2024
Uterine teratoma and the role of short-tandem repeat genotyping in understanding origins
AlAshqar A, Maruthi V, Abi-Raad R, Greenman M, Hui P, Ratner E, Altwerger G, Santin A, Andikyan V. Uterine teratoma and the role of short-tandem repeat genotyping in understanding origins. Gynecologic Oncology Reports 2024, 56: 101652. PMID: 39698441, PMCID: PMC11652878, DOI: 10.1016/j.gore.2024.101652.Peer-Reviewed Case Reports and Technical NotesUterine teratomaPluripotent stem cellsMolecular testingRare tumorLimitations of diagnostic imagingHistory of vaginal bleedingShort tandem repeat genotypingStem cellsAdvanced molecular testingRepeat genotypingFallopian tube tissueGerm cell layersLoss of heterozygosityFour-week historyVaginal bleedingSurgical resectionOvarian counterpartRare entityUterine massPrimiparous womenEndometrial samplesFetal tissuesTeratomaPresence of tissueDiploid karyotypeInitial data from a phase 1, first-in-human clinical trial for T-Plex, a multiplexed, enhanced T cell receptor-engineered T cell therapy (TCR-T) for solid tumors.
Thomas S, Pico B, Henick B, Leidner R, Samhouri Y, Isaacs J, Weiss J, Hurwitz M, Grewal J, Luke J, Chattopadhyay S, Wang Y, Motta M, Murray J, Barton D, Pinchasik D, MacBeath G, Moser J. Initial data from a phase 1, first-in-human clinical trial for T-Plex, a multiplexed, enhanced T cell receptor-engineered T cell therapy (TCR-T) for solid tumors. Journal Of Clinical Oncology 2024, 42: 2542-2542. DOI: 10.1200/jco.2024.42.16_suppl.2542.Peer-Reviewed Original ResearchT-cell receptor-engineered T-cell therapyLoss of heterozygositySolid tumorsHLA-A*02:01HLA matchingHLA allelesPatients evaluated to dateFirst-in-human clinical trialDose level 1Dose level 3Pre-identify patientsTarget HLA alleleAntitumor T cellsT-cell therapyLoss of heterozygosity testingT-cell attackMaster protocolProportion of patientsScreening protocolCombination of HLAHLA LOHHLA lossImmunosuppressive microenvironmentMAGE-A1HLA typingPersistent Cutaneous Lesions of Darier Disease and Second-Hit Somatic Variants in ATP2A2 Gene
Atzmony L, Zagairy F, Mawassi B, Shehade M, Tatour Y, Danial-Farran N, Khayat M, Warrour N, Dodiuk-Gad R, Cohen-Barak E. Persistent Cutaneous Lesions of Darier Disease and Second-Hit Somatic Variants in ATP2A2 Gene. JAMA Dermatology 2024, 160: 518-524. PMID: 38536168, PMCID: PMC10974685, DOI: 10.1001/jamadermatol.2024.0152.Peer-Reviewed Original ResearchConceptsSomatic variantsATP2A2 geneDeep sequencingResponse to environmental factorsCopy number variantsRestriction fragment length polymorphismLoss of heterozygosityWhole-exome sequencingChromosomal microarray analysisDarier's diseaseFragment length polymorphismPaired whole exome sequencingPathogenic germline variantsHeterozygous pathogenic germline variantsDD lesionsGenomic characteristicsGenetic analysisGenetic skin disordersGermline variantsSanger sequencingLength polymorphismSkin lesionsTransient lesionsHeterozygous variantsMicroarray analysisPreclinical efficacy of RAF/MEK clamp avutometinib in combination with FAK inhibition in low grade serous ovarian cancer
