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Ko, B. C. B.

Publications and source records attributed to Ko, B. C. B..

2 recordsLinked to original sources

Functional and sensitivity profiling of theKITMutation Landscape in Melanoma

Melanoma in Asia presents a unique epidemiological profile, with a higher prevalence of acral and mucosal subtypes compared to Western populations. While KIT mutations are found in up to 15% of Asian melanoma cases, clinical outcomes with KIT inhibitors have been modest due to heterogeneous mutation profiles and a lack of specific patient selection criteria. This study characterizes the landscape of KIT mutations in melanoma using the GENIE database, identifying 86 recurrent hotspots, many of which are variants of unknown significance (VUS). We validated drug sensitivities for key mutations using in vitro and in vivo models. Our results indicate that while the L576P mutation is highly sensitive to multiple inhibitors, the N822K mutation shows resistance to imatinib but responds to sunitinib, nilotinib, and nintedanib. These findings highlight the necessity of genotype-guided therapeutic strategies and provide a rationale for future clinical trials combining broad-spectrum KIT inhibitors with immune checkpoint inhibitors. Translational SignificanceMelanoma subtypes prevalent in Asia, specifically acral and mucosal melanoma, frequently harbor KIT mutations but show poor response rates (23-26%) to the standard-of-care inhibitor, imatinib. This study challenges the current clinical practice of treating all KIT-mutated melanomas uniformly. We demonstrate that specific recurrent mutations, such as N822K, are intrinsically resistant to imatinib but highly sensitive to broad-spectrum inhibitors like sunitinib and nintedanib. By establishing a comprehensive "lookup table" of drug sensitivities for both common and previously uncharacterized KIT variants, this work provides the evidence base required to transition from a "one-size-fits-all" approach to a genotype-guided precision medicine strategy. Furthermore, validating these targets informs the design of next-generation clinical trials, particularly those combining optimal KIT inhibitors with immune checkpoint blockade to improve survival in currently underserved patient populations.

cancer biology↗

Unconventional tonicity-regulated nuclear trafficking of NFAT5 mediated by KPNB1, XPOT and RUVBL2

NFAT5 is the only known mammalian tonicity-responsive transcription factor functionally implicated in diverse physiological and pathological processes. NFAT5 activity is tightly regulated by extracellular tonicity but the underlying mechanisms remain elusive. We demonstrated that NFAT5 enters the nucleus via the nuclear pore complex. We also found that NFAT5 utilizes a non-canonical nuclear localization signal (NFAT5-NLS) for nuclear imports. siRNA screening revealed that karyopherin {beta}1 (KPNB1) drives nuclear import of NFAT5 via directly interacting with NFAT5-NLS. Proteomics analysis and siRNA screening further revealed that nuclear export of NFAT5 under hypotonicity is mediated by Exportin-T, and that it requires RuvB-Like AAA type ATPase 2 (RUVBL2) as an indispensable chaperone. Our findings have identified KPNB1 and RUVBL2 as key molecules responsible for the unconventional tonicity-regulated nucleocytoplasmic shuttling of NFAT5. These findings offer an opportunity for developing novel NFAT5 targeting strategies that are potentially useful for the treatment of diseases associated with NFAT5 dysregulation.

cell biology↗