Maximum standardized uptake value of the primary tumor was a powerful prognostic determinant for patients with adenocarcinoma, but not with squamous cell carcinoma of the lung.

We analysed the results of radical segmentectomy achieved through a hybrid video-assisted thoracic surgery (VATS) approach that used both direct vision and television monitor visualization at a median follow-up of over 5 years. Between April 2004 and October 2010, 102 consecutive patients able to tolerate lobectomy to treat clinical T1N0M0 non-small cell lung cancer (NSCLC) underwent hybrid VATS segmentectomy in which we used electrocautery without a stapler to divide the intersegmental plane detected by selective jet ventilation in addition to the path of the intersegmental veins. Curative resection was achieved in all patients. The median surgical duration and blood loss during the surgery were 129 min (range, 60-275 min) and 50 ml (range, 10-350 ml), respectively. The complication rate was 9.8% (10/102) with the most frequent being prolonged air leak, and there was no case of in-hospital death or 30-day mortality post procedure. Five and seven patients developed locoregional and distant recurrences, respectively. The overall and disease-free 5-year survival rates were 89.8% and 84.7%, respectively. Radical hybrid VATS segmentectomy including atypical resection of (sub)segments is a useful option for clinical stage-I NSCLC. The exact identification of anatomical intersegmental plane followed by dissection using electrocautery is critical from oncological and functional perspectives.

Sublobar resection may be a potential alternative choice for clinical stage I NSCLC with ILD on HRCT.

BackgroundTo decrease the risk of postoperative complication, improving general and pulmonary conditioning preoperatively should be considered essential for patients scheduled to undergo lung surgery.ObjectiveThe aim of this study is to develop a short-term beneficial program of preoperative pulmonary rehabilitation for lung cancer patients.MethodsFrom June 2009, comprehensive preoperative pulmonary rehabilitation (CHPR) including intensive nutritional support was performed prospectively using a multidisciplinary team-based approach. Postoperative complication rate and the transitions of pulmonary function in CHPR were compared with historical data of conventional preoperative pulmonary rehabilitation (CVPR) conducted since June 2006. The study population was limited to patients who underwent standard lobectomy.ResultsPostoperative complication rate in the CVPR (n = 29) and CHPR (n = 21) were 48.3% and 28.6% (p = 0.2428), respectively. Those in patients with Charlson Comorbidity Index scores ≥2 were 68.8% (n = 16) and 27.3% (n = 11), respectively (p = 0.0341) and those in patients with preoperative risk score in Estimation of Physiologic Ability and Surgical Stress scores >0.3 were 57.9% (n = 19) and 21.4% (n = 14), respectively (p = 0.0362). Vital capacities of pre- and post intervention before surgery in the CHPR group were 2.63±0.65 L and 2.75±0.63 L (p = 0.0043), respectively; however, their transition in the CVPR group was not statistically significant (p = 0.6815). Forced expiratory volumes in one second of pre- and post intervention before surgery in the CHPR group were 1.73±0.46 L and 1.87±0.46 L (p = 0.0012), respectively; however, their transition in the CVPR group was not statistically significant (p = 0.6424).ConclusionsCHPR appeared to be a beneficial and effective short-term preoperative rehabilitation protocol, especially in patients with poor preoperative conditions.

Poly (ADP-ribose) polymerase (PARP) plays a critical role in responding to DNA damage, by activating DNA repair pathways responsible for cellular survival. Inhibition of PARP is used to treat certain solid cancers, such as breast and ovarian cancers. However, its effectiveness with other solid cancers, such as esophageal squamous cell carcinoma (ESCC), has not been clarified. We evaluated the effects of PARP inhibition on the survival of human esophageal cancer cells, with a special focus on the induction and repair of DNA double-strand breaks. The effects were monitored by colony formation assays and DNA damage responses, with immunofluorescence staining of cH2AX and RAD51. We found that PARP inhibition synergized with cisplatin, and the cells were highly sensitive, in a similar manner to the combination of cisplatin and 5-fluorouracil (5-FU). Comparable increases in RAD51 foci formation were observed after each combined treatment with cisplatin and either 3-aminobenzamide (3-AB) or 5-FU in three human esophageal cancer cell lines, TE11, TE14, and TE15. In addition, decreasing the amount of RAD51 by RNA interference rendered the TE11 cells even more hypersensitive to these treatments. Our findings suggested that the homologous recombinational repair pathway may be involved in the synergism between cisplatin and either 3-AB or 5-FU, and that 3-AB and 5-FU may similarly modify the cisplatin-induced DNA damage to types requiring the recruitment of RAD51 proteins for their repair. Understanding these mechanisms could be useful for improving the clinical outcome of ESCC patients who suffer from aggressive disease that presently lacks effective treatment options. (Cancer Sci 2013; 104: 1593-1599 G enomic integrity is maintained by the close cooperation of several DNA repair pathways. Any failure in these pathways can lead to unrepaired DNA lesions, which cause cell-cycle arrest and cell death, either directly or following DNA replication during the S phase of the cell cycle.(1,2) Therefore, the therapeutic effects of DNA-damaging agents may be enhanced by the inhibition of DNA repair. This feature makes DNA repair mechanisms a promising target for novel cancer treatment regimens.In recent years, poly (ADP-ribose) polymerase (PARP) inhibitors have emerged as a novel class of chemotherapeutic agents. An abundant nuclear protein that catalyzes the formation of PAR polymers from NAD + , PARP is attached primarily to glutamic acid residues on acceptor proteins.(3) It participates in maintaining genomic integrity, as it is a DNA damage-sensing protein that binds to DNA single-strand breaks (SSBs). (4,5) In addition, PARP plays a role in restarting stalled replication forks, by attracting Mre11 to these sites.(6,7) Therefore, the inhibition of PARP generates DNA damage, and the obstructed replication forks can be converted to replication-associated DNA double-strand breaks (DSBs), which lead to cell cycle arrest and cell death unless they are repaired by the homologous recombinational repair pathway (HR). (8,9) Recently, th...