Qi Wang

ORCID: 0000-0003-0858-9393
Publications
Citations
Views
---
Saved
---
About
Contact & Profiles
Research Areas
  • Lung Cancer Research Studies
  • Colorectal Cancer Treatments and Studies
  • Lung Cancer Treatments and Mutations
  • Cancer Mechanisms and Therapy
  • Microtubule and mitosis dynamics
  • Genetic factors in colorectal cancer
  • Chronic Lymphocytic Leukemia Research
  • interferon and immune responses
  • Cancer therapeutics and mechanisms
  • Neuroendocrine Tumor Research Advances
  • Peptidase Inhibition and Analysis
  • Phagocytosis and Immune Regulation
  • Cancer Genomics and Diagnostics
  • Cancer Immunotherapy and Biomarkers
  • RNA modifications and cancer
  • Chromatin Remodeling and Cancer
  • Computational Drug Discovery Methods
  • Advanced Breast Cancer Therapies
  • CAR-T cell therapy research
  • Immunotherapy and Immune Responses
  • Melanoma and MAPK Pathways
  • Neuroblastoma Research and Treatments
  • Cancer-related Molecular Pathways
  • Pancreatic and Hepatic Oncology Research
  • PI3K/AKT/mTOR signaling in cancer

The University of Texas MD Anderson Cancer Center
2019-2025

Harbin Medical University
2007-2025

Institute of Hematology & Blood Diseases Hospital
2019-2025

Chinese Academy of Medical Sciences & Peking Union Medical College
2019-2025

Guangzhou Medical University
2025

Shandong First Medical University
2023-2025

Tongji University
2025

Shanghai Pulmonary Hospital
2025

Xinjiang Institute of Materia Medica
2025

Xinjiang University
2025

Hepatocellular cell death and macrophage proinflammatory activation contribute to the pathology of various liver diseases, during which XBP1 plays an important role. However, function mechanism in thioacetamide (TAA)-induced acute injury (ALI) remains unknown. Here, we investigated effects inhibition on promoting hepatocellular pyroptosis activate STING signaling ALI. While both TAA- LPS-induced ALI triggered hepatocytes, hepatocyte-specific knockout mice exhibited exacerbated with increased...

10.1016/j.redox.2022.102305 article EN cc-by-nc-nd Redox Biology 2022-03-28

Molecular modifiers of KRASG12C inhibitor (KRASG12Ci) efficacy in advanced KRASG12C-mutant NSCLC are poorly defined. In a large unbiased clinicogenomic analysis 424 patients with non-small cell lung cancer (NSCLC), we identified and validated coalterations KEAP1, SMARCA4, CDKN2A as major independent determinants inferior clinical outcomes KRASG12Ci monotherapy. Collectively, comutations these three tumor suppressor genes segregated into distinct prognostic subgroups captured ∼50% those early...

10.1158/2159-8290.cd-22-1420 article EN Cancer Discovery 2023-04-17

Oxidative stress-mediated ferroptosis and macrophage-related inflammation play an important role in various liver diseases. Here, we explored if how hepatocyte regulates macrophage stimulator of interferon genes (STING) activation the development spontaneous damage, fibrosis, tumorigenesis.We used a transforming growth factor-beta-activated kinase 1 (TAK1) deficiency-induced model tumorigenesis to investigate its impact on STING signalling. Primary hepatocytes macrophages were for vitro...

10.1016/j.jhepr.2023.100695 article EN cc-by-nc-nd JHEP Reports 2023-02-03

Small cell lung cancer (SCLC) is an aggressive malignancy composed of distinct transcriptional subtypes, but implementing subtyping in the clinic has remained challenging, particularly due to limited tissue availability. Given known epigenetic regulation critical SCLC programs, we hypothesized that subtype-specific patterns DNA methylation could be detected tumor or blood from patients. Using genomic-wide reduced-representation bisulfite sequencing (RRBS) two cohorts totaling 179 patients...

10.1016/j.ccell.2024.01.001 article EN cc-by-nc-nd Cancer Cell 2024-01-25

Abstract Inactivating TP53 mutations leads to a loss of function p53, but can also often result in oncogenic gain-of-function (GOF) mutant p53 (mutp53) proteins which promotes tumor development and progression. The GOF activities are well documented, the mechanisms involved remain poorly understood. Here, we study mutp53 interactome find that by targeting minichromosome maintenance complex components (MCMs), predisposes cells replication stress chromosomal instability (CIN), leading...

10.1038/s41467-023-44239-2 article EN cc-by Nature Communications 2024-01-02

IntroductionThe combination of programmed cell death protein-1 or death-ligand 1 immune checkpoint blockade and chemotherapy has revolutionized the treatment advanced NSCLC, but mechanisms underlying this synergy remain incompletely understood. In study, we explored relationships between neoadjuvant microenvironment (IME) resectable NSCLC to identify novel by which may enhance effect blockade.MethodsGenomic, transcriptomic, profiling data 511 patients treated with followed surgery (NCT)...

