Endocrine Therapy and Growth Regulation of Breast Cancer by U. Eppenberger (auth.), Professor Dr. Urs Eppenberger, Priv.

By U. Eppenberger (auth.), Professor Dr. Urs Eppenberger, Priv. Doz. Dr. Aron Goldhirsch (eds.)

Key questions fascinated by the remedy of disseminated breast melanoma are mentioned during this well-presented review. it's the results of an initiative taken via the Swiss team for medical melanoma study to bare the latest advancements in experimental and medical examine. the subjects mentioned comprise: the comparability of in vitro cultures of epithelial cells with breast melanoma cells, the influence of steroids and their antagonists, the involvement of suppressor genes in tumour development, the modulation of reworking progress components by means of estrogen, and prognostic elements akin to cERB-2 and EGF-R in breast cancer.

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1984). In some cases, the ineffectiveness of the steroid receptor complex is due to abnormal receptors with defects distal to the initial steroid binding step (Danielson et al. 1986; Miesfeld et al. 1984; Westphal et al. 1984), but sometimes the receptors are normal (Darbre and King 1987c; Gaubert et al. 1986; King 1978; Sibley and Yamamoto 1979). The 22 P. D. Darbre et al. loss of hormone-sensitive parameters in the S115 cells also occurs without either loss of receptor number (King 1978) or of receptor function (Darbre and King 1987c).

To be published). The estrogen-induced 52K-cathepsin D is also constitutively produced by estrogen receptor-negative breast cancer cells and appears to be more related to cell proliferation than to hormone dependency (Garcia et al. 1987). Immunohistochemical studies have additionally indicated that it is elevated in high-risk mastopathies (Garcia et al. 1986). In conclusion, 52K-cathepsin D may have important autocrine and paracrine functions in stimulating the growth and invasion of hormone-responsive and -unresponsive breast cancers and appears to be a useful tissue marker to predict highrisk mastopathies and breast cancer invasiveness (Rochefort et al.

Examples of receptor-positive but steroid-insensitive cells have been described (Daniel et al. 1986; Darbre and King 1987c; Gaubert et al. 1986; Gehring 1986; George and Wilson 1986; King 1978; Kontula et al. 1986; Miesfeld et al. 1984; Nawata et al. 1981; Sedlacek and Horwitz 1984; Sibley and Yamamoto 1979; Westphal et al. 1984). In some cases, the ineffectiveness of the steroid receptor complex is due to abnormal receptors with defects distal to the initial steroid binding step (Danielson et al.

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