias del primer trimestre.

3.
Cancer Cell ; 11(3): 291-302, 2007 Mar.
Article in English | MEDLINE | ID: mdl-17349585

ABSTRACT

Pancreatic ductal adenocarcinoma (PDA), one of the deadliest human cancers, often involves somatic activation of K-Ras oncogenes. We report that selective expression of an endogenous K-Ras(G12V) oncogene in embryonic cells of acinar/centroacinar lineage results in pancreatic intraepithelial neoplasias (PanINs) and invasive PDA, suggesting that PDA originates by differentiation of acinar/centroacinar cells or their precursors into ductal-like cells. Surprisingly, adult mice become refractory to K-Ras(G12V)-induced PanINs and PDA. However, if these mice are challenged with a mild form of chronic pancreatitis, they develop the full spectrum of PanINs and invasive PDA. These observations suggest that, during adulthood, PDA stems from a combination of genetic (e.g., somatic K-Ras mutations) and nongenetic (e.g., tissue damage) events.


Subject(s)
Carcinoma in Situ/pathology , Carcinoma, Pancreatic Ductal/pathology , Genes, ras , Pancreatic Neoplasms/pathology , Pancreatitis, Chronic/pathology , Animals , Carcinoma in Situ/metabolism , Carcinoma, Pancreatic Ductal/metabolism , Cell Lineage , Cell Transformation, Neoplastic , Ceruletide , Doxycycline/pharmacology , Liver Neoplasms/secondary , Lung Neoplasms/secondary , Mice , Mice, Mutant Strains , Mutation , Neoplasm Invasiveness , Pancreas/pathology , Pancreatic Neoplasms/metabolism , Pancreatitis, Chronic/chemically induced , Signal Transduction
4.
Carcinogenesis ; 28(3): 584-94, 2007 Mar.
Article in English | MEDLINE | ID: mdl-17050554

ABSTRACT

AKT1/PKB is a serine/threonine protein kinase that regulates biological processes such as proliferation, apoptosis and growth in a variety of cell types. To assess the oncogenic capability of an activated form of AKT in vivo we have generated several transgenic mouse lines that overexpress in the mammary epithelium the murine Akt1 gene modified with a myristoylation signal, which renders active this protein by localizing it to the plasma membrane. We demonstrate that expression of myristoylated AKT in the mammary glands increases the susceptibility of these mice to the induction of mammary tumors of epithelial origin by the carcinogen 9,10-dimethyl-1,2 benzanthracene (DMBA). We have found that while carcinogen-treated wild-type mice show mostly mammary tumors of sarcomatous origin, AKT transgenic mice treated with DMBA developed mainly adenocarcinoma or adenosquamous tumors, all of them displaying activated AKT. We analyzed other possible molecular alterations cooperating with AKT and found that neither Ras nor beta-catenin/Wnt pathways seemed altered nor p53 mutated. We have found that 100% of mammary DMBA-induced tumors and benign lesions in myrAKT mice are estrogen receptor (ERalpha)-positive and are more frequent than in wild-type littermates. These data show that AKT activation cooperates with deregulation of the estrogen receptor in the DMBA-induced mammary tumorigenesis model and recapitulate two characteristics of some human breast tumors. Thus, our model might provide a preclinical relevant model system to study the role of AKT and ERalpha in breast tumorigenesis and the response of mammary gland tumors to chemotherapeutics.


Subject(s)
9,10-Dimethyl-1,2-benzanthracene/toxicity , Breast Neoplasms/genetics , Carcinogens/toxicity , Mammary Neoplasms, Animal/genetics , Myristic Acid/metabolism , Proto-Oncogene Proteins c-akt/genetics , Animals , Base Sequence , Breast Neoplasms/pathology , DNA Primers , Disease Models, Animal , Estrogens/analysis , Female , Humans , Mammary Neoplasms, Animal/pathology , Mice , Mice, Transgenic
5.
Cancer Res ; 66(1): 95-106, 2006 Jan 01.
Article in English | MEDLINE | ID: mdl-16397221

ABSTRACT

Several diverse genetically engineered mouse models of pancreatic exocrine neoplasia have been developed. These mouse models have a spectrum of pathologic changes; however, until now, there has been no uniform nomenclature to characterize these changes. An international workshop, sponsored by The National Cancer Institute and the University of Pennsylvania, was held from December 1 to 3, 2004 with the goal of establishing an internationally accepted uniform nomenclature for the pathology of genetically engineered mouse models of pancreatic exocrine neoplasia. The pancreatic pathology in 12 existing mouse models of pancreatic neoplasia was reviewed at this workshop, and a standardized nomenclature with definitions and associated images was developed. It is our intention that this nomenclature will standardize the reporting of genetically engineered mouse models of pancreatic exocrine neoplasia, that it will facilitate comparisons between genetically engineered mouse models and human pancreatic disease, and that it will be broad enough to accommodate newly emerging mouse models of pancreatic neoplasia.


Subject(s)
Disease Models, Animal , Pancreatic Neoplasms/pathology , Animals , Genetic Engineering , Humans , Mice , Pancreas, Exocrine/pathology , Pancreatic Neoplasms/genetics , Terminology as Topic
6.
Rev. esp. cardiol. (Ed. impr.) ; 53(7): 1005-1007, jul. 2000.
Article in Es | IBECS | ID: ibc-2856

ABSTRACT

Describimos el caso de una paciente que presentó un sarcoma del tabique interauricular con un crecimiento muy acelerado y una evolución clínica fulminante, documentado mediante técnicas diagnósticas de imagen no invasivas, habituales en la práctica cardiológica. La historia natural de algunos tipos de tumores cardíacos malignos tan agresivos como el descrito explica el habitual retraso diagnóstico, la dificultad para instaurar un tratamiento curativo como la cirugía y/o poliquimioterapia/radioterapia y el pronóstico tan sombrío a corto plazo (AU)


Subject(s)
Adult , Female , Humans , Sarcoma , Time Factors , Cell Division , Magnetic Resonance Imaging , Heart Neoplasms
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