McNamara B, Demirkiran C, Hartwich T, Bellone S, Manavella D, Mutlu L, Greenman M, Zipponi M, Yang-Hartwich Y, Yang K, Ratner E, Schwartz P, Coma S, Pachter J, Santin A. Preclinical efficacy of RAF/MEK clamp avutometinib in combination with FAK inhibition in low grade serous ovarian cancer. Gynecologic Oncology 2024, 183: 133-140. PMID: 38493021, DOI: 10.1016/j.ygyno.2024.01.028.Peer-Reviewed Original ResearchLow grade serous ovarian carcinomaWhole-exome-sequencingGain-of-function mutationsVS-4718Preclinical efficacyLow grade serous ovarian cancerSerous ovarian cancerControl-treated miceTumor growth inhibitionWild-type KRASLoss of heterozygosityDecreased p-ERKRAF/MEK inhibitionMedian survivalOvarian cancerRecurrence rateTherapeutic optionsOral gavageTumor growthTumor samplesIn vivo activityMAPK pathway genesRAF/MEK inhibitorsP-ERKEx vivo
2023
TP53 mutations and Their Impact on Survival in Patients with Myeloproliferative Neoplasms
Rolles B, De Oliveira Filho C, Keating J, Luskin M, DeAngelo D, Lindsley C, Kim A, Hem J, Kim C, Weeks L, Wazir M, How J, Marneth A, Liu Y, Aryee M, Tsai H, Stahl M, Mullally A. TP53 mutations and Their Impact on Survival in Patients with Myeloproliferative Neoplasms. Blood 2023, 142: 3160. DOI: 10.1182/blood-2023-185024.Peer-Reviewed Original ResearchMyeloproliferative neoplasms diagnosisLoss of heterozygosityVariant allele fractionTP53 mutation detectionSecondary AMLTP53 mutationsMyeloproliferative neoplasm subtypeMyeloproliferative neoplasm patientsMyeloproliferative neoplasmsOverall survivalEssential thrombocythemiaCourse of diseasePolycythemia veraDriver mutationsBlast phase myeloproliferative neoplasmsChronic phase myeloproliferative neoplasmsContext of myeloproliferative neoplasmsMyeloproliferative neoplasm driver mutationsNext-generation sequencingDetect TP53 mutationsDiagnosis to detectionPost-ET/PV myelofibrosisTP53-mutant patientsTP53-mutated patientsMutation detectionClinical and genomic differences in supratentorial versus infratentorial NF2 mutant meningiomas.
Tabor J, O'Brien J, Vasandani S, Vetsa S, Lei H, Jalal M, Marianayagam N, Jin L, Millares Chavez M, Haynes J, Dincer A, Yalcin K, Aguilera S, Omay S, Mishra-Gorur K, McGuone D, Morales-Valero S, Fulbright R, Gunel M, Erson-Omay E, Moliterno J. Clinical and genomic differences in supratentorial versus infratentorial NF2 mutant meningiomas. Journal Of Neurosurgery 2023, 139: 1648-1656. PMID: 37243548, DOI: 10.3171/2023.4.jns222929.Peer-Reviewed Original ResearchConceptsSubtotal resectionSupratentorial tumorsElevated Ki-67High-risk featuresProgression-free survivalChromosome 1p deletionInfratentorial counterpartsInfratentorial tumorsPostoperative managementSomatic driver mutationsCerebral convexityGrade IIInfratentorial meningiomasKi-67Posterior fossaLoss of heterozygosityMeningiomasResectionTumorsWhole-exome sequencing dataDriver mutationsHigh gradeSignificant differencesExome sequencing dataSporadic meningiomasEvolutionary characterization of lung adenocarcinoma morphology in TRACERx
