Hyun Ae Jung
성균관대학교 의료진프로필 · 의학
Hyun Ae Jung 교수의 연구실은 주로 암 치료의 최신 진료 전략과 약물 반응성에 초점을 맞추고 있으며, 특히 난소암, 구강암, 비소세포폐암 등에서의 표적치료 및 면역요법의 유효성과 부작용에 대한 연구를 진행하고 있습니다. 환자의 생존율 향상과 치료 내성 문제를 해결하기 위해 약물 조합, 뇌전이 예방, 치료 지속성 등에 대한 임상적 분석을 강화하고 있으며, 약물의 뇌침투성과 장기적 반응률에 대한 데이터 기반 연구도 수행하고 있습니다. 특히, 5-FU, afatinib, nivolumab, capecitabine 등의 약물에 대한 임상적 반응 패턴을 분석함으로써 개인화된 치료 전략 수립에 기여하고 있습니다.
표시된 성과는 수집된 데이터 기준으로 산출되며, 일부 차이가 있을 수 있습니다.
Article Free Access Share on Lower bounds and efficient algorithms for multiprocessor scheduling of dags with communication delays Authors: H. Jung Mathematics Dept., Humboldt Univ., GDR Mathematics Dept., Humboldt Univ., GDRView Profile , L. Kirousis Computer Technology Institute, Patras Univ., Greece Computer Technology Institute, Patras Univ., GreeceView Profile , P. Spirakis Computer Technology Institute, Patras Univ., Greece and Courant Inst. Math. Sciences, NYU Computer Technology Institut
In urachal cancer, curative surgery is still the recommended treatment with respect to overall survival. A 5-FU-based chemotherapy regimen could be considered for metastatic recurrent disease.
Through there are some limitation as a retrospective study, afatinib showed similar CNS response rates, superior CNS-PFS and cumulative incidence of CNS failure, compared with gefitinib or erlotinib.
Nivolumab plus gemcitabine showed promising efficacy with favorable toxicity profiles in patients with advanced NPC in whom platinum-based combination chemotherapy failed.
Optical gain spectra of GaInAsP/InP double heterostructures (DHs) have been recorded in the temperature range of 80–300 K. These data are compared with threshold currents of DHs injection lasers fabricated from the same wafers. An identical behavior of maximum optical gain and threshold current is observed, i.e., two T0 values (100 and 63 K) with a break-point temperature of TB ≃260 K are found. Furthermore, characteristic changes of the optical gain spectrum are observed close to the break-poin
Macrocytosis developed with more frequent and prolonged use of capecitabine. It is possible that association with treatment outcomes warrants further investigation.
The low-risk group with TRU subtype and TP53 wild-type without clinicopathologic risk factors might not need adjuvant EGFR-TKIs. In the high-risk group, with non-TRU subtype and/or TP 53 mutation, or clinicopathologic risk factors, a novel adjuvant strategy of EGFR-TKI with others, e.g., chemotherapy or antiangiogenic agents needs to be investigated. Given the poor outcome to EGFR-TKIs after recurrence in patients with the APOBEC mutation signature, an alternative adjuvant strategy might be need