the Int7G24A variant of the TGFBR1 gene predisposes to small cell lung cancer risk (meta-analysis)

no evidence to support the hypothesis that TGFBR1*6A is associated with lung cancer.

reduced TGF beta R1 expression could contribute to the development of malignant phenotype of non-small cell lung cancer

an association between a TGFBR1 haplotype and risk for non-small-cell lung cancer

Using microarray gene expression profiling of human lung tumors, dysregulation of transforming growth factor-beta signaling was identified as an important mediator of tumor invasion.

A haplotype of TGFBR1 is predominantly found in non-small cell lung cancer patients displaying TGFBR1 allelic-specific expression.

in lung cancer cells, SCUBE3 could serve as an endogenous autocrine and paracrine ligand of TGF-beta type II receptor, which could regulate TGF-beta receptor signaling and modulate EMT and cancer progression

High TGFBR-1 expression is associated with metastasis in non-small cell lung cancer.

data demonstrate that miR-142-3p influences the proliferation of non-small cell lung cancer cells through repression of TGFbetaR1

This paper highlights that targeting the BMP and TGFbeta type I and type II receptors causes a downregulation of XIAP, TAK1, and Id1 leading to cell death of lung cancer cells.

BIX02189 is a potent inhibitor of TGF-beta type I receptor that can block the lung tumor metastatic activity of TGF-beta1.

TGFbetaR1 signaling was involved in 14-3-3zeta-mediated cell proliferation and metastasis of lung squamous cell carcinoma cells.

This study shows that TFAP2C promoted lung tumor progression by upregulation of TGFBR1 and consequent activation of PAK1 signaling.

Results show that TGFBR1 is upregulated in nonsmall cell lung cancer (NSCLC) that its 3'UTR is a direct target for miR98.

Data indicate that PPAR-g agonists represent an attractive treatment tool and by suppression of cell growth (in vitro and ex vivo models) and of invasion via blockade of MAPK cascade and TGFb/SMADs signaling, respectively, and its role in cancer bioenergetics and metabolism indicate that PPAR-g agonists represent an attractive treatment tool for non small cell lung cancer .

ALK 5A4 IHC can serve as a robust diagnostic test for ALK-rearranged lung cancer and is associated with treatment response and survival. Optimized tissue allocation resulted in high success rates of combined reflex EGFR and ALK testing.

hese findings demonstrate that miR-195 and miR-497 act as a tumor suppressor by suppressing ubiquitination-mediated degradation of TGF-beta receptors through SMURF2, and suggest that miR-195 and miR-497 are potential therapeutic targets for lung cancer.

Inactivation of tumor suppressor gene Clusterin leads to hyperactivation of TAK1-NF-kappaB signaling axis in lung cancer cells and denotes a therapeutic opportunity.