Infigratinib in upper tract urothelial carcinoma versus urothelial carcinoma of the bladder and its association with comprehensive genomic profiling and/or cell-free DNA results.


Journal

Cancer
ISSN: 1097-0142
Titre abrégé: Cancer
Pays: United States
ID NLM: 0374236

Informations de publication

Date de publication:
01 06 2020
Historique:
received: 13 11 2019
revised: 29 12 2019
accepted: 06 01 2020
pubmed: 26 3 2020
medline: 23 1 2021
entrez: 26 3 2020
Statut: ppublish

Résumé

Infigratinib (BGJ398) is a potent and selective fibroblast grown factor receptor 1 to 3 (FGFR1-3) inhibitor with significant activity in patients with advanced or metastatic urothelial carcinoma bearing FGFR3 alterations. Given the distinct biologic characteristics of upper tract urothelial carcinoma (UTUC) and urothelial carcinoma of the bladder (UCB), the authors examined whether infigratinib had varying activity in these settings. Eligible patients had metastatic urothelial carcinoma with activating FGFR3 mutations and/or fusions. Comprehensive genomic profiling was performed on formalin-fixed, paraffin-embedded tissues. Blood was collected for cell-free DNA analysis using a 600-gene panel. Patients received infigratinib at a dose of 125 mg orally daily (3 weeks on/1 week off) until disease progression or intolerable toxicity occurred. The overall response rate (ORR; partial response [PR] plus complete response [CR]) and disease control rate (DCR; CR plus PR plus stable disease [SD]) were characterized. A total of 67 patients were enrolled; the majority (70.1%) had received ≥2 prior antineoplastic therapies. In 8 patients with UTUC, 1 CR and 3 PRs were observed (ORR, 50%); the remaining patients achieved a best response of SD (DCR, 100%). In patients with UCB, 13 PRs were observed (ORR, 22%), and 22 patients had a best response of SD (DCR, 59.3%). Notable differences in genomic alterations between patients with UTUC and those with UCB included higher frequencies of FGFR3-TACC3 fusions (12.5% vs 6.8%) and FGFR3 R248C mutations (50% vs 11.9%), and a lower frequency of FGFR3 S249C mutations (37.5% vs 59.3%). Differences in the cumulative genomic profile were observed between patients with UTUC and those with UCB in the current FGFR3-restricted experience, underscoring the distinct biology of these diseases. These results support a planned phase 3 adjuvant study predominantly performed in this population.

Sections du résumé

BACKGROUND
Infigratinib (BGJ398) is a potent and selective fibroblast grown factor receptor 1 to 3 (FGFR1-3) inhibitor with significant activity in patients with advanced or metastatic urothelial carcinoma bearing FGFR3 alterations. Given the distinct biologic characteristics of upper tract urothelial carcinoma (UTUC) and urothelial carcinoma of the bladder (UCB), the authors examined whether infigratinib had varying activity in these settings.
METHODS
Eligible patients had metastatic urothelial carcinoma with activating FGFR3 mutations and/or fusions. Comprehensive genomic profiling was performed on formalin-fixed, paraffin-embedded tissues. Blood was collected for cell-free DNA analysis using a 600-gene panel. Patients received infigratinib at a dose of 125 mg orally daily (3 weeks on/1 week off) until disease progression or intolerable toxicity occurred. The overall response rate (ORR; partial response [PR] plus complete response [CR]) and disease control rate (DCR; CR plus PR plus stable disease [SD]) were characterized.
RESULTS
A total of 67 patients were enrolled; the majority (70.1%) had received ≥2 prior antineoplastic therapies. In 8 patients with UTUC, 1 CR and 3 PRs were observed (ORR, 50%); the remaining patients achieved a best response of SD (DCR, 100%). In patients with UCB, 13 PRs were observed (ORR, 22%), and 22 patients had a best response of SD (DCR, 59.3%). Notable differences in genomic alterations between patients with UTUC and those with UCB included higher frequencies of FGFR3-TACC3 fusions (12.5% vs 6.8%) and FGFR3 R248C mutations (50% vs 11.9%), and a lower frequency of FGFR3 S249C mutations (37.5% vs 59.3%).
CONCLUSIONS
Differences in the cumulative genomic profile were observed between patients with UTUC and those with UCB in the current FGFR3-restricted experience, underscoring the distinct biology of these diseases. These results support a planned phase 3 adjuvant study predominantly performed in this population.

Identifiants

pubmed: 32208524
doi: 10.1002/cncr.32806
pmc: PMC7515773
mid: NIHMS1628289
doi:

Substances chimiques

Cell-Free Nucleic Acids 0
Phenylurea Compounds 0
Pyrimidines 0
infigratinib A4055ME1VK
FGFR3 protein, human EC 2.7.10.1
Receptor, Fibroblast Growth Factor, Type 3 EC 2.7.10.1

Types de publication

Comparative Study Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

2597-2606

Subventions

Organisme : NCI NIH HHS
ID : P30 CA008748
Pays : United States
Organisme : NCI NIH HHS
ID : P30 CA013330
Pays : United States
Organisme : NCI NIH HHS
ID : P30 CA014089
Pays : United States
Organisme : NCATS NIH HHS
ID : UL1 TR001863
Pays : United States

Informations de copyright

© 2020 American Cancer Society.