10.1016/j.jtho.2020.09.027 article EN cc-by-nc-nd Journal of Thoracic Oncology 2020-10-21

Background: Prostate cancer is usually considered as immune "cold" tumor with poor immunogenic response and low density of tumor-infiltrating cells, highlighting the need to explore clinically actionable strategies sensitize prostate immunotherapy.In this study, we investigated whether docetaxel-based chemohormonal therapy induces immunologic changes potentiates checkpoint blockade immunotherapy in cancer.Methods: We performed transcriptome histopathology analysis characterize...

10.7150/thno.73152 article EN cc-by Theranostics 2022-01-01

Methylthioadenosine phosphorylase, an essential enzyme for the adenine salvage pathway, is often deficient (MTAPdef) in tumors with 9p21 loss and hypothetically renders susceptible to synthetic lethality by antifolates targeting de novo purine synthesis. Here we report our single arm phase II trial (NCT02693717) that assesses pemetrexed MTAPdef urothelial carcinoma (UC) primary endpoint of overall response rate (ORR). Three 7 enrolled patients show (ORR 43%). Furthermore, a historic cohort...

10.1038/s41467-022-29397-z article EN cc-by Nature Communications 2022-04-04

Abstract Mitochondria are hubs where bioenergetics, redox homeostasis, and anabolic metabolism pathways integrate through a tightly coordinated flux of metabolites. The contributions mitochondrial to tumor growth therapy resistance evident, but drugs targeting have repeatedly failed in the clinic. Our study pancreatic ductal adenocarcinoma (PDAC) finds that cellular lipid composition influence cancer cell sensitivity pharmacological inhibition electron transport chain complex I. Profiling...

10.1038/s41467-023-37924-9 article EN cc-by Nature Communications 2023-04-17

Abstract Large granular lymphocytic leukemia (LGLL) is characterized by the clonal proliferation of cytotoxic T lymphocytes or NK cells. Standard first-line immunosuppressive treatments have limitations, achieving complete remission (CR) rates up to 50%. Immune system dysregulation implicated in LGLL. Promising results for thalidomide, an immunomodulatory drug, combined with prednisone and methotrexate (TPM), were observed our pilot study. This multicenter study evaluated efficacy safety a...

10.1038/s41392-025-02164-4 article EN cc-by Signal Transduction and Targeted Therapy 2025-03-12

Abstract Background With concerns about the disastrous health and economic consequences caused by influenza pandemic, comprehensively understanding global host response to virus infection is urgent. The role of microRNA (miRNA) has recently been highlighted in pathogen-host interactions. However, precise miRNAs pathogenesis humans, especially critically ill patients still unclear. Methods We identified cellular involved performing comprehensive miRNA profiling peripheral blood mononuclear...

10.1186/1471-2334-13-257 article EN cc-by BMC Infectious Diseases 2013-06-03

Abstract AXL, a TAM (TYRO3, and MERTK) family receptor tyrosine kinase, is increasingly being recognized as key determinant of resistance to targeted therapies, well chemotherapy radiation in non–small cell lung cancer (NSCLC) other cancers. We further show here that high levels AXL epithelial-to-mesenchymal transition were frequently expressed subsets both treatment-naïve treatment-relapsed NSCLC. Previously, we others have demonstrated role for mediating DNA damage response (DDR),...

10.1158/1541-7786.mcr-20-0414 article EN Molecular Cancer Research 2020-11-10

The transcription factor MYC is overexpressed in 30% of small cell lung cancer (SCLC) tumors and known to modulate the balance between two major pathways metabolism: glycolysis mitochondrial respiration. This duality underscores importance further investigation into its role SCLC metabolism could lead insights metabolic targeting approaches.We investigated differences transcriptional metabolomics datasets based on cMYC expression patient line samples. Metabolic pathway utilization was...

10.1186/s40170-021-00270-9 article EN cc-by Cancer & Metabolism 2021-09-23

Abstract Small-cell lung cancer (SCLC) is speculated to harbor complex genomic intratumor heterogeneity (ITH) associated with high recurrence rate and suboptimal response immunotherapy. Here, using multi-region whole exome/T cell receptor (TCR) sequencing as well immunohistochemistry, we reveal a rather homogeneous mutational landscape but extremely cold heterogeneous TCR repertoire in limited-stage SCLC tumors (LS-SCLCs). Compared localized non-small cancers, LS-SCLCs have similar predicted...

10.1038/s41467-021-26821-8 article EN cc-by Nature Communications 2021-11-17

COVID-19 is an infectious disease caused by SARS-CoV-2, which enters host cells via the cell surface proteins ACE2 and TMPRSS2. Using a variety of normal malignant models tissues from aerodigestive respiratory tracts, we investigated expression regulation

10.1101/2020.05.28.122291 preprint EN cc-by-nc-nd bioRxiv (Cold Spring Harbor Laboratory) 2020-05-29

Abstract Purpose: Therapeutic resistance to frontline therapy develops rapidly in small cell lung cancer (SCLC). Treatment options are also limited by the lack of targetable driver mutations. Therefore, there is an unmet need for developing better therapeutic strategies and biomarkers response. Aurora kinase B (AURKB) inhibition exploits inherent genomic vulnerability SCLC a promising approach. Here, we identify response develop rational combinations with AURKB improve treatment efficacy....

10.1158/1078-0432.ccr-23-0375 article EN Clinical Cancer Research 2023-06-08
Coming Soon ...