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1.
Clin Breast Cancer ; 15(5): e243-8, 2015 Oct.
Artículo en Inglés | MEDLINE | ID: mdl-25922244

RESUMEN

BACKGROUND: Recent studies suggest that axillary lymph node dissection (ALND) may be omitted in select breast cancer patients with a positive sentinel lymph node biopsy (SLNB). As we trend away from ALND, we must understand the burden of axillary disease among various patient subgroups. For patients with positive nodes determined using ultrasound-guided needle biopsy (USNB), there are no data regarding the extent of axillary disease. PATIENTS AND METHODS: An institutional breast cancer registry was retrospectively reviewed to identify women with invasive cancer and a positive USNB/SLNB who had completion ALND. For statistical analysis, we used χ(2) and 1-way analysis of variance. RESULTS: One hundred ninety-nine USNB-positive (USNB(+)) patients and 434 SLNB(+) patients were eligible for the study. Positive USNB patients were significantly older, had larger tumors, and were more likely to be estrogen receptor-negative/progesterone receptor-negative and HER2/neu(+) than SLNB(+) patients. USNB(+) patients had much higher rates of N2 (33.2% vs. 12.4%; P < .05) and N3 (17.1% vs. 3.9%; P < .05) disease compared with SLNB(+) patients. Higher axillary disease burden was demonstrated in USNB patients who were clinically node negative and those who met Z11 criteria. CONCLUSION: Patients with invasive breast cancer with a positive node on USNB have a significantly greater burden of axillary disease compared with patients with a positive SLNB. USNB(+) patients represent a distinct patient population and further research is required to determine if these patients can be safely exempted from axillary dissection.


Asunto(s)
Neoplasias de la Mama/patología , Neoplasias de la Mama/cirugía , Biopsia Guiada por Imagen , Escisión del Ganglio Linfático , Biopsia del Ganglio Linfático Centinela , Adulto , Femenino , Humanos , Metástasis Linfática , Persona de Mediana Edad , Estadificación de Neoplasias , Sistema de Registros , Estudios Retrospectivos
2.
Proc Natl Acad Sci U S A ; 99(14): 9380-5, 2002 Jul 09.
Artículo en Inglés | MEDLINE | ID: mdl-12089333

RESUMEN

Certain HIV-encoded proteins modify host-cell gene expression in a manner that facilitates viral replication. These activities may contribute to low-level viral replication in nonproliferating cells. Through the use of oligonucleotide microarrays and high-throughput Western blotting we demonstrate that one of these proteins, gp120, induces the expression of cytokines, chemokines, kinases, and transcription factors associated with antigen-specific T cell activation in the absence of cellular proliferation. Examination of transcriptional changes induced by gp120 in freshly isolated peripheral blood mononuclear cells and monocyte-derived-macrophages reveals a broad and complex transcriptional program conducive to productive infection with HIV. Observations include the induction of nuclear factor of activated T cells, components of the RNA polymerase II complex including TFII D, proteins localized to the plasma membrane, including several syntaxins, and members of the Rho protein family, including Cdc 42. These observations provide evidence that envelope-mediated signaling contributes to the productive infection of HIV in suboptimally activated T cells.


Asunto(s)
Proteína gp120 de Envoltorio del VIH/fisiología , VIH-1/fisiología , Leucocitos Mononucleares/metabolismo , Leucocitos Mononucleares/virología , Proteínas Nucleares , Replicación Viral/fisiología , Animales , Células CHO , División Celular , Quimiocinas/genética , Cricetinae , Citocinas/genética , Proteínas de Unión al ADN/genética , Expresión Génica/efectos de los fármacos , Proteína gp120 de Envoltorio del VIH/farmacología , Humanos , Técnicas In Vitro , Leucocitos Mononucleares/citología , Leucocitos Mononucleares/efectos de los fármacos , Activación de Linfocitos , Macrófagos/citología , Macrófagos/efectos de los fármacos , Macrófagos/metabolismo , Macrófagos/virología , Fusión de Membrana/efectos de los fármacos , Fusión de Membrana/genética , Factores de Transcripción NFATC , Proteínas Quinasas/genética , Proteínas Recombinantes/metabolismo , Proteínas Recombinantes/farmacología , Transducción de Señal , Linfocitos T/efectos de los fármacos , Linfocitos T/metabolismo , Linfocitos T/virología , Factores de Transcripción/genética
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