Karasaki T, Moore D, Veeriah S, Naceur-Lombardelli C, Toncheva A, Magno N, Ward S, Bakir M, Watkins T, Grigoriadis K, Huebner A, Hill M, Frankell A, Abbosh C, Puttick C, Zhai H, Gimeno-Valiente F, Saghafinia S, Kanu N, Dietzen M, Pich O, Lim E, Martínez-Ruiz C, Black J, Biswas D, Campbell B, Lee C, Colliver E, Enfield K, Hessey S, Hiley C, Zaccaria S, Litchfield K, Birkbak N, Cadieux E, Demeulemeester J, Van Loo P, Adusumilli P, Tan K, Cheema W, Sanchez-Vega F, Jones D, Rekhtman N, Travis W, Hackshaw A, Marafioti T, Salgado R, Le Quesne J, Nicholson A, McGranahan N, Swanton C, Jamal-Hanjani M. Evolutionary characterization of lung adenocarcinoma morphology in TRACERx. Nature Medicine 2023, 29: 833-845. PMID: 37045996, PMCID: PMC7614478, DOI: 10.1038/s41591-023-02230-w.Peer-Reviewed Original ResearchConceptsPrimary tumor regionLung adenocarcinomaPresence of micropapillary patternLoss of chromosome 3pSolid pattern tumorsHigh-grade patternsClonal evolution analysisSomatic copy number alterationsTumor regionLoss of heterozygosityWhole-exome sequencing dataCopy number alterationsAdenocarcinoma morphologyIntrathoracic recurrenceLepidic tumorsRNA sequencing dataMicropapillary patternRelapse riskGene alterationsMetastatic samplesHistological spectrumMicropapillary tumorsChromosome 3pHigh-gradeHistopathological analysis
2022
Recurrent Loss of Heterozygosity in Pancreatic Neuroendocrine Tumors
Parilla M, Chapel D, Hechtman J, Wanjari P, Jabbour T, Sharma A, Ritterhouse L, Segal J, Vanderbilt C, Klimstra D, Setia N, Tang L. Recurrent Loss of Heterozygosity in Pancreatic Neuroendocrine Tumors. The American Journal Of Surgical Pathology 2022, 46: 823-831. PMID: 35125451, PMCID: PMC9106831, DOI: 10.1097/pas.0000000000001860.Peer-Reviewed Original ResearchConceptsPancreatic neuroendocrine tumorsNeuroendocrine tumorsChromosomal copy number alterationsLoss of chromosome 11Loss of chromosome 1Recurrent loss of heterozygosityLoss of heterozygosityCopy number alterationsDisease-specific mortalityPrognostic markerChromosome aneuploidyTumor typesNext-generation sequencingChromosomal subgroupsAggressive subgroupTumorRecurrent lossChromosome 1Chromosome 11Third groupSubgroupsMortalityStatistical analysisMultivariate statistical analysisAneuploidy
2021
The somatic molecular evolution of cancer: Mutation, selection, and epistasis
Dasari K, Somarelli JA, Kumar S, Townsend JP. The somatic molecular evolution of cancer: Mutation, selection, and epistasis. Progress In Biophysics And Molecular Biology 2021, 165: 56-65. PMID: 34364910, PMCID: PMC8819680, DOI: 10.1016/j.pbiomolbio.2021.08.003.Peer-Reviewed Original ResearchConceptsCancer evolutionEpistatic interactionsNeutral mutation rateCancer progressionEvolution of neoplasmsSingle nucleotide variantsMolecular evolutionRate of fixationGenetic interactionsEvolutionary biologyPhylogenetic analysisCopy number aberrationsPhylogenetic relationsNeutral mutationsGenomic dataSelective pressureSynonymous mutationsMutation rateChromosomal instabilityPhenotypic changesLoss of heterozygosityFitness landscapeClonal deconvolutionTumor microenvironmentEnvironment interactionSequential filtering for clinically relevant variants as a method for clinical interpretation of whole exome sequencing findings in glioma
