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FGFR3 alterations in bladder cancer:Sensitivity and resistance to targeted therapies

Cancer Communications 2024年第10期44卷 1189-1208页

作者： Maxim Noeraparast Katarina Krajina Renate Pichler dora Nieders-beke Shahrokh F Shariat Viktor Grünwald Sascha Ahyai Martin Pichler Translational Oncology II.Med Clinics Hematology and OncologyAugsburgGermany Department of Urology Medical University of InnsbruckInnsbruckAustria Department of Hematology and Oncology Clinics OttakringViennaAustria Department of Urology Medical University of ViennaViennaAustria Interdisciplinary Genitourinary Oncology Clinic for UrologyClinic for Medical OncologyUniversity Hospital EssenHufelandstrase 55EssenGermany Department of Urology Medical University of GrazGrazAustria

In this review,we revisit the pivotal role of fibroblast growth factor receptor 3(FGFR3)in bladder cancer(BLCA),underscoring its prevalence in both nonmuscle-invasive and muscle-invasive forms of the ***3 mutations in up to half of BLCAs play a well-established role in tumorigenesis,shaping distinct tumor initiation patterns and impacting the tumor microenvironment(TME).Emphasizing the importance of considering epithelial-mesenchymal transition profile and TME status,we revisit their relevance in predicting responses to immune checkpoint inhibitors in FGFR3-mutated *** writing highlights the initially promising yet transient efficacy of the FGFR inhibitor Erdafitinib on FGFR3-mutated BLCA,stressing the pressing need to unravel resistance mechanisms and identify co-targets for future combinatorial studies.A thorough analysis of recent preclinical and clinical evidence reveals resistance mechanisms,including secondarymutations,epigenetic alterations in pathway effectors,phenotypic heterogeneity,and population-specific variations within FGFR3 mutational ***,we discuss the potential of combinatorial treatments and concepts like synthetic lethality for discovering more effective targeted therapies against FGFR3-mutated BLCA.

关键词： Bladder Cancer Erdafitinib FGFR inhibition FGFR3 mutations Resistance to Erdafitinib Tumor Microenvironment

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A Synonymous Polymorphism of APCDD1 Affects Translation Efficacy and is Associated with Androgenic Alopecia

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Journal of Life Sciences 2014年第2期8卷 106-114页

作者： Nikoletta Nagy Katalin Farkas Agnes Kinyo Barbara Fazekas Kornelia Szabo Edit Kollar Balazs Sztano Angela Meszes dora beke Lajos Kemeny Laszlo Royo Marta Szell Department of Medical Genetics University of Szeged Szeged 6720 Hungary Department of Dermatology andAllergology University ofSzeged Szeged 6720 Hungary Dermatological Research Group Hungarian Academy of Sciences Szeged 6720 Hungary Department of Rhino-Laryngology and Head-Neck Surgery University ofSzeged Szeged 6720 Hungary

The APCDDI （adenomatosis polyposis coli down-regulated 1） gene is an inhibitor of the Wnt signaling pathway, and a rare mutation of this gene has been associated with hereditary hypotrichosis simplex. In this study, the authors aimed to investigate whether common APCDD1 gene polymorphisms contribute to the development of androgenic alopecia. Patients （n = 210） with androgenic alopecia and 98 controls were investigated. SNPs （Single nucleotide polymorphisms） in the coding region of the gene were sequenced. A significant difference in genotype distribution was found for the c. 1781C/T, p.L476L SNP （rs3185480） of the APCDD1 gene. This SNP is located in exon 5 and is associated with a 3.5- and a 2.8-fold increase in risk for the development of androgenic alopecia for homozygote （CI 0.933-13.125; nominal regression P = 0.063） and heterozygote （CI 1.086-7.217; nominal regression P = 0.033） carriers, respectively. These data suggest that the rs3185480 polymorphism contributes to the development of androgenic alopecia. Protein expression experiments revealed that the polymorphism is associated with reduced APCDDI protein abundance. This reduction is likely due to altered codon usage for leucine from a preferred codon （CTC） to a rare codon （CTT）, which might influence translation efficiency and, thus, APCDDI protein level.

关键词： Adenomatosis polyposis coli down-regulated 1 gene hereditary hypotrichosis simplex androgenic alopecia,polymorphism synonymous translation efficacy preferable codon.

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