data describe percentage of bone marrow cells expressing receptors for interleukin-1, platelet-derived growth factor, fibroblast growth factor, transforming growth factor-beta, epidermal growth factor and c-Fos and c-Myc in untreated lung & breast cancer

bFGF, FGFR1, and FGFR2 are frequently overexpressed in squamous cell carcinoma and adenocarcinoma of the lung and may have a role in neoplasm pathogenesis

Focal FGFR1 amplification is common in squamous cell lung cancer and associated with tumor growth and survival, suggesting that FGFR inhibitors may be a viable therapeutic option in this cohort of patients.

These studies show that FGFR1 amplification is common in squamous cell lung cancer, and that FGFR1 may represent a promising therapeutic target in non-small cell lung cancer.

An increased FGFR1 gene copy number was found in 32 (32%) lung cancer patients

There were no significant associations between FGFR1 and clinicopathological parameters in lung cancer

Conclude that FGFR1 amplification is one of the most frequent therapeutically tractable genetic lesions in pulmonary carcinomas.

The incidence of FGFR1 amplification within Chinese patient non-small cell lung carcinoma tumors was 6 of 48 squamous origin and 5 of 76 adenocarcinoma.

FGFR1 amplification is associated with squamous cell carcinoma of the lung.

Data indicate that FGFR1 amplification is an independent negative prognostic factor in surgically resected squamous cell carcinoma of the lung (SCCL) and is associated with cigarette smoking in a dose-dependent manner.

FGFR1 amplification is much more common in squamous cell lung cancers (21%) than in lung adenocarcinoma (3.4%). Survival of FGFR1-amplified lung cancer cell lines was additionally shown to be dependent on overexpression of the FGFR1 kinase.

In this study, we provide evidence that 5% of Small-cell lung cancer cases show targetable high-level FGFR1 amplification

Fibroblast growth factor receptor 1 gene locus amplification is associated with lung squamous cell carcinoma.

high level of gene amplifications brain metastases of adenocarcinomas but not in squamous cell carcinomas of the lung

Increased expression of SOX2 and FGFR1 indicate poor prognosis in small cell lung cancer patients.

Amplification of FGFR1 is one of the most frequent candidate targets in lung cancer.

We further demonstrated that miR-198 directly targets fibroblast growth factor receptor 1 (FGFR1) in lung cancer cells.

Our findings suggested that FGFR inhibition could delay breast tumor progression, impair lung metastasis and break immunosuppression by effecting on tumor microenvironment, which may provide a promising therapeutic approach for breast cancer patient.

Amplification owing to polysomy of chromosome 8, where FGFR1 locates, was observed in small-cell lung cancer.

Increased SOX2 gene copy number is associated with FGFR1 and PIK3CA gene gain in non-small cell lung cancer and predicts improved survival in early stage disease

High FGFR1 mRNA and protein expression, not gene copy number, predict FGFR TKI sensitivity across all lung cancer histologies.

FGFR1 tyrosine kinase fusions are associated with aggressive molecular subtype of non-small cell lung cancer.

FGFR1 amplification is common in early-stage squamous cell carcinomas of the lung and is an independent and adverse prognostic marker.

We found that only inhibition of JNK significantly decreased the activation of MMP26 in response to FGF1 stimulation, suggesting that activation of FGFR1 signaling may activate JNK to activate MMP26 in non-small-cell lung cancer

FGFR1 protein expression is correlated with FGFR1 mRNA levels and FGFR1 gene copy number in small cell lung cancer.

Frequency of FGFR1 amplification is similar in squamous cell carcinoma of lung with and without lymph node metastases

This meta-analysis strongly suggests that FGFR1 amplification occurs more frequently in male, squamous cell lung cancer (SQCC) and smokers, and it is a risk factor for poor prognosis among Asian patients with SQCC.

High FGFR1 expression is associated with non-small cell lung cancer.

FGFR1 amplification was identified in all types of lung carcinoma

FGFR1 amplification is associated with advanced squamous non-small cell lung cancer.

endothelin-A receptor-activated ABCB1 expression has a role in nintedanib resistance in FGFR1-driven small cell lung cancer

FGFR1/MAPK may be important for brachyury activation in lung cancer, and this pathway may be an appealing therapeutic target for a subset of brachyury-driven lung cancer.

Amplification of gene FGFR1 is associated with lung adenocarcinoma.

It has been found that the adaptor protein receptor for activated PKC kinase (RACK1) formed a complex with FGFR1 and PKM2, and activated the FGFR1/PKM2 signaling. The study shows that RACK1 forms a complex with FGFR1 and PKM2, and stimulates the growth and migration of squamous lung cancer cells.

Loss of FGFR1 does generate a gene signature that is reverse correlated with FGFR1 gene amplification and/or upregulation in human breast cancer. Our results suggest that FGFR1 signaling is a key pathway driving breast cancer lung metastasis and that targeting FGFR1 in breast cancer is an exciting approach to inhibit metastasis.

This study reports a highly specific internalizing antibody fragment that can serve as a therapeutic targeting agent for efficient delivery of cytotoxic drugs into FGFR1-positive lung cancer cells.

High levels of FGFR1 is associated with non-small cell lung cancer.

Lysosomal sequestration - resulting in an organelle-specific and pH-dependent nintedanib fluorescence - was identified as an intrinsic resistance mechanism in FGFR-driven lung cancer cells. Accordingly, combination of nintedanib with agents compromising lysosomal acidification (bafilomycin A1, chloroquine) exerted distinctly synergistic growth inhibitory effects

These results suggest that FGFR1 gene amplification is a frequent alteration in squamous cell carcinoma of the lung and appears not to be a negative but rather a favorable prognostic marker for women and particularly for patients with advanced disease

Study found that YAP1 and FGFR1 were co-overexpressed in lung cancer. In addition, YAP1 regulates FGFR1 expression at the transcriptional level and strongly modulates the CSC phenotypes of FGFR1- amplified lung cancer cells in vitro and in vivo.

our findings reveal that activation of FGFR1 promotes cell proliferation, EMT, and metastasis by the newly defined FGFR1-ERK1/2-SOX2 axis in FGFR1-amplified lung cancer.

miR802 expression was demonstrated to be decreased in nonsmall cell lung cancer (NSCLC) tissues and low expression was significantly correlated with the tumor stage, lymph node metastasis and brain metastasis. FGFR1 was confirmed as the target gene of miR802 in NSCLC cells. miR802 could downregulate FGFR1 expression, thereby deactivating the PI3K/Akt/mTOR pathway and inhibiting the malignant development of NSCLC.

The results of the present study identified miR497 as a potential tumor suppressor gene in nonsmall cell lung cancer that may function via repressing FGFR1 expression, and AKT and JNK signaling.

FGFR1 regulates proliferation and metastasis by targeting CCND1 in FGFR1 amplified lung cancer.

FGFR1 Is Critical for RBL2 Loss-Driven tumor Development and Requires PLCG1 Activation for Continued Growth of Small Cell lung cancer.