Breast tumors biopsy

Noseda A, Berens ME, White JG, Modest EJ (1988) In vitro antiproliferative activity of combinations of ether lipid analogues and DNA interactive agents against human tumor cells. Cancer Res 48 1788-1791 Obeid LM, Linardic CM, Karolak LA, Hannun YA (1993) Programmed cell death induced by ceramide. Science 259 1769-1771 O Brian CA, Vogel, VG, Singletary SE, Ward NE (1989a) Elevated protein kinase C expression in human breast tumor biopsies relative to normal breast tissue. Cancer Res 49 3215-3217... 

O Brian C, Vogel VG, Singletary SE, et al. Elevated protein kinase C expression in human breast tumor biopsies relative to normal breast tissue. Cancer Res 1989 49(12) 3215-3217. 

Whereas quantitative assays for ERP and PRP have repeatedly proved their clinical utility, the increasing use of breast tumor biopsies by fine needle aspiration requires an assay that is able to identify the ERP and PRP in small tissue samples. Immunocytochemical procedures are ideal for this and in Section 11.3 a detailed explanation of this method is given. The fine needle aspiration can be used as an... 

A double immunohistochemical method has been used for determining the expression patterns of ER, PR, and EGF receptors in breast biopsies (Van Agthoven et al., 1994). It was demonstrated that ER/PR and EGF receptors in breast tumor cells were inversely related at the single cell level. However, the expression of these three receptors in individual normal luminal cells was not mutually exclusive. 

Analyses of the p53 status in tumor biopsies have revealed that patients with tumors with increased protein expression of p53 or a mutant p53 have a worse prognosis. This has been demonstrated for patients with bladder, breast, colon, gastric, nonsmall cell lung, oesophagus, ovarian and prostate carcinoma and the group of soft-tissue sarcomas (11,21-37). 

Non-carcinomatous spindle cell proliferation in a breast core biopsy sample includes fibromatosis, myofibroblastoma, stromal component of phyllodes tumor, or rare primary sarcomas. 

The causative roles attributed to CCL5 in breast cancer motivated the search for better identification of its modes of action in this disease. First, it is possible that the chemokine acts directly on the cancer cells to promote their ability to exert promalignancy properties. Such an activity of the chemokine necessitates the expression of the corresponding receptors for CCL5 by the tumor cells. Indeed, CCL5 was found to bind to breast tumor cells, and CCR5 and CCR1 receptors were detected in breast tumor cells in culture and/or in biopsies of breast cancer patients ([39 41,43,46, 56-58] and A. Ben-Baruch et al., unpublished results). 

John, C.S., Vilner, B.J., Schwartz, A.M., Bowen, W.D., 1996. Characterization of sigma receptor binding sites in human biopsied solid breast tumors. J. Nucl. Med. 37, 267P. 

It may not be possible to obtain better correlation between the cy tochemical and the biochemical methods for aspirates and excision biopsies due to the heterogeneity of breast tumors with respect to receptor concentration. Earlier studies demonstrated that cells from different areas of a tumor may show different characteristics (K12). 

The presence of estrogen receptors (ER) in biopsies of breast cancers is a good predictor of responsiveness to tamoxifen therapy 60% of women with ER-positive tumors will have a remission, as opposed to fewer than 10% with ER-negative tumors. Overall, 35 to 40% of women with breast cancer will respond to some degree, with antitumor effects lasting an average of 9 to 12 months. Complete remissions may occur in 10 to 15% of patients and may last several months to a few years. Therapy should be continued for at least 6 weeks to establish efficacy. 

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