Zobrazeno 1 - 10
of 16
pro vyhledávání: '"Bo Hong"'
Autor:
Varun V. Prabhu, David T. Dicker, Bo Hong, Joshua E. Allen, Wafik S. El-Deiry, Shengliang Zhang, Amriti R. Lulla
Publikováno v:
Cancer Research. 76:1989-1999
Tumor suppressor p53 is frequently mutated or inactivated in colorectal cancer. In contrast, p53 family member p73 is rarely mutated in colorectal cancer and p73 activation elicits p53-like tumor suppression. Colorectal cancer stem cells (CRCSC) comp
Autor:
A. Pieter J. van den Heuvel, Christina Leah B. Kline, Varun V. Prabhu, David T. Dicker, Bo Hong, Wafik S. El-Deiry, Levy Kopelovich, Shengliang Zhang, Noel A. Warfel, Lanlan Zhou
Publikováno v:
Cancer Research. 75:3842-3852
The tumor-suppressor p53 prevents cancer development via initiating cell-cycle arrest, cell death, repair, or antiangiogenesis processes. Over 50% of human cancers harbor cancer-causing mutant p53. p53 mutations not only abrogate its tumor-suppressor
Autor:
Bo Hong, Levy Kopelovich, A. Pieter J. van den Heuvel, Shengliang Zhang, Wafik S. El-Deiry, Varun V. Prabhu, David T. Dicker
Publikováno v:
Cancer Research. 74:1153-1165
p53 reactivation offers a broad-based strategy for cancer therapy. In this study, we report the identification of prodigiosin that can reactivate p53 family-dependent transcriptional activity in p53-deficient human colon cancer cells. Prodigiosin and
Publikováno v:
Cancer Research. 77:3419-3419
The goal of this study is to elucidate the functional consequences of FBXW7 mutations in the context of endometrial carcinoma (EC). EC is a heterogeneous disease, consisting of multiple histological subtypes associated with distinct clinical outcomes
Autor:
Wafik S. El-Deiry, Shengliang Zhang, Joshua E. Allen, Amriti R. Lulla, Bo Hong, Varun V. Prabhu, David T. Dicker
Publikováno v:
Cancer Research. 75:1215-1215
Tumor suppressor p53 is frequently mutated or inactivated in colorectal cancer while p53 family member p73 is rarely mutated in cancer cells. Small molecules that activate p73 can elicit a p53-like tumor suppressive function and represent a novel app
Autor:
Wafik S. El-Deiry, Shengliang Zhang, Varun V. Prabhu, David T. Dicker, Joshua E. Allen, Bo Hong
Publikováno v:
Cancer Research. 74:202-202
Tumor suppressor p53 is frequently mutated or inactivated in colorectal cancer while p53 family member p73 is rarely mutated in cancer cells. Small molecules that activate p73 can elicit a p53-like tumor suppressive function and represent a novel app
Autor:
Prabhu, Varun V.1,2, Bo Hong1, Allen, Joshua E.1, Shengliang Zhang1,2, Lulla, Amriti R.1,2, Dicker, David T.1,2, El-Deiry, Wafik S.1,2 wafik.eldeiry@fccc.edu
Publikováno v:
Cancer Research. 4/1/2016, Vol. 76 Issue 7, p1989-1999. 11p.
Publikováno v:
Cancer Research. 73:LB-53
Rescue of mutant p53 function is an attractive strategy for cancer therapy development. Using high throughput drug screening, we identified prodigiosin, which can reactivate p53-dependent transcriptional activity in p53 mutant cancer cells. We find t
Autor:
Bo Hong, Shengliang Zhang, Lanlan Zhou, Noel A. Warfel, Antonius Van den heuvel, Wafik S. El-Deiry, David T. Dicker, Levy Kopelovich
Publikováno v:
Cancer Research. 73:2171-2171
Tumor suppressor p53 is critical for protection against cancer. Over 50% of human cancers harbor mutant p53 which is hyper-stabilized and blocks p53 family member p73/p63 activity. Mutations not only abrogate the p53 tumor suppressor function, but al
Publikováno v:
Cancer Research. 72:2758-2758
Discovery of the molecular targets of chemotherapeutic medicines and their chemical footprints can validate and improve the use of such medicines. In the present study, we investigated the effect of mitomycin C (MMC), a well-known chemotherapeutic ag