FGFR genes mutation is an independent prognostic factor and associated with lymph node metastasis in squamous non-small cell lung cancer

Li, Jing Jing; Shi, Yan; Pan, Yaqi; Liu, Zhen; Liu, Ying; Deng, Qiuju; Tan, Qin; Woodward, Emma R.; Wu, Nan

doi:10.1080/15384047.2018.1480294

Cited by 8 publications

(8 citation statements)

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“…A 3.5-fold amplification of this gene was recognized as the distribution cut-off for patient survival and may represent a stratification factor for clinical trials 127–129. In addition, a recent study demonstrated that FGFR mutations might increase the risk of lymph node metastasis in squamous NSCLC and be an independent predictive factor for inferior survival 130. There are currently two types of FGFR inhibitors: 1) molecules directed against the FGFR domain, which are selective FGFR TKIs; 2) multitarget inhibitors that are nonselective FGFR TKIs.…”

Section: Fgfr1 Amplificationmentioning

confidence: 99%

<p>Recent Progress in Rare Oncogenic Drivers and Targeted Therapy For Non-Small Cell Lung Cancer</p>

Guo¹,

Cao²,

Zhang³

et al. 2019

OTT

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Non-small cell lung cancer (NSCLC) is frequently associated with oncogenic driver mutations, which play an important role in carcinogenesis and cancer progression. Targeting epidermal growth factor receptor (EGFR) mutations and anaplastic lymphoma kinase rearrangements has become standard therapy for patients with these aberrations because of the greater improvement of survival, tolerance, and quality-of-life compared to chemotherapy. Clinical trials for emerging therapies that target other less common driver genes are generating mixed results. Here, we review the literature on rare drivers in NSCLC with frequencies lower than 5% (e.g., ROS1, RET, MET, BRAF, NTRK, HER2, NRG1, FGFR1, PIK3CA, DDR2, and EGFR exon 20 insertions). In summary, targeting rare oncogenic drivers in NSCLC has achieved some success. With the development of new inhibitors that target these rare drivers, the spectrum of targeted therapy has been expanded, although acquired resistance is still an unavoidable problem.

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Section: Fgfr1 Amplificationmentioning

confidence: 99%

<p>Recent Progress in Rare Oncogenic Drivers and Targeted Therapy For Non-Small Cell Lung Cancer</p>

Guo¹,

Cao²,

Zhang³

et al. 2019

OTT

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“…Several trials have shed light on the specific patient population who would benefit from FGFR-targeted drugs (30)(31)(32)(33)(34)(35)(36)(37)(38)(39); however, studies that have investigated the distribution of FGFR aberrations in different cancers have focused primarily on Caucasians (20). A few studies investigated FGFR mutations in Chinese squamous non-small cell lung cancer patients and their associated clinical significance (40,41). However, there lacks a study that interrogates the FGFR mutation spectrum in Chinese cancer patients.…”

Section: Introductionmentioning

confidence: 99%

A comprehensive pan-cancer study of fibroblast growth factor receptor aberrations in Chinese cancer patients

