By E. Edward Bittar, Gloria Heppner, William P. Peters and Daniel W. Visscher (Eds.)
Breast melanoma study hasn't ever been in such a thrilling and hopeful part as at the present time. From a medical viewpoint, the invention of genetic markers of danger in a percentage of familial breast melanoma circumstances has unfolded new vistas for knowing and eventually combating this ailment. however, competitive - even bold - cures are being confirmed to be powerful opposed to complicated breast melanoma. For the breast melanoma experimentalist, this is often additionally a time of serious strengthen. even if animal and mobile tradition breast melanoma types have confirmed to be of significant use, there are actually expanding possibilities to check the strategies built in those versions in genuine medical samples and situations. it truly is pleasurable to work out how good those innovations "translate" into the medical atmosphere. a truly energetic sector of analysis that's linking the laboratory to the sanatorium is the dissection of the biology and elucidation of the importance of proliferate breast affliction and the identity of real, "high threat" or "preneoplastic" legions in the formerly ill-defined spectrum of fibrocystic or benign breast disorder. One anticipates that discoveries made right here also will bring about previous detection, intervention and prevention of life-threatening cancer.Even, notwithstanding, as we glance with optimism to the eventual eradication of breast melanoma, we're once more compelled to stand the truth that we've got no longer but completed our aim. hence, we're saddened through the a lot too untimely dying of Dr. Helene Smith from breast melanoma. Helena's paintings was once on the vanguard of efforts to appreciate the biology of human breast melanoma on the molecular point. Her perception, open-mindedness, and refusal to sacrifice relevance for comfort will proceed to set the normal for all breast melanoma researchers. This quantity is devoted to her reminiscence.
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Extra resources for Breast Cancer
1992). Because the molecular mechanisms underlying the acquisition of resistance to antihormone therapy in breast cancer are poorly understood, ER+ breast cancer cell lines have been studied in vitro and in vivo in many model systems that attempt to re-create changes in tumor behavior seen in patients in response to hormone ablation. Such manipulation has successfully generated E2-independent or antiestrogen-insensitive cell lines from ER-H precursors, but most retain ER expression. , 1987; Welshons and Jordan, 1987) or by serial passage through nude mice in vivo in the absence of E2 and 20 DAVID L.
1993). Although AR expression correlates with ER expression in breast tumors, tumors that overexpress EGFR also express AR in 35% of cases. , 1993). , 1995). , 1989). All three proteins, like EGF, TGF-a, and AR, are synthesized as transmembrane precursors that are proteolytically cleaved to yield a soluble form. , 1992). , 1991). , 1993). , 1996). , 1989). , 1994); the natural receptor for cripto-1 remains unidentified. In contrast to the multiple growth factors shown to bind and activate EGFR specifically, only two ligands for c-erbB-2 have been described.
MILLER and FRANCIS C. , 1993). Given the plethora of growth factors with angiogenic potential, essentially all of which have been found to be expressed in tumors or tumor cell lines, it is impossible at this point to determine which factor or combination of factors is driving the process in tumors. , 1989; Leung et al, 1989). In addition to being an endothelial cell mitogen, this factor also allows neovascularization by promoting remodeling of the extracellular matrix and was originally described as Vascular Permeability Factor (VPF).