2024
Emerging therapeutic options for follicular-derived thyroid cancer in the era of immunotherapy
Turner N, Hamidi S, Ouni R, Rico R, Henderson Y, Puche M, Alekseev S, Colunga-Minutti J, Zafereo M, Lai S, Kim S, Cabanillas M, Nurieva R. Emerging therapeutic options for follicular-derived thyroid cancer in the era of immunotherapy. Frontiers In Immunology 2024, 15: 1369780. PMID: 38868771, PMCID: PMC11167082, DOI: 10.3389/fimmu.2024.1369780.Peer-Reviewed Original ResearchConceptsAnaplastic thyroid cancerFollicular-derived thyroid cancersAdvanced thyroid cancerThyroid cancerFood and Drug AdministrationManagement of advanced thyroid cancerEra of immunotherapyTargeted kinase inhibitorsU.S Food and Drug AdministrationImmune milieuRefractory diseaseExcellent prognosisTherapeutic optionsTreatment optionsKinase inhibitorsDrug AdministrationGenetic driversTherapeutic avenuesCancerImmunotherapyGenetic landscapeRadioiodineTreatmentMolecular basisOptions
2022
Interleukin-6 blockade abrogates immunotherapy toxicity and promotes tumor immunity
Hailemichael Y, Johnson D, Abdel-Wahab N, Foo W, Bentebibel S, Daher M, Haymaker C, Wani K, Saberian C, Ogata D, Kim S, Nurieva R, Lazar A, Abu-Sbeih H, Fa'ak F, Mathew A, Wang Y, Falohun A, Trinh V, Zobniw C, Spillson C, Burks J, Awiwi M, Elsayes K, Soto L, Melendez B, Davies M, Wargo J, Curry J, Yee C, Lizee G, Singh S, Sharma P, Allison J, Hwu P, Ekmekcioglu S, Diab A. Interleukin-6 blockade abrogates immunotherapy toxicity and promotes tumor immunity. Cancer Cell 2022, 40: 509-523.e6. PMID: 35537412, PMCID: PMC9221568, DOI: 10.1016/j.ccell.2022.04.004.Peer-Reviewed Original ResearchConceptsImmune checkpoint blockadeExperimental autoimmune encephalomyelitisInterleukin-6 blockadeInterleukin-6Anti-cytotoxic T-lymphocyte-associated antigen 4T-lymphocyte-associated antigen 4Anti-programmed death-1Experimental autoimmune encephalomyelitis symptomsImmune-related adverse eventsICB-treated patientsPromote tumor immunityAnti-CTLA-4Anti-PD-1Improve tumor controlEffector T cellsT helper 1T helper 17Expression of interleukin-6Chemotactic markersImmunotherapy toxicityReduced Th17Antitumor immunityCheckpoint blockadeTumor controlDeath-1
2016
Protein stabilization improves STAT3 function in autosomal dominant hyper-IgE syndrome
Bocchini C, Nahmod K, Katsonis P, Kim S, Kasembeli M, Freeman A, Lichtarge O, Makedonas G, Tweardy D. Protein stabilization improves STAT3 function in autosomal dominant hyper-IgE syndrome. Blood 2016, 128: 3061-3072. PMID: 27799162, PMCID: PMC5201093, DOI: 10.1182/blood-2016-02-702373.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCD4-Positive T-LymphocytesCD8-Positive T-LymphocytesCytokinesDiterpenesDNA-Binding ProteinsHalf-LifeHeat Shock Transcription FactorsHerpesvirus 4, HumanHumansInterleukin-17Job SyndromeMiceModels, MolecularMutant ProteinsMutationPhosphotyrosineProtein BindingProtein StabilitySpleenSTAT3 Transcription FactorTranscription FactorsConceptsAutosomal dominant hyper-IgE syndromeSTAT3 mutationsPeripheral blood mononuclear cellsAD-HIESProtein stabilityEpstein-Barr virus-transformed BPY-STAT3Human peripheral blood mononuclear cellsHeat shock proteinsHyper-IgE syndromeSTAT3 target genesProtein half-lifeMouse splenocytesUpregulating heat shock proteinsAD-HIES patientsLevel of STAT3T cellsDominant-negative mutationsTreatment of human peripheral blood mononuclear cellsCD8<sup>+</sup> T cellsSTAT3 functionEpstein-Barr virus-transformed B cellsProtein functionHuman CD4<sup>+</sup>MRNA levels