2020
mTOR inhibition overcomes primary and acquired resistance to Wee1 inhibition by augmenting replication stress in epithelial ovarian cancers.
Li F, Guo E, Huang J, Lu F, Yang B, Xiao R, Liu C, Wu X, Fu Y, Wang Z, Peng S, Lei Y, Guo Z, Li L, Xi L, Sun C, Liu S, Chen G. mTOR inhibition overcomes primary and acquired resistance to Wee1 inhibition by augmenting replication stress in epithelial ovarian cancers. American Journal Of Cancer Research 2020, 10: 908-924. PMID: 32266099, PMCID: PMC7136919.Peer-Reviewed Original ResearchEpithelial ovarian cancerOvarian cancerReplication stressWEE1 inhibitorSynergistically inhibited tumor growthOvarian cancer cell linesCombination of Wee1Patient-derived xenograftsDNA replication stressHeterogeneity of patient tumorsOvarian cancer cellsActivated mTOR pathwaySubstrate dNTPCheckpoint deficiencyTP53 mutationsCancer cell linesPatient tumorsClinical efficacyFork stallingTumor growthCell cycleTherapeutic windowDrug combinationsWEE1 inhibitionG2/M checkpoint
2014
The combination of HTATIP2 expression and microvessel density predicts converse survival of hepatocellular carcinoma with or without sorafenib
Wang W, Liu L, Xu H, Sun H, Wu C, Zhu X, Zhang W, Xu J, Liu C, Long J, Ni Q, Tang Z, Yu X. The combination of HTATIP2 expression and microvessel density predicts converse survival of hepatocellular carcinoma with or without sorafenib. Oncotarget 2014, 5: 3895-3906. PMID: 25008315, PMCID: PMC4116529, DOI: 10.18632/oncotarget.2019.Peer-Reviewed Original ResearchConceptsSurvival of hepatocellular carcinomaMicrovessel densityHepatocellular carcinomaSorafenib treatmentDissemination of hepatocellular carcinomaAssociated with inhibition of angiogenesisAdvanced hepatocellular carcinomaMicrovessel density valuesCurative HCC resectionSuppressor of tumor growthInhibition of angiogenesisNegative prognostic indicatorAssociated with inhibitionSorafenib interventionHCC resectionSorafenib administrationOverall survivalDisease recurrencePrognostic factorsTissue microarrayPrognostic indicatorTumor growthSorafenibPersonalized treatmentPredictive value
2012
OPA1 downregulation is involved in sorafenib-induced apoptosis in hepatocellular carcinoma
Zhao X, Tian C, Puszyk W, Ogunwobi O, Cao M, Wang T, Cabrera R, Nelson D, Liu C. OPA1 downregulation is involved in sorafenib-induced apoptosis in hepatocellular carcinoma. Laboratory Investigation 2012, 93: 8-19. PMID: 23108376, PMCID: PMC3860369, DOI: 10.1038/labinvest.2012.144.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisCarcinoma, HepatocellularCell Line, TumorCytochromes cDown-RegulationGene Knockdown TechniquesGTP PhosphohydrolasesHumansLiverLiver NeoplasmsMiceMice, SCIDMitochondriaNiacinamidePhenylurea CompoundsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRaf KinasesRas ProteinsRNA, Small InterferingSignal TransductionSorafenibXenograft Model Antitumor AssaysConceptsHepatocellular carcinomaSorafenib-induced apoptosisHCC xenograft tumor growthOptic atrophy 1HCC cellsPatients' hepatocellular carcinomaNon-tumor tissue samplesAdvanced hepatocellular carcinomaPathogenesis of HCCNovel therapeutic targetTumorigenesis of HCCXenograft tumor growthTumor tissue analysisNormal human primary hepatocytesHuman primary hepatocytesCell growth inhibitionSorafenib treatmentHCC patientsTherapeutic targetExposure of cellsTumor growthMitochondrial injuryPatientsSorafenibOPA1 expression
2010
Inhibition of Neovascularization to Simultaneously Ameliorate Graft-vs-Host Disease and Decrease Tumor Growth
Penack O, Henke E, Suh D, King C, Smith O, Na I, Holland A, Ghosh A, Lu S, Jenq R, Liu C, Murphy G, Lu T, May C, Scheinberg D, Gao D, Mittal V, Heller G, Benezra R, van den Brink M. Inhibition of Neovascularization to Simultaneously Ameliorate Graft-vs-Host Disease and Decrease Tumor Growth. Journal Of The National Cancer Institute 2010, 102: 894-908. PMID: 20463307, PMCID: PMC2886094, DOI: 10.1093/jnci/djq172.Peer-Reviewed Original ResearchMeSH KeywordsAngiogenesis InhibitorsAnimalsAntibodies, MonoclonalAntigens, CDBone Marrow TransplantationCadherinsFemaleFlow CytometryFluorescent Antibody TechniqueGraft vs Host DiseaseHematopoietic Stem Cell TransplantationMiceMice, Inbred C57BLNeoplasmsNeovascularization, PathologicTransplantation, HomologousConceptsTumor growthAllo-BMTHost diseaseAllogeneic hematopoietic stem cell transplantationHematopoietic stem cell transplantationEndothelial cellsAllo-BMT recipientsGVHD target tissuesAllogeneic BM transplantationStem cell transplantationEndothelial progenitor cellsDecreases tumor growthInhibition of neovascularizationTumor-bearing miceTissue endothelial cellsAmeliorate graftDonor BMBM transplantationCell transplantationGVHDBone marrowTherapeutic targetingNeovascularizationOverall outcomeTumor vasculature
2009
Depletion of Vascular Endothelial Progenitor Cells Simultaneously Ameliorates GVHD and Inhibits Tumor Growth
Penack O, Henke E, Suh D, King C, Smith M, Na I, Holland A, Ghosh A, Lu S, Jenq R, Liu C, May C, Murphy G, Lu T, Gao D, Mittal V, Benezra R, van den Brink M. Depletion of Vascular Endothelial Progenitor Cells Simultaneously Ameliorates GVHD and Inhibits Tumor Growth. Transplantation And Cellular Therapy 2009, 15: 1. DOI: 10.1016/j.bbmt.2008.12.007.Peer-Reviewed Original Research
2008
Depletion of Vascular Endothelial Progenitor Cells Inhibits Inflammation
Penack O, Henke E, Suh D, King C, Smith M, Na I, Holland A, Ghosh A, Lu S, Jenq R, Liu C, Murphy G, Lu T, May C, Scheinberg D, Gao D, Mittal V, Benezra R, Van Den Brink M. Depletion of Vascular Endothelial Progenitor Cells Inhibits Inflammation. Blood 2008, 112: 694. DOI: 10.1182/blood.v112.11.694.694.Peer-Reviewed Original ResearchDepletion of EPCsAllo-BMT recipientsEndothelial progenitor cellsDonor T cellsRole of EPCsDay of BMTGVHD target organsDonor BM cellsAllo-BMTT cellsTumor growthImproved survivalA20 lymphomaInflamed colonPeripheral bloodEndothelial cellsInflammatory diseasesBM cellsTarget organsBM-derived endothelial progenitor cellsAllogeneic hematopoietic stem cell transplantationDay 0Donor endothelial progenitor cellsAllogeneic bone marrow transplantationBALB/c recipients