Tenghui Chen

ORCID: 0000-0003-0683-8974
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About
Contact & Profiles
Research Areas
  • Cancer Genomics and Diagnostics
  • Chronic Lymphocytic Leukemia Research
  • Genomics and Rare Diseases
  • Immune Response and Inflammation
  • Bioactive Compounds and Antitumor Agents
  • Genomics and Phylogenetic Studies
  • Estrogen and related hormone effects
  • Gene expression and cancer classification
  • PI3K/AKT/mTOR signaling in cancer
  • Bioinformatics and Genomic Networks
  • Ubiquitin and proteasome pathways
  • NF-κB Signaling Pathways
  • Advanced Breast Cancer Therapies
  • Nutrition, Genetics, and Disease
  • Immune cells in cancer
  • RNA modifications and cancer
  • Lung Cancer Treatments and Mutations
  • Cancer Immunotherapy and Biomarkers
  • Genetics, Bioinformatics, and Biomedical Research
  • CAR-T cell therapy research
  • Genetic Associations and Epidemiology
  • Wnt/β-catenin signaling in development and cancer
  • Ferroptosis and cancer prognosis
  • Nuclear Receptors and Signaling
  • Morinda citrifolia extract uses

Shenzhen University
2022

The University of Texas MD Anderson Cancer Center
2014-2019

Xiamen University
2010-2014

The Ohio State University
2012

Large-scale sequencing efforts are uncovering the complexity of cancer genomes, which composed causal "driver" mutations that promote tumor progression along with many more pathologically neutral "passenger" events. The majority mutations, both in known drivers and uncharacterized genes, generally low occurrence, highlighting need to functionally annotate long tail infrequent present heterogeneous cancers. Here we describe a mutation assessment pipeline enabled by high-throughput engineering...

10.1158/0008-5472.can-15-1654 article EN Cancer Research 2015-12-02

Further advances of targeted cancer therapy require comprehensive in-depth profiling somatic mutations that are present in subpopulations tumor cells a clinical sample. However, it is unclear to what extent such intratumor heterogeneity and whether may affect decision-making. To study this question, we established deep sequencing platform identify potentially actionable DNA alterations samples.We assayed 515 formalin-fixed paraffin-embedded (FFPE) samples matched germline (475 patients) from...

10.1373/clinchem.2014.231100 article EN Clinical Chemistry 2015-01-27

Lung cancer remains the leading cause of death. Genome sequencing lung tumors from patients with squamous cell carcinoma has identified SMAD4 to be frequently mutated. Here, we use a mouse model determine molecular mechanisms by which Smad4 loss leads progression. Mice ablation Pten and in airway epithelium develop metastatic adenosquamous tumors. Comparative transcriptomic vivo cistromic analyses that PTEN results ELF3 ErbB2 pathway activation due decreased expression ERRFI1, negative...

10.1016/j.celrep.2015.02.014 article EN cc-by-nc-nd Cell Reports 2015-03-01

Here we report that mice deficient for the proteasome activator, REGγ, exhibit a marked resistance to TPA (12-O-tetradecanoyl-phorbol-13-acetate)-induced keratinocyte proliferation, epidermal hyperplasia and onset of papillomas compared with wild-type counterparts. Interestingly, massive increase REGγ in skin tissues or cells resulting from induces activation p38 mitogen-activated protein kinase (MAPK/p38). Blocking MAPK prevents elevation HaCaT treatment. AP-1, downstream effector MAPK/p38,...

10.1038/ncomms7875 article EN cc-by Nature Communications 2015-04-24

Identifying subclonal mutations and their implications requires accurate estimation of mutant allele fractions from possibly duplicated sequencing reads. Removing duplicate reads assumes that polymerase chain reaction amplification library constructions is the primary source. The alternative-sampling coincidence DNA fragmentation-has not been systematically investigated.With sufficiently high-sequencing depth, sampling-induced read duplication non-negligible, removing can overcorrect counts,...

10.1093/bioinformatics/btt771 article EN Bioinformatics 2014-01-02

// Ka Bian 2 , Naveen Reddy Muppani 1 Lobna Elkhadragy Wei Wang 3 Cheng Zhang Tenghui Chen 4 Sungyun Jung Ole Morten Seternes 5 and Weiwen Long 1,2 Department of Biochemistry Molecular Biology, Wright State University, Dayton, OH, USA Otorhinolaryngology, Tangdu Hospital, The Fourth Military Medical Xi'an, China Cellular Baylor College Medicine, Houston, TX, Bioinformatics Computational University Texas MD Anderson Cancer Center, Pharmacy, Tromsoe, N-Tromsoe, Norway Correspondence to: Long,...

