Objective To explore the relationships among pulmonary function,DVH and acute radiation pneumonitis after three-dimensional conformal radiation treatment in patients with non-small-cell lung cancer.MethodsPulmonary function tests were conducted on 68 inoperable patients (male 42,female 26,median age 52,KPS≥80) before and after three months radiotherapy respectively.After 3 months of follow-up,radiation pneumonitis were graded,and V20,V30 and MLD were derived from dose volume histogram (DVH).ResultsAll patients were treated with radiotherapy at the irradiation dose of 60～70Gy.Acute radiation pneumonitis occurred in 24 patients with 11 Grade Ⅰ,7 Grade Ⅱ,3 Grade Ⅲ,3 Grade Ⅳ.There were no significant difference between the pre-irradiation and the three months after irradiation for FVC (P＞0.05).But there were significant different between pre-irradiation and three months after irradiation for FEV1.0 and DLCO (P＜0.05).V20,V30 and MLD were observed in patients treated with high radiation pneumonitis.ConclusionsThere were close relationships among pulmonary function,DVH and radiation pneumonitis in patients with non-small cell lung cancer.

Unlike healthy, non-transformed cells, the proteostasis network of cancer cells is taxed to produce proteins involved in tumor development. Cancer cells have a higher dependency on molecular chaperones to maintain proteostasis. The chaperonin T-complex protein ring complex (TRiC) contains eight paralogous subunits (CCT1-8), and assists the folding of as many as 10% of cytosolic proteome. TRiC is essential for the progression of some cancers, but the roles of TRiC subunits in osteosarcoma remain to be explored. Here, we show that CCT4/TRiC is significantly correlated in human osteosarcoma, and plays a critical role in osteosarcoma cell survival. We identify a compound anticarin-β that can specifically bind to and inhibit CCT4. Anticarin-β shows higher selectivity in cancer cells than in normal cells. Mechanistically, anticarin-β potently impedes CCT4-mediated STAT3 maturation. Anticarin-β displays remarkable antitumor efficacy in orthotopic and patient-derived xenograft models of osteosarcoma. Collectively, our data uncover a key role of CCT4 in osteosarcoma, and propose a promising treatment strategy for osteosarcoma by disrupting CCT4 and proteostasis.