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Article Title: Modulation of Notch Signaling Elicits Signature Tumors and Inhibits Hras1-Induced Oncogenesis in the Mouse Mammary Epithelium
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Figure Lengend Snippet: Nonregressing hN1IC-dependent tumors. Nonregressing hN1IC-dependent papillary invasive adenocarcinomas with low-grade nuclei and necrotic areas. A: Invasion of adipose tissue by a papillary adenocarcinoma. B: An invasive tumor (Inv) is found adjacent to a benign papillary lesion in a terminal breast duct (arrow). DCIS is also visible in this section and is indicated by an asterisk. C: Invasive tumor with evident papillary structure composed of (enlargement in D) a uniform population of cancer cells with low-grade nuclei, sharp nuclear borders, and inconspicuous nucleoli. Regressing papillary hN1IC neoplasias are more sensitive to apoptosis than the invasive tumors. E and F: Apoptotic cells identified by TUNEL analysis (brown staining) in hN1IC lactation-dependent tumors from animals sacrificed either during lactation (E) or during involution (F). Note the increased number of the TUNEL-positive cells in F, as compared to E, consistent with the notion that tumors induced during lactation retain the ability to respond to apoptotic signals during involution. G and H: TUNEL analysis in nonregressing tumors during lactation and involution, respectively. The scarcity of apoptotic nuclei, as compared to that of the regressing tumors shown in E and F indicates that these lesions are resistant to the apoptotic stimuli encountered during involution. Original magnifications: ×4 (B); ×10 (A, C); ×60 (D).
Article Snippet: However, terminal differentiation of the mammary epithelium during lactation could proceed normally. fig ft0 fig mode=article f1 fig/graphic|fig/alternatives/graphic mode="anchored" m1 Open in a separate window Figure 6 caption a7 The expression of the Notch signal antagonist Deltex inhibits apoptosis during involution.
Techniques: TUNEL Assay, Staining