Ülgen E, Can Ö, Bilguvar K, Akyerli Boylu C, Kılıçturgay Yüksel Ş, Erşen Danyeli A, Sezerman OU, Yakıcıer MC, Pamir MN, Özduman K. Sequential filtering for clinically relevant variants as a method for clinical interpretation of whole exome sequencing findings in glioma. BMC Medical Genomics 2021, 14: 54. PMID: 33622343, PMCID: PMC7903763, DOI: 10.1186/s12920-021-00904-3.Peer-Reviewed Original ResearchConceptsTumor mutational burdenSomatic copy number alterationsWhole-exome sequencing findingsMicrosatellite instabilityGermline variantsClinical interpretationIndividual brain tumorsShort variantRecurrent tumorsMSI incidenceMutational burdenBrain tumorsLoss of heterozygosityPathway enrichment analysisPrimary gliomasClinical settingTumorsWES analysisCopy number alterationsTumor samplesSequencing findingsDiffuse gliomasClinical analysisGliomasChr10 loss
2020
Pervasive chromosomal instability and karyotype order in tumour evolution
Watkins T, Lim E, Petkovic M, Elizalde S, Birkbak N, Wilson G, Moore D, Grönroos E, Rowan A, Dewhurst S, Demeulemeester J, Dentro S, Horswell S, Au L, Haase K, Escudero M, Rosenthal R, Bakir M, Xu H, Litchfield K, Lu W, Mourikis T, Dietzen M, Spain L, Cresswell G, Biswas D, Lamy P, Nordentoft I, Harbst K, Castro-Giner F, Yates L, Caramia F, Jaulin F, Vicier C, Tomlinson I, Brastianos P, Cho R, Bastian B, Dyrskjøt L, Jönsson G, Savas P, Loi S, Campbell P, Andre F, Luscombe N, Steeghs N, Tjan-Heijnen V, Szallasi Z, Turajlic S, Jamal-Hanjani M, Van Loo P, Bakhoum S, Schwarz R, McGranahan N, Swanton C. Pervasive chromosomal instability and karyotype order in tumour evolution. Nature 2020, 587: 126-132. PMID: 32879494, PMCID: PMC7611706, DOI: 10.1038/s41586-020-2698-6.Peer-Reviewed Original ResearchConceptsSomatic copy number alterationsWhole-genome doublingChromosomal instabilityHuman leukocyte antigenChromosomal instability resultsSomatic copy number alteration analysisLoss of chromosome 8pFocal somatic copy number alterationsLoss of heterozygosityCopy number alterationsMetastatic samplesTumor evolutionKaryotype remodelingChromosome 8q24.1Clear cell renal cellChromosome 1q21Evolutionary eventsHER2+ breast cancerChromosome 8pChromosome 11q13.3Focal amplificationHaploid copiesRecurrent lossSubclonal frequenciesClonal events
2019
Haplotype-resolved and integrated genome analysis of the cancer cell line HepG2
Zhou B, Ho S, Greer S, Spies N, Bell J, Zhang X, Zhu X, Arthur J, Byeon S, Pattni R, Saha I, Huang Y, Song G, Perrin D, Wong W, Ji H, Abyzov A, Urban A. Haplotype-resolved and integrated genome analysis of the cancer cell line HepG2. Nucleic Acids Research 2019, 47: 3846-3861. PMID: 30864654, PMCID: PMC6486628, DOI: 10.1093/nar/gkz169.Peer-Reviewed Original ResearchConceptsGenome sequenceStructural variantsGenomic structural featuresSomatic genomic rearrangementsFunctional genomics dataAllele-specific expressionEntire chromosome armsIntegrated genome analysisCRISPR/Cas9Cell linesMain cell linesGenome structureEpigenomic characteristicsChromosome armsGenome analysisDNA methylationGenome characteristicsRetrotransposon insertionChromosomal segmentsGenomic rearrangementsGenomic dataRegulatory complexityCell line HepG2Copy numberLoss of heterozygosity
2018
Real-Time Genomic Characterization of Metastatic Pancreatic Neuroendocrine Tumors Has Prognostic Implications and Identifies Potential Germline Actionability.
