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Autor:
Xiaodong Shu, Shan Cheng, Jianhong Xia, Duanqing Pei, Qiuling Huang, Xiaofei Zhang, Haiyun Wang
Publikováno v:
Molecular Cancer Research. 20:253-264
Dysregulation of Notch signaling has been implicated in cellular transformation and tumorigenesis in a variety of cancers while potential roles of MIB1, an E3 ubiquitin ligase required for efficient Notch activation, remains to be investigated. We an
Publikováno v:
Molecular Cancer Research. 20:3-10
Centromere dysfunctions leading to numerical chromosome alterations are believed to be closely related to human cancers. As a centromere-specific protein, centromere protein A (CENP-A) replaces the histone H3 in centromeres and is therefore considere
Autor:
Purna Chaitanya Konduri, Jung-whan Kim, Parinaz Sadat Alemi, Chantal Vidal, Adnin Ashrafi, Nivesh Jain, Sanchareeka Dey, Narges Salamat, Li Zhang, Sarada Preeta Kalainayakan, Poorva Ghosh
Publikováno v:
Molecular Cancer Research. 20:139-149
Lung adenocarcinoma (ADC) and squamous cell carcinoma (SCC) are two most common subtypes of lung cancer. Here, to identify new, targetable molecular properties of both subtypes, we monitored changes in the levels of heme- and oxidative phosphorylatio
Publikováno v:
Molecular Cancer Research. 20:30-44
Kirsten Rat Sarcoma (KRAS) gene somatic point mutations is one of the most prominently mutated proto-oncogenes known to date, and accounts for approximately 60% of all colorectal cancer cases. One of the most exciting drug development areas against c
Autor:
Emad A. Rakha, Ying Zhang, Hamid Band, Lulu Yu, Dhananjaya Pal, Mohsin Raza, Zhi-Ming Zheng, Vimla Band, M. Jordan Rowley, Achyuth Kalluchi, Bhopal Mohapatra, Michel M. Ouellette, Sameer Mirza, Irfana Saleem, Fang Qiu, Mansour Alsaleem, Alexei Lobanov
Publikováno v:
Mol Cancer Res
High-risk human papillomaviruses (HPV), exemplified by HPV16/18, are causally linked to human cancers of the anogenital tract, skin, and upper aerodigestive tract. Previously, we identified Ecdysoneless (ECD) protein, the human homolog of the Drosoph
Autor:
Li Ji, Jingjing Wang, Lingli Gong, Yaling Hu, Jian Zou, Ying Yin, Xusheng Yang, Yingdi Jiang, Zhenhao Zhang, Zhening Pu, Bo Zhang
Publikováno v:
Molecular Cancer Research. 20:92-101
Previous studies have demonstrated that glucocorticoid receptor β (GRβ) functions as an oncoprotein, regulating the malignant phenotypes and stem-like cell maintaining in human glioblastoma (GBM). Of the glucocorticoid receptor (GR) isoforms, GRβ
Autor:
Elisha Martin, Yehenew M. Agazie
Publikováno v:
Molecular Cancer Research. 19:1946-1956
Previous studies have reported dysregulated cytoplasmic and nuclear expression of the β-catenin protein in triple-negative breast cancer (TNBC) in the absence of Wnt signaling pathway dysregulation. However, the mechanism that sustains β-catenin pr
Autor:
Daqian Zhan, Alan K. Meeker, Hernando Lopez-Bertoni, Charles G. Eberhart, Yi Fu, Ding Ma, Yunqing Li, Bachchu Lal, John Laterra, Shuli Xia, Mingyao Ying, Shuang Wei
Publikováno v:
Mol Cancer Res
Heterozygous isocitrate dehydrogenase (IDH) R132H mutation (IDH1R132H/WT) is an early event during gliomagenesis. Clinically, patients with glioma carrying mutant IDH1 respond better to antitumor therapies. However, the mechanism by which IDH1 mutati
Autor:
George E. Sandusky, Max Jacobsen, Constance J. Temm, Poornima Bhat-Nakshatri, Harikrishna Nakshatri, Calli Maguire, Brijesh Kumar
Publikováno v:
Mol Cancer Res
Breast cancers are classified into five intrinsic subtypes and 10 integrative clusters based on gene expression patterns and genomic aberrations, respectively. Although the cell-of-origin, adaptive plasticity, and genomic aberrations shape dynamic tr
Autor:
Jochen Hess, Karam Khorani, Ina Kurth, Karim Zaoui, Sebastian Burkart, Christa Flechtenmacher, Peter K. Plinkert, Dana Holzinger, Julia Schwaerzler
Publikováno v:
Molecular Cancer Research. 19:1676-1687
Recent studies highlighted SOX2 and SOX9 as key determinants for cancer-cell plasticity and demonstrated that cisplatin-induced adaptation in oral squamous cell carcinoma (SCC) is acquired by an inverse regulation of both transcription factors. Howev