IJMMS_2024v14n5

International Journal of Molecular Medical Science, 2024, Vol.14, No.5, 305-314 http://medscipublisher.com/index.php/ijmms 314 Kim M., Woo S., Park B., Yoon K., Kim Y., Joo J., Lee W., Han S., Park S., and Kong S., 2018, Prognostic implications of multiplex detection of KRAS mutations in cell-free DNA from patients with pancreatic ductal adenocarcinoma, Clinical Chemistry, 64(4): 726-734 . https://doi.org/10.1373/clinchem.2017.283721 Koga T., Suda K., Fujino T., Ohara S., Hamada A., Nishino M., Chiba M., Shimoji M., Takemoto T., Arita T., Gmachl M., Hofmann M., Soh J., and Mitsudomi T., 2021, KRAS secondary mutations that confer acquired resistance to KRAS G12C inhibitors, sotorasib and adagrasib, and overcoming strategies: insights from the in vitro experiments, Journal of Thoracic Oncology: Official Publication of the International Association for the Study of Lung Cancer, 16(8): 1321-1332. https://doi.org/10.1016/j.jtho.2021.04.015 Liou G., Döppler H., DelGiorno K., Zhang L., Leitges M., Crawford H., Murphy M., and Storz P., 2016, Mutant KRas-induced mitochondrial oxidative stress in acinar cells upregulates EGFR signaling to drive formation of pancreatic precancerous lesions, Cell Reports, 14(10): 2325-2336. https://doi.org/10.1016/j.celrep.2016.02.029 Luo J., 2021, KRAS mutation in pancreatic cancer, Seminars in Oncology, 48(1): 10-18. https://doi.org/10.1053/j.seminoncol.2021.02.003 Lyu H., Minelli R., Deckard C., Seth S., Huang J., Jiang H., Peoples M., Lam M., Bristow C., Gerlach D., Tontsch-Grunt U., Li C., Ho I., Vellano C., Hofmann M., Heffernan T., Marszalek J., Viale A., and Carugo A., 2022, Abstract LB079: pancreatic clonal replica tumors display functional heterogeneity in response to KRAS pharmacological inhibition and reveal unique epigenetic vulnerabilities to overcome resistance, Cancer Research, 82(12): LB079. https://doi.org/10.1158/1538-7445.am2022-lb079 Muzumdar M., Chen P., Dorans K., Chung K., Bhutkar A., Hong E., Noll E., Sprick M., Trumpp A., and Jacks T., 2017, Survival of pancreatic cancer cells lacking KRAS function, Nature Communications, 8(1): 1090. https://doi.org/10.1038/s41467-017-00942-5 Pei Y., Chen L., Huang Y., Wang J., Feng J., Xu M., Chen Y., Song Q., Jiang G., Gu X., Zhang Q., Gao X., and Chen J., 2019, Sequential targeting TGF-β signaling and KRAS mutation increases therapeutic efficacy in pancreatic cancer, Small, 15(24): e1900631. https://doi.org/10.1002/smll.201900631 Singh H., Keller R., Kapner K., Dilly J., Raghavan S., Yuan C., Cohen E., Tolstorukov M., Hill E., Andrews E., Brais L., Silva A., Perez K., Rubinson D., Schlechter B., Rosenthal M., Hornick J., Nardi V., Li Y., Gupta H., Cherniack A., Meyerson M., Cleary J., Nowak J., Wolpin B., and Aguirre A., 2022, Abstract A001: clinical-genomic analysis of KRAS wild-type pancreatic cancer confirms alternative targetable drivers and provides insight for age and risk related clinical stratification, Cancer Research, 82(22): A001. https://doi.org/10.1158/1538-7445.panca22-a001 Tanaka N., Lin J., Li C., Ryan M., Zhang J., Kiedrowski L., Michel A., Syed M., Fella K., Sakhi M., Baiev I., Juric D., Gainor J., Klempner S., Lennerz J., Siravegna G., Bar-Peled L., Hata A., Heist R., and Corcoran R., 2021, Clinical acquired resistance to KRASG12C inhibition through a novel KRAS switch-II pocket mutation and polyclonal alterations converging on RAS-MAPK reactivation, Cancer Discovery, 11(8): 1913-1922. https://doi.org/10.1158/2159-8290.CD-21-0365 Teufel M., Laethem J., Riess H., Giurescu M., Garosi V., Schulz A., Vonk R., Seidel H., Reischl J., and Childs B., 2015, Abstract 5239: KRAS wild-type status as detected by circulating tumor DNA analysis may be a prognostic or predictive factor for clinical benefit in patients with unresectable, locally advanced or metastatic pancreatic cancer (PC) treated with the MEK inhibitor refametin, Cancer Research, 75: 5239. https://doi.org/10.1158/1538-7445.AM2015-5239 Tímár J., and Kashofer K., 2020, Molecular epidemiology and diagnostics of KRAS mutations in human cancer, Cancer Metastasis Reviews, 39: 1029-1038. https://doi.org/10.1007/s10555-020-09915-5 Voutsadakis I., and Digklia A., 2023, Pancreatic adenocarcinomas without KRAS, TP53, CDKN2A and SMAD4 mutations and CDKN2A/CDKN2B copy number alterations: a review of the genomic landscape to unveil therapeutic avenues, Chinese Clinical Oncology, 12(1): 2. https://doi.org/10.21037/cco-22-108 Watanabe F., Suzuki K., Tamaki S., Abe I., Endo Y., Takayama Y., Ishikawa H., Kakizawa N., Saito M., Futsuhara K., Noda H., Konishi F., and Rikiyama T., 2019, Longitudinal monitoring of KRAS-mutated circulating tumor DNA enables the prediction of prognosis and therapeutic responses in patients with pancreatic cancer, PLoS ONE, 14(12): e0227366. https://doi.org/10.1371/journal.pone.0227366 Waters A., and Der C., 2018, KRAS: the critical driver and therapeutic target for pancreatic cancer, Cold Spring Harbor Perspectives in Medicine, 8(9): a031435. https://doi.org/10.1101/cshperspect.a031435

RkJQdWJsaXNoZXIy MjQ4ODYzNQ==