Robert B. Boxer, Ph.D.

Affiliations: 
2004 University of Pennsylvania, Philadelphia, PA, United States 
Area:
Molecular Biology, Cell Biology, Oncology
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"Robert Boxer"

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Lewis A. Chodosh grad student 2004 Penn
 (Studies on proto-oncogene function: The roles of c-MYC and Akt1 in mammary development and tumorigenesis.)
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Publications

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Chen CC, Stairs DB, Boxer RB, et al. (2012) Autocrine prolactin induced by the Pten-Akt pathway is required for lactation initiation and provides a direct link between the Akt and Stat5 pathways. Genes & Development. 26: 2154-68
Chen CC, Boxer RB, Stairs DB, et al. (2010) Akt is required for Stat5 activation and mammary differentiation. Breast Cancer Research : Bcr. 12: R72
Sarkisian CJ, Keister BA, Stairs DB, et al. (2007) Dose-dependent oncogene-induced senescence in vivo and its evasion during mammary tumorigenesis. Nature Cell Biology. 9: 493-505
Boxer RB, Stairs DB, Dugan KD, et al. (2006) Isoform-specific requirement for Akt1 in the developmental regulation of cellular metabolism during lactation. Cell Metabolism. 4: 475-90
Jang JW, Boxer RB, Chodosh LA. (2006) Isoform-specific ras activation and oncogene dependence during MYC- and Wnt-induced mammary tumorigenesis. Molecular and Cellular Biology. 26: 8109-21
Boxer RB, Jang JW, Sintasath L. (2005) Persistence of cancer after oncogene targeting Cancer Biology and Therapy. 4
Boxer RB, Jang JW, Sintasath L, et al. (2004) Lack of sustained regression of c-MYC-induced mammary adenocarcinomas following brief or prolonged MYC inactivation. Cancer Cell. 6: 577-86
Chodosh L, Boxer R, Moody S, et al. (2003) Reversibility and progression in conditional transgenic mouse models of breast cancer Breast Cancer Research. 5: 5-5
Gunther EJ, Belka GK, Wertheim GB, et al. (2002) A novel doxycycline-inducible system for the transgenic analysis of mammary gland biology. Faseb Journal : Official Publication of the Federation of American Societies For Experimental Biology. 16: 283-92
D'Cruz CM, Gunther EJ, Boxer RB, et al. (2001) c-MYC induces mammary tumorigenesis by means of a preferred pathway involving spontaneous Kras2 mutations. Nature Medicine. 7: 235-9
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