MYCL1, FHIT, SPARC, p16(INK4) and TP53 genes associated to lung cancer in idiopathic pulmoary fibrosis

High SPARC expression showed a trend toward longer survival in non-small cell lung cancer.

Data show that the nonsteroidal anti-inflammatory drug NS398 reactivates SPARC expression via promoter demethylation to attenuate invasiveness of lung cancer cells.

SPARC expression is higher in squamous cell carcinoma than in adenocarcinoma in non-small cell lung cancer. SPARC was a prognostic factor of overall survival but not disease-free survival.

Data indicat that the SPARC overexpression may play an important role in the initiation and development of non-small cell lung cancer (NSCLC), whereas KLF4 inhibits this process.

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

The SPARC drives pathological responses in non-small cell lung cancer and idiopathic pulmonary fibrosis by promoting microvascular remodelling and excessive deposition of ECM proteins.

Weekly NAB-paclitaxel might be effective for heavily pretreated non-small-cell lung cancer patients. SPARC expression in tumor stroma cells might be a potential negative predictor of NAB-paclitaxel.

Plasma samples from lung cancer patients and healthy heavy-smokers controls were tested for levels of COL11A1 and COL10A1 (n = 57 each) and SPARC (n = 90 each). Higher plasma levels of COL10A1 were detected in patients (p

angiogenesis of lung cancer may be related to the interaction of SPARC, TGFbeta1 and Endoglin

Potential Prognostic Role of SPARC Methylation in Non-Small-Cell lung cancer.