Robert M. Gemmill

ORCID: 0000-0003-0747-5984
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About
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Research Areas
  • Angiogenesis and VEGF in Cancer
  • Axon Guidance and Neuronal Signaling
  • Genomic variations and chromosomal abnormalities
  • RNA modifications and cancer
  • Cancer, Hypoxia, and Metabolism
  • Cancer-related gene regulation
  • Genetics and Neurodevelopmental Disorders
  • Epigenetics and DNA Methylation
  • Renal and related cancers
  • Cancer-related Molecular Pathways
  • Cancer Genomics and Diagnostics
  • PI3K/AKT/mTOR signaling in cancer
  • Bacterial Genetics and Biotechnology
  • Genomics and Chromatin Dynamics
  • Chromosomal and Genetic Variations
  • Chromatin Remodeling and Cancer
  • Lung Cancer Treatments and Mutations
  • RNA Research and Splicing
  • Ubiquitin and proteasome pathways
  • Bacteriophages and microbial interactions
  • Cancer Cells and Metastasis
  • Histone Deacetylase Inhibitors Research
  • Wnt/β-catenin signaling in development and cancer
  • Hedgehog Signaling Pathway Studies
  • Sarcoma Diagnosis and Treatment

Medical University of South Carolina
2013-2024

MUSC Hollings Cancer Center
2009-2024

University of Colorado Health
1999-2023

University of Colorado Anschutz Medical Campus
1991-2023

University of Charleston
2010-2017

Ralph H. Johnson VA Medical Center
2017

Palmetto Hematology Oncology
2017

University of Colorado Denver
1998-2013

The Ohio State University
2013

University of South Carolina
2011

The epidermal growth factor receptor (EGFR) is overexpressed in the majority of non-small cell lung cancers (NSCLC). EGFR tyrosine kinase inhibitors, such as gefitinib and erlotinib, produce 9% to 27% response rates NSCLC patients. E-Cadherin, a calcium-dependent adhesion molecule, plays an important role prognosis progression, interacts with EGFR. zinc finger transcriptional repressor, ZEB1, inhibits E-cadherin expression by recruiting histone deacetylases (HDAC). We identified significant...

10.1158/0008-5472.can-05-1988 article EN Cancer Research 2006-01-15

Elevated tumor cyclooxygenase-2 (COX-2) expression is associated with invasion, metastasis, and poor prognosis in non-small cell lung cancer (NSCLC). Here, we report that COX-2-dependent pathways contribute to the modulation of E-cadherin NSCLC. First, whereas genetically modified COX-2-sense (COX-2-S) NSCLC cells expressed low showed diminished capacity for cellular aggregation, genetic or pharmacologic inhibition COX-2 led increased resulted augmented homotypic aggregation among vitro. An...

10.1158/0008-5472.can-05-3635 article EN Cancer Research 2006-05-15

PURPOSE: E-cadherin (E-cad) and its associated intracellular molecules, catenins, are critical for intercellular epithelial adhesion often expressed in non–small-cell lung carcinomas (NSCLCs). We constructed tissue microarrays (TMAs) to investigate the expression of cadherins catenins their prognostic significance NSCLC. PATIENTS AND METHODS: Tumor samples from 193 patients with stages I III NSCLC were obtained University Colorado Cancer Center Johns Hopkins Medical Institutions. Viable...

10.1200/jco.2002.08.159 article EN Journal of Clinical Oncology 2002-05-15

The US2 and US11 gene products of human cytomegalovirus promote viral evasion by hijacking the endoplasmic reticulum (ER)-associated degradation (ERAD) pathway. initiate dislocation newly translocated major histocompatibility complex class I (MHC I) from ER to cytosol for proteasome-mediated degradation, thereby decreasing cell surface MHC I. Despite being instrumental in elucidating mammalian ERAD pathway, responsible E3 ligase or ligases remain unknown. Using a functional small interfering...

10.1083/jcb.200906110 article EN cc-by-nc-sa The Journal of Cell Biology 2009-08-31

Epithelial-mesenchymal transition (EMT) is one mechanism of acquired resistance to inhibitors the epidermal growth factor receptor-tyrosine kinases (EGFR-TKIs) in non-small cell lung cancer (NSCLC). The precise mechanisms EMT-related EGFR-TKIs NSCLC remain unclear. We generated erlotinib-resistant HCC4006 cells (HCC4006ER) by chronic exposure EGFR-mutant increasing concentrations erlotinib. HCC4006ER an EMT phenotype and activation TGF-β/SMAD pathway, while lacking both T790M secondary EGFR...

10.1371/journal.pone.0147344 article EN cc-by PLoS ONE 2016-01-20

HOX genes encode transcription factors that control patterning and cell fates. Alterations in expression have been clearly implicated leukemia, but their role most other malignant diseases remains unknown. By using degenerate reverse transcription-PCR subsequent real-time quantitative assays, we examined lung cancer lines, direct tumor-control pairs, bronchial epithelial cultures. As of the HOX9 paralogous group HOXA10 were frequently overexpressed. For HOXB9, confirmed elevated RNA was...

