Through my work, I have helped launch ERACE, or Engaging Research to Achieve Cancer Care Equity , which aims to bring the latest data, technology, and top US oncologists and cancer research centers together to create a race and ethnicity-based oncology registry.
The registry is intended to generate insight into what is driving these inequalities, bring to bear positive outcomes for populations where disparities exist, and support the next generation of researchers in their search for innovative solutions.
We also believe that it will expand access for minority populations to cutting-edge cancer care. Although individuals from racial and ethnic backgrounds will comprise the majority of the U. Building a national registry of minority cancer patients will address systemic geographic and structural barriers to achieve more equitable care and outcomes for all patients and not just the privileged few. The collective efforts that have recently launched to explicitly address these health inequities may finally move the needle in a positive direction.
The National Foundation for Cancer Research is seeking funding to expand on genomic sequencing work led by Dr. And leading cancer research organizations like the Dana-Farber Cancer Institute are increasingly turning their attention and formidable resources to cancer disparities, both to better understand biological factors and to actively address the social forces that increase the risk for disease and limit access to treatment.
Now we need to hold ourselves accountable and make the case for more funding, for private-public partnerships, and for institutions to create space for their leading researchers to focus on this issue. This analysis consisted of the following three steps.
The ARACNe method uses information-theoretic approaches to calculate the mutual information MI between every transcription factor and its putative targets, assesses the statistical significance of each MI value, and discards insignificant interactions as well as false positive interactions identified by the data processing inequality.
This approach, using as few as Parsa, or Carro et al. In particular, it predicted direct transcriptional targets of ZFHX4, of which were represented in our transcriptional profiling studies Figure 4G , Table S3. Recent work implicates alterations in epigenetic regulation as a key step during gliomagenesis Lewis et al.
Here we show that a transcription factor with previously unknown roles in cancer interacts with a core member of an epigenetic regulatory complex and thereby drives a specific gene expression program and regulates the GBM TIC state. Further studies of ZFHX4 and its downstream effectors, as well as its interaction with CHD4 and the NuRD complex, will enhance our understanding of glioma and may eventually lead to new targeted differentiation-based therapies for brain tumor patients.
Materials, cell lines, and shRNA and expression constructs used, as well as detailed methods, are described in Extended Experimental Procedures. After 1 wk, 2 selected and 2 unselected replicates were assayed for relative cell number using CellTiter-Glo Luminescent Assay Promega.
Two additional unselected replicates were stained for DNA and Tubulin and imaged on an automated microscope. Cellular objects were identified, characterized, and classified by phenotype using CellProfiler and CellProfiler Analyst software Carpenter et al. The confirmation screen was performed as described in Extended Experimental Procedures.
Mice were sacrificed upon exhibiting signs of morbidity, and brains were excised and processed for histology and IHC. This network was parsed to identify interactions for ZFHX4; of these were represented in transcriptional profiles obtained after suppressing CHD4. Significance of enrichment was calculated using a non-parametric test with sample shuffling. Maire for technical assistance, L.
Solomon, L. Gaffney, and T. DiCesare for extensive graphical help preparing manuscript figures, E. Spooner for mass spectrometric analysis, H. Le, S. Ponduru, M.
Vokes, V. Ljosa, A. C and M. Supplemental Information includes Extended Experimental Procedures, four figures, three tables, one data file, and supplemental references. Read article at publisher's site DOI : Brief Bioinform , 22 5 , 01 Sep J Mol Cell Biol , 13 3 , 01 Jul Ann Transl Med , 9 12 , 01 Jun JCI Insight , 6 4 , 22 Feb Int J Mol Sci , 22 2 , 06 Jan This data has been text mined from the article, or deposited into data resources.
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Chheda MG Show less. Affiliations 1 author 1. Share this article Share with email Share with twitter Share with linkedin Share with facebook. Abstract Glioblastoma GBM harbors subpopulations of therapy-resistant tumor-initiating cells TICs that are self-renewing and multipotent. ZFHX4 is required to maintain TIC-associated and normal human neural precursor cell phenotypes in vitro, suggesting that ZFHX4 regulates differentiation, and its suppression increases glioma-free survival in intracranial xenografts.
Free full text. Cell Rep. Author manuscript; available in PMC Jul PMID: Fine , 15, 16 Anne E. Carpenter , 3 Serena J. Silver , 3 Roel G. Embryonic stem cells are characterized by rapid growth and renewal.
Frampton, Warren A. Whyte, Sabrina A. Stratton, Michelle C. Barton, Preethi H. Gunaratne, Richard A. Young, and Thomas P. Genes Dev. ScienceDaily, 25 June Baylor College of Medicine. Ronin recruits protein 'allies' to sustain embryonic stem cell growth. Retrieved November 10, from www. These cells are difficult to isolate and study because of their low abundance and For this purpose, the stem cells simultaneously modify the blueprints for The observed mechanism is essential for the self-renewal of stem Previously unclear was how its protein abundance is regulated in the cells.
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