Background: It is believed that bloody spontaneous nipple discharge (SND) portends a greater chance of malignancy than nonbloody discharge, and that cytologic evaluation of SND assists in treatment planning. Our aims were to assess (1) the pathology of women with/without SND who require diagnostic breast surgery, (2) whether bloody SND is associated with a different spectrum of pathologic findings than nonbloody, and (3) whether SND cytology is influenced by pathologic findings.
Methods: One hundred seventy-five women who underwent breast operation were enrolled.
Human kallikreins (hK) 2, 3, 6 and 10 are expressed in breast and prostate tissue. hK2 and hK3 (prostate-specific antigen, PSA) are used to screen for prostate cancer. hK6 and hK10 are downregulated in breast cancer compared to normal breast tissue.
View Article and Find Full Text PDFPurpose: Loss of heterozygosity (LOH) and microsatellite instability (MSI) have been identified in a variety of human cancers. The purpose of this prospective study was to determine whether (a) DNA can be isolated from nipple aspirate fluid (NAF) and PCR amplified to large fragments, (b) LOH and MSI are detectable in NAF, and (c) LOH and MSI in tissue and NAF increase with disease progression from precursor lesions to cancer.
Experimental Design: Forty-six matched samples from breast lesions, normal breast, and NAF were microdissected, and DNA was extracted.
Reorganization of skin during wound healing, inflammatory disorders, or cancer growth is the result of expression changes of multiple genes associated with tissue morphogenesis. We wanted to identify proteins involved in skin remodeling and select those that may be targeted for agonistic or antagonist therapeutic approaches in various disease processes. Full-thickness human skin was grafted to severe combined immunodeficient mice and injected intradermally with 38 different adenoviral vectors inserted with 37 different genes coding for growth factors, cytokines, proteolytic enzymes and their inhibitors, adhesion receptors, oncogenes, and tumor suppressor genes.
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