10.18632/oncotarget.6682 article EN Oncotarget 2015-12-19

An important step towards personalizing cancer treatment is to integrate heterogeneous evidences catalog mutational hotspots that are biologically and therapeutically relevant thus represent where targeted therapy would likely be beneficial. However, existing methods do not sufficiently delineate varying functionality of individual mutations within the same genes. We observed a large discordancy mutation rates across different subtypes tumor types, nominated 702 hotspot in 549 genes Catalog...

10.1186/s12864-016-2727-x article EN cc-by BMC Genomics 2016-06-01

Identification of cancer driver mutations is critical for advancing research and personalized medicine. Due to inter-tumor genetic heterogeneity, many occur at low frequencies, which make it challenging distinguish them from passenger mutations. Here, we show that a novel Bayesian hierarchical modeling approach, named rDriver can achieve enhanced prediction accuracy by identifying not only have high functional impact scores but also are associated with systemic variation in gene expression...

10.1371/journal.pone.0196939 article EN cc-by PLoS ONE 2018-05-08

Steroid receptor coactivator 3 (SRC-3) is a multifunctional protein that plays an important role in regulation of bacterial LPS-induced inflammation. However, its involvement host defense against infection remains unclear. In this study, we used SRC-3 knockout mice to assess the antibacterial Escherichia coli-induced septic peritonitis. After E. coli bacteria were injected i.p., SRC-3-deficient exhibited excessive local and systemic inflammatory responses more severe burdens, leading...

10.4049/jimmunol.0903802 article EN The Journal of Immunology 2010-09-30

10.1016/j.cels.2017.09.004 article EN publisher-specific-oa Cell Systems 2017-10-10

Mycoepoxydiene (MED) is a polyketide isolated from marine fungus associated with mangrove forests. MED has been shown to be able induce cell cycle arrest and cancer apoptosis. However, its effects on inflammatory response are unclear. Herein we showed that exhibited inhibitory effect induced by lipopolysaccharide (LPS). significantly inhibited LPS-induced expression of pro-inflammatory mediators such as tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, IL-6, nitric oxide (NO) in...

10.1371/journal.pone.0044890 article EN cc-by PLoS ONE 2012-09-11

Abstract It has been reported that the proteasome activator REG γ is associated with multiple oncogenic pathways in human cancers. However, role of development melanoma and underlying mechanisms remain unclear. In this study, we attempted to investigate effects on cell proliferation vitro vivo. We demonstrated knockdown inhibited growth arrested at G1 phase. Furthermore, depletion also xenograft melanoma. Mechanistically, activates Wnt/β‐catenin signal pathway by degrading GSK ‐3β lines...

10.1111/exd.13394 article EN Experimental Dermatology 2017-06-12

Mycoepoxydiene (MED) is a polyketide isolated from marine fungus associated with mangrove forests.MED has been shown to be able induce cell cycle arrest and cancer apoptosis.However, its effects on inflammatory response are unclear.Herein we showed that MED exhibited inhibitory effect induced by lipopolysaccharide (LPS).MED significantly inhibited LPS-induced expression of pro-inflammatory mediators such as tumor necrosis factora (TNF-a), interleukin (IL)-1b, IL-6, nitric oxide (NO) in...

10.1371/annotation/9a2fb76a-b2c3-43b4-a0b1-e8ae773378b7 article EN cc-by PLoS ONE 2012-11-01

Abstract Background: Immune checkpoint blockade including anti-CTLA-4 (ipilimumab, BMS) and anti-PD1 (nivolumab, as monotherapies have been known to clinical activity against metastatic renal cell carcinoma (MRCC), but with relatively low response rate (10-25%). Anti-VEGF antibody bevacizumab is a standard therapy for MRCC also (<20%). Since use distinct mechanisms T activation can promote the function of antigen presenting cells, we hypothesize that combination nivolumab + or...

10.1158/1538-7445.am2017-ct083 article EN Cancer Research 2017-07-01

3574 Background: A limited understanding of the immune microenvironment mismatch repair-proficient metastatic colorectal cancer (mCRC) impedes efforts to develop effective immunotherapy treatments for majority CRC patients. Liver disease is common and associated with poor outcomes. While T-cell infiltration liver metastases positively correlates survival, most mCRC patients do not benefit from checkpoint-blockade therapy. Tissue macrophages (TAMs) have been an suppressive environment, but...

10.1200/jco.2017.35.15_suppl.3574 article EN Journal of Clinical Oncology 2017-05-20

Abstract Background Cancer therapy is challenged by diverse molecular implementations of oncogenic processes and variations in therapeutic responses. So far, whole genome sequencing (WGS) exome (WES) has been implemented both research clinical settings to identify events cancer genomes. However, a large number passenger mutations have identified true driver disguised. Distinguishing “driver” from “passenger” will be key challenge for the realization targeted therapy. To elucidate that are...

10.1158/1538-7445.am2014-4275 article EN Cancer Research 2014-10-01
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