10.1073/pnas.97.23.12776 article EN Proceedings of the National Academy of Sciences 2000-11-07

E-cadherin loss in cancer is associated with de-differentiation, invasion, and metastasis. Drosophila DE-cadherin regulated by Wnt/β-catenin signaling, although this has not been demonstrated mammalian cells. We previously reported that expression of WNT7a, encoded on 3p25, was frequently downregulated lung cancer, or β-catenin a poor prognostic feature. Here we show WNT7a both activates via specific mechanism cells involved positive feedback loop. Li + , GSK3β inhibitor, led to induction an...

10.1073/pnas.1734137100 article EN Proceedings of the National Academy of Sciences 2003-08-22

The 3;8 chromosomal translocation, t(3;8)(p14.2;q24.1), was described in a family with classical features of hereditary renal cell carcinoma. Previous studies demonstrated that the 3p14.2 breakpoint interrupts fragile histidine triad gene ( FHIT) its 5′ noncoding region. However, evidence FHIT is causally related to or other malignancies controversial. We now show 8q24.1 region encodes 664-aa multiple membrane spanning protein, TRC8, similarity basal carcinoma/segment polarity gene, patched...

10.1073/pnas.95.16.9572 article EN Proceedings of the National Academy of Sciences 1998-08-04

Beta-catenin forms complexes with Tcf and Lef-1 functions as a transcriptional activator in the Wnt signalling pathway. Although recent investigations have been focused on role of adenomatous polyposis coli (APC)/ beta-catenin/Tcf pathway human tumorigenesis, there very few reports mutations beta-catenin gene variety tumour types. Using PCR single-strand conformational polymorphism analysis, we examined 93 lung, 9 breast, 6 kidney, 19 cervical 7 ovarian carcinoma cell lines for exon 3 gene....

10.1054/bjoc.2001.1863 article EN cc-by-nc-sa British Journal of Cancer 2001-07-01

Loss of heterozygosity (LOH) involving 3p occurs in many carcinomas but is complicated by the identification four distinct homozygous deletion regions. One putative target, 3p14.2, contains common fragile site, FRA3B, a hereditary renal carcinoma-associated 3;8 translocation and candidate tumor suppressor gene, FHIT. Using approximately 300 kb comsid/lambda contig, we identified deletions cervix, breast, lung colorectal carcinoma cell lines. The smallest (CC19) was shown not to involve FHIT...

10.1093/hmg/6.2.193 article EN Human Molecular Genetics 1997-02-01

The nucleotide sequence of the control region leu operon Salmonella typhimurium was determined. A prominent feature this is a signal for termination transcription. In vitro, transcription does terminate at site, yielding leader RNA about 160 nucleotides as major product. This potentially translatable into peptide containing 28 amino acids, 4 which are adjacent leucine residues. Several regions base complementarity exist within leader, positioned such that pairing one precludes another....

10.1073/pnas.76.10.4941 article EN Proceedings of the National Academy of Sciences 1979-10-01

We report that CD47 was upregulated in different EMT-activated human breast cancer cells versus epithelial MCF7 cells. Overexpression of SNAI1 or ZEB1 activated EMT and while siRNA-mediated targeting mesenchymal MDA-MB-231 reversed strongly decreased CD47. Mechanistically, by binding directly to E-boxes the promoter. TCGA METABRIC data sets from patients revealed correlated with Vimentin. At functional level, were less efficiently phagocytosed macrophages vs. The phagocytosis rescued using...

10.1080/2162402x.2017.1345415 article EN OncoImmunology 2017-07-05

Abstract Background The etiology of hemangiosarcoma remains incompletely understood. Its common occurrence in dogs suggests predisposing factors favor its development this species. These could represent a constellation heritable characteristics that promote transformation events and/or facilitate the establishment microenvironment is conducive for survival malignant blood vessel-forming cells. hypothesis study was characteristic molecular features distinguish from non-malignant endothelial...

10.1186/1471-2407-10-619 article EN cc-by BMC Cancer 2010-11-09

Abstract Loss of SEMA3F occurs frequently in lung cancer and correlates with advanced stage disease. We previously reported that blocked tumor formation by H157 cells a rat orthotopic model. This was associated loss activated αVβ3 integrin, impaired cell adhesion to extracellular matrix components, down-regulation phospho-extracellular signal-regulated kinase 1/2 (ERK1/2). These results suggested might interfere integrin outside-in signaling. In the present report, we found decreased...

10.1158/0008-5472.can-06-3612 article EN Cancer Research 2007-09-15

The epithelial to mesenchymal transition (EMT) enables cells with a migratory phenotype. It is activated in cancer and involved invasion, metastasis stem-like properties. ZEB1, an E-box binding transcription factor, major suppressor of genes lung cancer. In the present study, we show that H358 non-small cell cells, ZEB1 downregulates EpCAM (coding for adhesion molecule), ESRP1 (epithelial splicing regulatory protein), ST14 (a membrane associated serine protease HGF processing) RAB25 small...

10.3390/cancers5020334 article EN Cancers 2013-04-03
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