Sun¹,

Gao²,

Zhu³

et al. 2020

Ann Transl Med

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Background: The prevalence and types of fibroblast growth factor receptor (FGFR) mutations vary significantly among different ethnic groups. The optimal application of FGFR inhibitors depends on these variations being comprehensively understood. However, such an analysis has yet to be conducted in Chinese patients. Methods:We retrospectively screened the genomic profiling results of 10,582 Chinese cancer patients across 16 cancer types to investigate the frequency and distribution of FGFR aberrations.Results: FGFR aberrations were identified in 745 patients, equating to an overall prevalence of 7.0%. A majority of the aberrations occurred on FGFR1 (56.8%), which was followed by FGFR3 (17.7%), FGFR2 (14.4%), and FGFR4 (2.8%). Further, 8.5% of patients had aberrations of more than 1 FGFR gene. The most common types of aberrations were amplification (53.7%), other mutations (38.8%), and fusions (5.6%). FGFR fusion and amplification occurred concurrently in 1.9% of the patients. FGFR aberrations were detected in 12 of the 16 cancers, with the highest prevalence belonging to colorectal cancer (CRC) (31%). Other FGFR-aberrant cancer types included stomach (16.8%), breast (14.3%), and esophageal (12.7%) cancer. Breast tumors were also more likely than other cancer types to have concurrent FGFR rearrangements and amplifications (P<0.001). In comparison with the public dataset, our cohort had a significantly higher number of FGFR aberrations in colorectal (P<0.001) and breast cancer (P=0.05).Conclusions: Among the Chinese cancer patients in our study, the overall prevalence of FGFR aberrations was 7.0%. FGFR1 amplification was the most common genetic alteration in CRC, breast cancer, and lung cancer; while FGFR2 amplification was more commonly observed in gastric cancer than in other cancers in our cohort. Our study advances the understanding of the distribution of FGFR aberrations in various cancer types in the Chinese population, which will facilitate the further development of FGFR inhibitors.

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“…Growing evidence suggests that FGFR GAs are associated with worse outcomes in different tumor types [ 14 , 15 , 16 ]. In spite of the general correlation of FGFR GA with lower grades and stages of nonmuscle-invasive UC, there is no evidence to support that FGFR GAs are associated with a favorable phenotype once urothelial carcinoma advances [ 17 ].…”

Section: Discussionmentioning

confidence: 99%

Prognostic Value and Clinical Significance of FGFR Genomic Alterations (GAs) in Metastatic Urothelial Cancer Patients

Fernández

Madurga

Moreno

et al. 2022

JCM

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Fibroblast growth factor receptor (FGFR) genomic alterations (GAs) represent an actionable target, key to the pathogenesis of some urothelial cancers (UCs). Though FGFR GAs are common in noninvasive UC, little is known about their role in the metastatic(m) setting and response to therapy. This study aimed to assess the impact of FGFR alterations on sensitivity to systemic treatments and survival and to validate Bajorin’s and Bellmunt’s prognostic scores in mUC patients according to their FGFR status. We retrospectively analyzed data from 98 patients with tumor-sequenced UC who received treatment between January 2010 and December 2020. Up to 77 developed metastatic disease and were deemed the study population. Twenty-six showed FGFR GAs. A trend toward a better response to cisplatin and checkpoint inhibitors was suggested favoring FGFR GA tumors. FGFR GA patients who received an FGFR inhibitor as first-line had poorer responses compared with other options (20% vs. 68.4%, p = 0.0065). Median PFS was 6 vs. 5 months in the FGFR GA vs. FGFR WT cohort (p = 0.71). Median OS was significantly worse in the FGFR GA vs. FGFR WT cohort (16.2 vs. 31.9 months, p = 0.045). Multivariate analyses deemed FGFR GAs as a factor independently associated with the outcome (HR 2.59 (95% CI 1.21–5.55)). Bajorin’s model correctly predicted clinical outcomes in the whole study population but not in FGFR GA cases. FGFR GAs are a relevant biomarker in mUC that could condition the response to systemic therapy. New prognostic models, including this molecular determination, should be designed and validated.

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FGFR genes mutation is an independent prognostic factor and associated with lymph node metastasis in squamous non-small cell lung cancer

Cited by 8 publications

References 45 publications

<p>Recent Progress in Rare Oncogenic Drivers and Targeted Therapy For Non-Small Cell Lung Cancer</p>

<p>Recent Progress in Rare Oncogenic Drivers and Targeted Therapy For Non-Small Cell Lung Cancer</p>

A comprehensive pan-cancer study of fibroblast growth factor receptor aberrations in Chinese cancer patients

Prognostic Value and Clinical Significance of FGFR Genomic Alterations (GAs) in Metastatic Urothelial Cancer Patients

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