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Whitney Banach-Petrosky

Researcher at Rutgers University

Publications -  20
Citations -  1766

Whitney Banach-Petrosky is an academic researcher from Rutgers University. The author has contributed to research in topics: PTEN & Prostate cancer. The author has an hindex of 13, co-authored 16 publications receiving 1679 citations. Previous affiliations of Whitney Banach-Petrosky include Center for Advanced Biotechnology and Medicine & University of Medicine and Dentistry of New Jersey.

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Cooperativity of Nkx3.1 and Pten loss of function in a mouse model of prostate carcinogenesis

TL;DR: It is demonstrated that the Nkx3.1 homeobox gene undergoes epigenetic inactivation through loss of protein expression, which results in synergistic activation of Akt (protein kinase B), a key modulator of cell growth and survival.
Journal Article

Nkx3.1 Mutant Mice Recapitulate Early Stages of Prostate Carcinogenesis

TL;DR: It is found that PIN-like lesions from Nkx3.1 mutants can undergo progressively severe histopathological alterations after serial transplantation in nude mice, and the tissue recombination assay provides an empirical test to examine the relationship of PIN to prostate carcinoma.
Journal Article

Nkx3.1; Pten Mutant Mice Develop Invasive Prostate Adenocarcinoma and Lymph Node Metastases

TL;DR: It is concluded that Nkx3.1 (+/-); Pten(+/-) mice recapitulate key features of advanced prostate cancer and represent a useful model for investigating associated molecular mechanisms and for evaluating therapeutic approaches.
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Targeting the Transforming Growth Factor-β pathway inhibits human basal-like breast cancer metastasis

TL;DR: These studies support the notion that TGF-β plays an important role in both bone-and lung metastases of basal-like breast cancer, and that inhibiting T GF-β signaling results in a therapeutic effect independently of the tissue-tropism of the metastatic cells.
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Combinatorial activities of Akt and B-Raf/Erk signaling in a mouse model of androgen-independent prostate cancer

TL;DR: It is proposed that androgen independence emerges by means of epithelial–stromal competition, in which activation of Akt and Erk promotes AR activity in the prostate epithelium while counteracting antagonistic effects of the stroma.