Références

Cancer Discov. 2018 Jul;8(7):812-821
pubmed: 29848605
Nucleic Acids Res. 2019 Jan 8;47(D1):D941-D947
pubmed: 30371878
J Clin Oncol. 2017 Jan 10;35(2):157-165
pubmed: 27870574
Lancet Oncol. 2017 Mar;18(3):312-322
pubmed: 28131785
Mol Cancer Ther. 2017 Jun;16(6):1010-1020
pubmed: 28341788
Lancet Oncol. 2018 Jan;19(1):51-64
pubmed: 29217288
N Engl J Med. 2019 Jul 25;381(4):338-348
pubmed: 31340094
Cancer. 2016 Mar 1;122(5):702-11
pubmed: 26651075
Clin Cancer Res. 2019 Feb 1;25(3):967-976
pubmed: 30352907
Urol Oncol. 2016 Dec;34(12):556-565
pubmed: 27836246
Clin Cancer Res. 2018 Sep 15;24(18):4437-4443
pubmed: 29567812
Cancer. 2018 May 15;124(10):2115-2124
pubmed: 29517810
Ann Oncol. 2017 Oct 1;28(10):2458-2463
pubmed: 28945843
J Clin Oncol. 2005 Jul 20;23(21):4602-8
pubmed: 16034041
Nat Commun. 2019 Jul 5;10(1):2977
pubmed: 31278255
N Engl J Med. 2017 Mar 16;376(11):1015-1026
pubmed: 28212060
JCI Insight. 2019 May 30;5:
pubmed: 31145100
Cancer Sci. 2019 May;110(5):1771-1779
pubmed: 30887605
Cell Res. 2017 Jan;27(1):96-108
pubmed: 27981969
J Clin Oncol. 2016 Sep 10;34(26):3119-25
pubmed: 27269937
Lancet. 2018 Feb 24;391(10122):748-757
pubmed: 29268948
Curr Oncol Rep. 2019 Feb 26;21(3):24
pubmed: 30806823
Eur Urol. 2019 Nov;76(5):599-603
pubmed: 31272788
Eur Urol. 2017 Oct;72(4):641-649
pubmed: 28601352

Auteurs

Sumanta K Pal (SK)

Department of Medical Oncology & Experimental Therapeutics, City of Hope Comprehensive Cancer Center, Duarte, California.

Dean Bajorin (D)

Genitourinary Oncology, Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, New York.
Department of Medicine, Weill Cornell Medical College, New York, New York.

Nazli Dizman (N)

Department of Medical Oncology & Experimental Therapeutics, City of Hope Comprehensive Cancer Center, Duarte, California.

Jean Hoffman-Censits (J)

Departments of Medical Oncology and Urology, Sidney Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, Pennsylvania.

David I Quinn (DI)

University of Southern California Norris Comprehensive Cancer Center Keck School of Medicine at USC, Los Angeles, California.

Daniel P Petrylak (DP)

Department of Medicine, Division of Oncology, Yale School of Medicine, New Haven, Connecticut.

Matthew D Galsky (MD)

Department of Medicine, Division of Hematology/Oncology, Tisch Cancer Institute, The Mount Sinai Hospital, New York, New York.

Ulka Vaishampayan (U)

Department of Oncology, Karmanos Cancer Institute, Wayne State University, Detroit, Michigan.

Ugo De Giorgi (U)

Department of Medical Oncology, Scientific Institute of Romagna for the Study and Treatment of Cancer, IRCCS, Meldola, Italy.

Sumati Gupta (S)

Division of Medical Oncology, Huntsman Cancer Institute, University of Utah, Salt Lake City, Utah.

Howard A Burris (HA)

Sarah Cannon Research Institute and Tennessee Oncology, Nashville, Tennessee.

Harris S Soifer (HS)

Department of Translational Medicine, QED Therapeutics Inc, San Francisco, California.

Gary Li (G)

Department of Translational Medicine, QED Therapeutics Inc, San Francisco, California.

Hao Wang (H)

Department of Biostatistics and Data Management, QED Therapeutics Inc, San Francisco, California.

Carl L Dambkowski (CL)

Department of Strategy and Operations, QED Therapeutics Inc, San Francisco, California.

Susan Moran (S)

Department of Clinical Development, QED Therapeutics Inc, San Francisco, California.

Siamak Daneshmand (S)

Institute of Urology, Keck School of Medicine, University of Southern California, Los Angeles, California.

Jonathan E Rosenberg (JE)

Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, New York.

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