Raj N, Shah R, Stadler Z, Mukherjee S, Chou J, Untch B, Li J, Kelly V, Saltz L, Mandelker D, Ladanyi M, Berger M, Klimstra D, Reidy-Lagunes D, Osoba M. Real-Time Genomic Characterization of Metastatic Pancreatic Neuroendocrine Tumors Has Prognostic Implications and Identifies Potential Germline Actionability. JCO Precision Oncology 2018, 2018: 1-18. PMID: 30687805, PMCID: PMC6345401, DOI: 10.1200/po.17.00267.Peer-Reviewed Original ResearchMemorial Sloan Kettering-Integrated Mutation Profiling of Actionable Cancer TargetsNext-generation sequencingPancreatic neuroendocrine tumorsGermline genetic analysisLoss of heterozygosityMetastatic PanNETsNeuroendocrine tumorsHigh-penetrance cancer susceptibility genesPresence of loss of heterozygosityAdvanced pancreatic neuroendocrine tumorsMetastatic pancreatic neuroendocrine tumorsGenetic analysisSomatic loss of heterozygosityInferior overall survivalCancer susceptibility genesIncreasing tumor gradeTarget of rapamycin pathway genesRoutine clinical practice settingClonal evolution patternsMammalian target of rapamycin pathway genesChromatin remodeling factorsReal-time molecular profilingFrequent somatic mutationsClinical practice settingSequence of pre-Prospective Evaluation of Germline Alterations in Patients With Exocrine Pancreatic Neoplasms
Lowery M, Wong W, Jordan E, Lee J, Kemel Y, Vijai J, Mandelker D, Zehir A, Capanu M, Salo-Mullen E, Arnold A, Yu K, Varghese A, Kelsen D, Brenner R, Kaufmann E, Ravichandran V, Mukherjee S, Berger M, Hyman D, Klimstra D, Abou-Alfa G, Tjan C, Covington C, Maynard H, Allen P, Askan G, Leach S, Iacobuzio-Donahue C, Robson M, Offit K, Stadler Z, O’Reilly E. Prospective Evaluation of Germline Alterations in Patients With Exocrine Pancreatic Neoplasms. Journal Of The National Cancer Institute 2018, 110: 1067-1074. PMID: 29506128, PMCID: PMC6186514, DOI: 10.1093/jnci/djy024.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedAged, 80 and overAllelesAntineoplastic AgentsAntineoplastic Combined Chemotherapy ProtocolsBiomarkers, TumorFemaleGenetic Association StudiesGenetic Predisposition to DiseaseGerm-Line MutationHeterozygoteHumansKaplan-Meier EstimateLoss of HeterozygosityMaleMiddle AgedPancreas, ExocrinePancreatic NeoplasmsConceptsPathogenic germline alterationsExocrine pancreatic neoplasmsOverall survivalGermline testingGermline alterationsPancreatic neoplasmsHereditary cancer predisposition genesInstitutional review board-approved protocolProspective cohort of patientsTherapeutic implicationsHereditary pancreatic cancerCancer predisposition genesBoard-approved protocolResponse to platinumCohort of patientsKaplan-Meier curvesLoss of heterozygosityPotential therapeutic implicationsMedian OSPredisposition genesSomatic tumorsExocrine neoplasmsPredictive biomarkersCancer susceptibilityPancreas cancerWidespread somatic loss of heterozygosity as a possible marker of disease aggressiveness in metastatic well differentiated pancreatic neuroendocrine tumors.
