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C: Midregion PTHrP and human breast cancer cells. Sci World J 2010, 1:1016–1028.CrossRef 19. Henderson MA, Danks JA, Slavin JL, et al.: Parathyroid hormone related protein localization in breast cancers click here predict improved prognosis. Cancer Res 2006, 66:2250–2256.PubMedCrossRef 20. Yoneda T, Hiraga T: Crosstalk between cancer cell and bone microenviroment in bone metastasis. Biochem Biophys Res Commun 2005, 328:679–687.PubMedCrossRef 21. Yonou H, Ogawa Y, Ochiai A: Mechanism of osteoblastic bone metastasis of prostate PLX-4720 cost cancer. Clin Calcium 2006, 16:557–564.PubMed Competing Interests The authors have declared that no competing interests exist. Authors’ contributions ZZ carried RGFP966 solubility dmso out the protocol design, participated in the patients enrollment and TMA assay, drafted the manuscript. Z-WC carried out

the patients enrollment. X-HY carried out the TMA immunohistochemistry assay. These authors contributed equally to this work. All authors read and approved the final manuscript.”
“Introduction Lung cancer is a significant worldwide health problem, accounting for more than 1.5 million new cases DOK2 and 1.3 million cancer-related deaths annually [1, 2]. The 5-year survival rate of lung cancer

still remains at 13 to 15 % for the past 3 decades, despite recent advances in lung cancer early diagnosis, surgical techniques, and the development of novel chemotherapeutic agents [3]. The single most important risk factor for lung cancer is tobacco smoke, responsible for 85 % of lung cancer incidence. However, lung cancer incidence in developed countries, like several European countries and the USA, was noticeably reduced since 2000, mostly due to tobacco cessation campaigning, whereas the incidence rate in Asian countries, including China and Japan was still shown to be increased [4]. Histologically, lung cancer can be divided into small cell lung cancer and non-small cell lung cancer (NSCLC), which have totally different etiology and treatment options. NSCLC mainly includes squamous cell carcinoma, adenocarcinoma, and large cell carcinoma [5]. Molecularly, NSCLC development is believed to be initiated by the activation of oncogenes or inactivation of tumor suppressor genes [6]. Previous studies demonstrated that mutations in the KRAS proto-oncogene are responsible for 10–30 % of lung adenocarcinomas, while mutations and amplification of EGFR are common in NSCLC and provide the basis for treatment with EGFR-inhibitors [7].