High coexpression of both insulin-like growth factor receptor-1 (IGFR-1) and epidermal growth factor receptor (EGFR) is associated with shorter disease-free survival in resected non-small-cell lung cancer patients.

Overexpression of IGF1R is associated with squamous cell carcinoma in non-small-cell lung cancer patients.

These results suggest that IGFR-1 expression may be useful as a prognostic marker in patients with small-cell lung cancer -extensive disease.

Notch-1 stimulates survival of lung adenocarcinoma cells during hypoxia by activating the IGF-1R pathway.

In non-small cell lung carcinoma IGF1R protein and gene expression does not associate with survival, whereas high IGF1R gene copy number harbors positive prognostic value.

small cell lung cancer is characterized by frequent high-IGF1R protein expression, increased gene copy number, and occasional occurrence of true gene amplification.

The IGF-IR expression is related to tumor size and T stage in lung adenocarcinoma, while there is no relation between IGF-IR expression and prognosis.

intensity of anti-IGF-1R immunostaining for 21 patients with small-cell lung cancer was correlated to survival.

Propose a Systems Biology approach to understand the molecular biology of EGFR and IGF1R pathways in non-small cell lung cancer.

the present study demonstrated that expression of IGF1R was lower in moderately to poorly differentiated lung adenocarcinoma, and that low IGF1R expression was associated with poor prognosis in patients with lung adenocarcinoma.

High IGF1R is associated with postoperative recurrence in patients with adenocarcinoma in non-small-cell lung cancer.

High IGF-1R expression was associated with squamous cell carcinoma than adenocarcinoma in non-small-cell lung cancer.

Inactivation of TROP2 due to loss of heterozygosity or by DNA methylation may play an important role in lung cancer tumourigenicity through losing its suppressive effect on IGF-1R signalling and tumour growth.

IGF-1R is highly expressed in lung squamous cell carcinoma and mucinous adenocarcinoma, although copy number alterations in the IGF-1R gene were rare.

show that IGF-IR-mediated POU5F1 expression to form a complex with beta-catenin and SOX2 is crucial for the self-renewal and oncogenic potentials of lung adenocarcinoma stem-like cells

miR-486 directly targets components of insulin growth factor (IGF) signaling including IGF1, IGF1 receptor, and phosphoinositide-3-kinase, regulatory subunit 1alpha (PIK3R1, or p85a) and functions as a potent tumor suppressor of lung cancer.

FBLN3 suppresses both epithelial-to-mesenchymal transition and self-renewal of lung cancer stem cells by modulating the IGF1R pathway.

IGF1R activation is a molecular mechanism that confers acquired resistance to erlotinib in lung cancers with the wild-type EGFR

Hypoxia increased the population of lung cancer stem cells resistant to gefitinib in EGFR mutation-positive non-small cell lung cancer by activating IGF1R.

single nucleotide polymorphisms and mutations in the insulin-like growth factor 1 receptor can be detected and may harbor prognostic value in non-small cell lung cancers

Data indicate that insulin-like growth factor 1 receptor (IGF1R) was a target of miR-195 in non-small cell lung cancer (NSCLC)cells.

High IGF1R mRNA expression is associated with advanced non-small cell lung cancer.

There was also no correlation with IGF1R expression and survival in non-small cell lung cancer.

Low IGF-1R expression is associated with squamous cell tumours in non-small-cell lung cancer.

High IGF1R gene copy number and protein overexpression are frequent in non-small cell lung carcinoma but they are not prognostically relevant.

TM4SF4 expression was correlated with the increased expression of IGF1, consequently resulting in IGF1R activation in lung adenocarcinoma.

The results demonstrate that miR-30a influences non-small cell lung cancer progression through PI3K/AKT signaling pathway by targeting IGF1R in A549 cells.

Our results indicated that miR-139-5p acts as a tumor suppressor in non-small cell lung cancer partially via down-regulating IGF1R expression.

Low EI24 and high IGF-1R expressions in lung cancer patients.

Suggest that IGF1R plays an important role in acquired drug resistance against EGFR-TKIs by inducing epithelial mesenchymal transformation in non-small cell lung cancer.

progression of lung cancer in mice treated with IGF-1 was significantly increased as compared to the group treated with IGF-1+AG1024 or the control group, with the same trend mirrored in IGF-1/p-IGF-1R/IGF-1R at the protein and/or mRNA levels

Results showed that IGF1R genetic variants are related to EGFR mutation in female lung adenocarcinoma patients and may be a predictive factor for tumor lymph node metastasis in Taiwanese patients with non-small-cell lung carcinoma.

Data suggest that IGF-I/IGF-IR system triggers stimulatory actions through both GPER and DDR1 in aggressive tumors as mesothelioma and lung tumors.

Our findings imply that APBB1 plays an important role in the maintenance of EMT-associated CSC-like properties and gamma-radiation resistance via activation of IGF1Rbeta/AKT/GSK3beta pathway in lung cancer cells, highlighting APBB1 as a potential target for therapeutic cancer treatment.

Findings indicated both cezanne-1 and IGF1R expressions were negative independent predictive factors for the prognosis of lung adenocarcinoma, respectively. There was a close positive interrelationship between cezanne-1 and IGF1R expression.

In 16 pleuropulmonary blastomas (PPBs), 25% of the tumors had an amplification of the IGF1R gene and 44% showed a gain of chromosome 8. All of the tumors with IGF1R amplification were PPBs type 3, indicating that it is a later event in tumor progression, while the gain of chromosome 8 was found in both type 2 and type 3 tumors indicating that these changes are probably earlier events in tumor development.

This study explores the prognostic effect of MET, MET gene copy number, polysomy of chromosome 7, IGF1R gene copy number and IGF-1 expression in tumor epithelial cells of primary non-small-cell lung cancer in 326 patients.

This meta-analysis revealed that high expression of IGF-1R was associated with poor prognosis in non-small cell lung cancer.

There is an accelerated loss of IGF1R, following loss of UBQLN1 in lung adenocarcinoma cells.

High IGF1R expression is associated with non-small cell lung cancer.

Study characterises nuclear trafficking of IGF1R by intracellular amphiregulin as an important component of lung cancer biology, and demonstrates its contribution to the resistance of lung tumor cells to EGFR-tyrosine kinase inhibitor gefitinib.

Study found that the expression of IGF1R was significantly increased in nonsmall cell lung cancer (NSCLC) and associated with poor prognosis. The mRNA expression of IGF1R in human NSCLC tissues was positively correlated with the level of EGFRAS1.

Activation of insulin-like growth factor-1 receptor confers acquired resistance to osimertinib in non-small cell lung cancer with EGFR T790M mutation.

IGF2 Autocrine-Mediated IGF1R Activation Is a Clinically Relevant Mechanism of Osimertinib Resistance in lung cancer.

Insulin-like growth factor-1 receptor induces immunosuppression in lung cancer by upregulating B7-H4 expression through the MEK/ERK signaling pathway.

LINC00324 affects non-small cell lung cancer cell proliferation and invasion through regulation of the miR-139-5p/IGF1R axis.

These findings implicate IGF-IR as an important initiator of lung tumorigenesis