Akala O, Shah R, Untch B, Kelly V, Chou J, Ladanyi M, Berger M, Klimstra D, Reidy D, Raj N. Widespread somatic loss of heterozygosity as a possible marker of disease aggressiveness in metastatic well differentiated pancreatic neuroendocrine tumors. Journal Of Clinical Oncology 2018, 36: 275-275. DOI: 10.1200/jco.2018.36.4_suppl.275.Peer-Reviewed Original ResearchLoss of heterozygositySomatic loss of heterozygosityNext-generation sequencingPancreatic neuroendocrine tumorsAltered tumorsWild typeNeuroendocrine tumorsOverall survivalWT tumorsCancer-related genesMarkers of disease aggressivenessGenome-wideClinically heterogeneous tumorsHigh grade pathologySequencing platformsInferior overall survivalAggressive pathological featuresKi-67 indexNGS platformChromosome 1Allele-specificSomatic lossMEN1 alterationsGenetic alterationsGrade pathology
2016
Candidate predisposing germline copy number variants in early onset colorectal cancer patients
Brea-Fernandez AJ, Fernandez-Rozadilla C, Alvarez-Barona M, Azuara D, Ginesta MM, Clofent J, de Castro L, Gonzalez D, Andreu M, Bessa X, Llor X, Xicola R, Jover R, Castells A, Castellvi-Bel S, Capella G, Carracedo A, Ruiz-Ponte C. Candidate predisposing germline copy number variants in early onset colorectal cancer patients. Clinical And Translational Oncology 2016, 19: 625-632. PMID: 27888432, DOI: 10.1007/s12094-016-1576-z.Peer-Reviewed Original ResearchMeSH KeywordsAge of OnsetColorectal NeoplasmsDNA Copy Number VariationsDNA MethylationDNA Mutational AnalysisGenetic Predisposition to DiseaseGenetic VariationGenome-Wide Association StudyHumansIntercellular Signaling Peptides and ProteinsLoss of HeterozygosityNerve Tissue ProteinsReal-Time Polymerase Chain ReactionConceptsColorectal cancerEarly-onset colorectal cancer patientsEarly-onset CRC patientsMethods/patientsWeColorectal cancer patientsHereditary colorectal cancerIdentifiable germline mutationsCopy number variantsPenetrant copy number variantsSomatic mutation analysisCRC patientsGenome-wide copy number analysisCancer patientsReal-time quantitative PCRMultiplex ligation probe amplificationCRC tumorsColorectal carcinogenesisLoss of heterozygosityPatientsSLIT2 geneGenetic susceptibilityDuplex real-time quantitative PCREarly onsetGermline mutationsConclusionsThese findingsWhole exome and targeted deep sequencing identify genome-wide allelic loss and frequent SETDB1 mutations in malignant pleural mesotheliomas
Kang HC, Kim HK, Lee S, Mendez P, Kim JW, Woodard G, Yoon JH, Jen KY, Fang LT, Jones K, Jablons DM, Kim IJ. Whole exome and targeted deep sequencing identify genome-wide allelic loss and frequent SETDB1 mutations in malignant pleural mesotheliomas. Oncotarget 2016, 7: 8321-8331. PMID: 26824986, PMCID: PMC4884995, DOI: 10.18632/oncotarget.7032.Peer-Reviewed Original ResearchMeSH KeywordsBlotting, WesternExomeFemaleGenome, HumanHigh-Throughput Nucleotide SequencingHistone-Lysine N-MethyltransferaseHumansImmunoenzyme TechniquesLoss of HeterozygosityLung NeoplasmsMesotheliomaMesothelioma, MalignantMiddle AgedMutationPleural NeoplasmsPrognosisProtein MethyltransferasesReal-Time Polymerase Chain ReactionReverse Transcriptase Polymerase Chain ReactionRNA, MessengerSurvival RateConceptsMalignant pleural mesotheliomaPrimary cancerPleural mesotheliomaGenetic mechanismsDeep sequencingAdditional primary cancersMultiple primary cancersPrimary lung cancerPrimary cancer developmentAllelic lossNew genetic mechanismWhole-exome sequencingDistinct genomic alterationsMPM patientsRare malignancyPerineural invasionPoor prognosisTherapeutic optionsLung cancerLoss of heterozygosityTP53 mutationsCancer developmentPatientsExome sequencingCancerGenomic characterization of sarcomatoid transformation in clear cell renal cell carcinoma.
