Scott Powers

ORCID: 0000-0003-2769-1932
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About
Contact & Profiles
Research Areas
  • Cancer Genomics and Diagnostics
  • Fungal and yeast genetics research
  • Protein Kinase Regulation and GTPase Signaling
  • RNA modifications and cancer
  • Nanoplatforms for cancer theranostics
  • Advanced Nanomaterials in Catalysis
  • Cancer-related Molecular Pathways
  • Neutrophil, Myeloperoxidase and Oxidative Mechanisms
  • Epigenetics and DNA Methylation
  • RNA Research and Splicing
  • Cancer Cells and Metastasis
  • Genomics and Chromatin Dynamics
  • Ubiquitin and proteasome pathways
  • Pancreatic and Hepatic Oncology Research
  • Protease and Inhibitor Mechanisms
  • Genomic variations and chromosomal abnormalities
  • Microtubule and mitosis dynamics
  • CRISPR and Genetic Engineering
  • Single-cell and spatial transcriptomics
  • PI3K/AKT/mTOR signaling in cancer
  • Polyamine Metabolism and Applications
  • Advanced biosensing and bioanalysis techniques
  • Protein Tyrosine Phosphatases
  • Endoplasmic Reticulum Stress and Disease
  • Peptidase Inhibition and Analysis

Stony Brook University
2015-2024

Stony Brook School
2021-2024

MetroHealth
2024

Cold Spring Harbor Laboratory
2009-2022

State University of New York
2022

Stony Brook University Hospital
2018

Stony Brook Medicine
2017

University of Maryland, Baltimore
2015

Woodbury University
2012

Institut de Biologie Moléculaire et Cellulaire
2012

We have developed a methodology we call ROMA (representational oligonucleotide microarray analysis), for the detection of genomic aberrations in cancer and normal humans. By arraying probes designed from human genome sequence, hybridizing with "representations" cells, detect regions altered "copy number." achieve an average resolution 30 kb throughout genome, resolutions as high probe every 15 are practical. illustrate characteristics on array accuracy measurements obtained using ROMA. Using...

10.1101/gr.1349003 article EN cc-by-nc Genome Research 2003-01-01

Large-scale integrated cancer genome characterization efforts including the atlas and cell line encyclopedia have created unprecedented opportunities to study biology in context of knowing entire catalog genetic alterations. A clinically important challenge is discover subtypes their molecular drivers a comprehensive context. Curtis et al. [Nature (2012) 486(7403):346-352] has recently shown that integrative clustering copy number gene expression 2,000 breast tumors reveals novel subgroups...

10.1073/pnas.1208949110 article EN Proceedings of the National Academy of Sciences 2013-02-21

Human colorectal cancers (CRCs) display a large number of genetic and epigenetic alterations, some which are causally involved in tumorigenesis (drivers) others that have little functional impact (passengers). To help distinguish between these two classes we used transposon-based screen mice to identify candidate genes for CRC. Mice harboring mutagenic Sleeping Beauty (SB) transposons were crossed with expressing SB transposase gastrointestinal tract epithelium. Most the offspring developed...

10.1126/science.1163040 article EN Science 2009-02-27

Genetic alterations in specific driver genes lead to disruption of cellular pathways and are critical events the instigation progression hepatocellular carcinoma (HCC). As a prerequisite for individualized cancer treatment, we sought characterize landscape recurrent somatic mutations HCC. We performed whole-exome sequencing on 87 HCCs matched normal adjacent tissues an average coverage 59×. The overall mutation rate was roughly two per Mb, with median 45 nonsynonymous that altered amino acid...

10.1002/hep.26540 article EN Hepatology 2013-05-31

Immune evasion is a hallmark of KRAS-driven cancers, but the underlying causes remain unresolved. Here, we use mouse model pancreatic ductal adenocarcinoma to inactivate KRAS by CRISPR-mediated genome editing. We demonstrate that at an advanced tumor stage, dependence on for growth reduced and manifested in suppression antitumor immunity. KRAS-deficient cells retain ability form tumors immunodeficient mice. However, they fail evade host immune system syngeneic wild-type mice, triggering...

10.1038/s41467-021-21736-w article EN cc-by Nature Communications 2021-03-05

Abstract The tumor microenvironment (TME) profoundly influences tumorigenesis, with gene expression in the breast TME capable of predicting clinical outcomes. is complex and includes distinct cancer-associated fibroblast (CAF) subtypes whose contribution to tumorigenesis remains unclear. Here, we identify a subset myofibroblast CAFs (myCAF) that are senescent (senCAF) mouse human tumors. Utilizing MMTV-PyMT;INK-ATTAC (INK) model, found senCAF-secreted extracellular matrix specifically limits...

10.1158/2159-8290.cd-23-0426 article EN Cancer Discovery 2024-04-29

The acidification of various ligands was measured on a cell by basis for suspensions correlated dual fluorescence flow cytometry. Mouse 3T3 cells were incubated with mixture fluorescein- and rhodamine-conjugated ligands, the ratio fluorescein rhodamine used as measure endosome pH. calibration this both fluorometry cytometry is described. Dual parameter histograms average pH per versus amount internalization calculated from data, samples in absence presence chloroquine added to neutralize...

10.1083/jcb.98.5.1757 article EN The Journal of Cell Biology 1984-05-01
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