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1.
Clin Breast Cancer ; 15(5): e243-8, 2015 Oct.
Article in English | MEDLINE | ID: mdl-25922244

ABSTRACT

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.


Subject(s)
Breast Neoplasms/pathology , Breast Neoplasms/surgery , Image-Guided Biopsy , Lymph Node Excision , Sentinel Lymph Node Biopsy , Adult , Female , Humans , Lymphatic Metastasis , Middle Aged , Neoplasm Staging , Registries , Retrospective Studies
2.
Proc Natl Acad Sci U S A ; 99(14): 9380-5, 2002 Jul 09.
Article in English | MEDLINE | ID: mdl-12089333

ABSTRACT

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.


Subject(s)
HIV Envelope Protein gp120/physiology , HIV-1/physiology , Leukocytes, Mononuclear/metabolism , Leukocytes, Mononuclear/virology , Nuclear Proteins , Virus Replication/physiology , Animals , CHO Cells , Cell Division , Chemokines/genetics , Cricetinae , Cytokines/genetics , DNA-Binding Proteins/genetics , Gene Expression/drug effects , HIV Envelope Protein gp120/pharmacology , Humans , In Vitro Techniques , Leukocytes, Mononuclear/cytology , Leukocytes, Mononuclear/drug effects , Lymphocyte Activation , Macrophages/cytology , Macrophages/drug effects , Macrophages/metabolism , Macrophages/virology , Membrane Fusion/drug effects , Membrane Fusion/genetics , NFATC Transcription Factors , Protein Kinases/genetics , Recombinant Proteins/metabolism , Recombinant Proteins/pharmacology , Signal Transduction , T-Lymphocytes/drug effects , T-Lymphocytes/metabolism , T-Lymphocytes/virology , Transcription Factors/genetics
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