Bi X, Zhao S, Adeniran A, Kluger H, Xie Z, Nawaf C, Merino M, Valera V, Pantuck A, Said J, Belldegrun A, Lifton R, Shuch B. Genomic characterization of sarcomatoid transformation in clear cell renal cell carcinoma. Journal Of Clinical Oncology 2016, 34: 509-509. DOI: 10.1200/jco.2016.34.2_suppl.509.Peer-Reviewed Original ResearchDriver genesCancer driver genesSomatic mutationsProtein traffickingIllumina sequencingSomatic cellsGenomic characterizationCell differentiationCell adhesionLoss of heterozygosityClear cell renal cell carcinomaGenesMutational signaturesCell renal cell carcinomaClonal divergenceGenetic alterationsMutationsTP53 mutationsRepair deficiencySarcomatoid transformationSubset of tumorsCcRCCHypermutationRenal cell carcinomaBAP1Microsatellite Alterations With Allelic Loss at 9p24.2 Signify Less-Aggressive Colorectal Cancer Metastasis
Koi M, Garcia M, Choi C, Kim H, Koike J, Hemmi H, Nagasaka T, Okugawa Y, Toiyama Y, Kitajima T, Imaoka H, Kusunoki M, Chen Y, Mukherjee B, Boland C, Carethers J. Microsatellite Alterations With Allelic Loss at 9p24.2 Signify Less-Aggressive Colorectal Cancer Metastasis. Gastroenterology 2016, 150: 944-955. PMID: 26752111, PMCID: PMC4808397, DOI: 10.1053/j.gastro.2015.12.032.Peer-Reviewed Original ResearchMeSH KeywordsBiomarkers, TumorChi-Square DistributionChromosome AberrationsChromosomes, Human, Pair 9Colorectal NeoplasmsDisease ProgressionDisease-Free SurvivalFemaleGenetic Predisposition to DiseaseHumansJapanKaplan-Meier EstimateLiver NeoplasmsLogistic ModelsLoss of HeterozygosityMaleMicrosatellite RepeatsMiddle AgedNeoplasm Recurrence, LocalNeoplasm StagingOdds RatioPhenotypeProportional Hazards ModelsProto-Oncogene Proteins B-rafProto-Oncogene Proteins p21(ras)Republic of KoreaRisk FactorsTime FactorsTreatment OutcomeConceptsPrimary colorectal tumorsLoss of heterozygosityLiver metastasesColorectal cancerColorectal tumorsElevated microsatellite alterationsMicrosatellite alterationsStage IICurative treatment of patientsStage III colorectal cancerOverall survival of patientsSurvival of patientsIII colorectal cancerTumor to liverColorectal cancer recurrenceTreatment of patientsMatched liver metastasesCancer cell nucleiMatched metastasesDisease recurrenceOverall survivalPrognostic factorsAllelic lossNo significant differenceCurative treatment
2013
LOH in the HLA Class I Region at 6p21 Is Associated with Shorter Survival in Newly Diagnosed Adult Glioblastoma
Yeung JT, Hamilton RL, Ohnishi K, Ikeura M, Potter DM, Nikiforova MN, Ferrone S, Jakacki RI, Pollack IF, Okada H. LOH in the HLA Class I Region at 6p21 Is Associated with Shorter Survival in Newly Diagnosed Adult Glioblastoma. Clinical Cancer Research 2013, 19: 1816-1826. PMID: 23401227, PMCID: PMC3618546, DOI: 10.1158/1078-0432.ccr-12-2861.Peer-Reviewed Original ResearchConceptsHLA class IT cell infiltrationHLA class IILoss of heterozygosityHLA class IIIClass IOverall survivalAdult glioblastomaClass IIIHLA class I expressionHuman leukocyte antigen (HLA) class IClass IIEfficacy of immunotherapyShorter overall survivalCytotoxic T cellsClass I expressionAntigen class ICross-sectional analysisAdult patientsShorter survivalImmunohistochemical evaluationT cellsHLA class I regionI expressionDownregulated expression
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