These results suggest that lower lymphocyte Hsp27 levels might be associated with an increased risk of lung cancer.

downregulation of expression sensitizes lung adenocarcinoma cells to TRAIL-induced apoptosis

Single nucleotide polymorphisms in HSPB1 promoter is asociated with lung cancer.

data suggest that serum HSP27 levels might serve as a possible tool to discriminate between early and advanced stages of non-small cell lung cancer

Study shows that Hsp27 is expressed in nearly 80% of non-small cell lung cancer patients and that erlotinib or chemotherapy increases its expression levels leading to chemoresistance.

Stromal expression of heat-shock protein 27 is associated with worse clinical outcome in patients with colorectal cancer lung metastases

The genetic polymorphisms in LIG4 rs1805388 and HSPB1 rs2868371 were not obviously correlated with the risk of radiation pneumonitis and radiation-induced lung injury of lung cancer.

In clinical specimens of non-small cell lung cancer, HSPB1 expression was absent from tumor endothelial cells undergoing the endothelial-to-mesenchymal transition

High p-Hsp27 expression is associated with cisplatin resistance in lung cancer.

High HSP27 expression is associated with non-small cell lung cancer metastasis.

low expression of HSPB1 is also significantly associated with better overall survival of non-small cell lung cancer patients

High HSP27 expression is associated with invasive non-small cell lung cancer.

Study revealed that constitutive overexpression of Redd1 induced HSP27 and HSP70 expression in lung cancer cells. The expression of Redd1, HSP27 and HSP70 was highly increased in lung cancer tissues compared with that in normal lung tissues. Constitutive overexpression of Redd1 led to AKT activation and HSP27 and HSP70 induction, all of which were involved in lung cancer cell survival and resistance to ionizing radiation.

lung cancer patients carrying the HSPB1 rs7459185 CC genotype were associated with a significantly higher risk of acute grade 3 radiation-induced esophageal toxicity (RIET) than those carrying the GG/GC genotypes

silencing of HSPB1 increased the radiosensitivity of nonsmall cell lung carcinoma (NSCLC) cells by reducing cell viability, depolarizing the MMP, arresting the cell cycle in the G2/M phase and promoting cell apoptosis. Therefore, HSPB1 may be a novel target for increasing radiosensitivity in the treatment of NSCLC

HSPB1 depletion in a mouse model of lung tumorigenesis induced the endothelial-to-mesenchymal transition