J Clin Oncol 2006, 24: 5034–5042 PubMedCrossRef 18 Coombs NJ, Go

J Clin Oncol 2006, 24: 5034–5042.PubMedCrossRef 18. Coombs NJ, Gough AC, Primrose

JN: Optimisation of DNA and RNA extraction from archival formalin-fixed learn more tissue. Nucleic Acids Res 1999, 27: e12.PubMedCrossRef 19. Board RE, Ellison G, Orr MC, Kemsley KR, McWalter G, Blockley LY, Dearden SP, Morris C, Ranson M, Cantarini MV, et al.: Detection of BRAF mutations in the tumour and serum of patients enrolled in the AZD6244 (ARRY-142886) advanced melanoma phase II study. Br J Cancer 2009, 101: 1724–1730.PubMedCrossRef 20. Kimura H, Suminoe M, Kasahara K, Sone T, Araya T, Tamori S, Koizumi F, Nishio K, Miyamoto K, Fujimura M, et al.: Evaluation of epidermal growth factor receptor mutation status in serum DNA as a predictor of response to gefitinib (IRESSA). Br J Cancer 2007, 97: 778–784.PubMedCrossRef 21. Horiike A, Kimura H, Nishio K, Ohyanagi F, Satoh Y, Okumura S, Ishikawa Y, Nakagawa K, Horai T, Nishio M: Detection of epidermal growth factor receptor mutation in transbronchial needle aspirates of non-small cell lung cancer. Chest 2007, 131: 1628–1634.PubMedCrossRef 22. Kimura H, Fujiwara Y, Sone T, Kunitoh H, Tamura T, Kasahara K, Nishio K: High sensitivity detection of epidermal

growth factor receptor mutations in the pleural effusion of non-small cell lung cancer patients. Cancer Sci 2006, 97: 642–648.PubMedCrossRef Competing interests GE, ED, GM, LF, JS, MC, MO and GS are employees and shareholders of AstraZeneca. LK is a former employee of AstraZeneca and has no additional competing interests to declare. Authors’ contributions GE carried out the molecular Navitoclax order genetic studies and drafted the manuscript. ED, GM, LK, LF and JS carried out the molecular analysis. MC, MO and GS participated in the design and coordination of the study. JM drafted the manuscript. All authors reviewed the draft manuscript and read and approved the final version for submission.”
“Introduction Dickkopf-1(DKK-1) gene was first discovered in 1998 as a head formation inducer and an antagonist of Wnt signaling pathway [1]. In normal

tissues of human body, DKK-1 mRNA was highly expressed in placenta and at a very low level in prostate only [2, 3]. Recent studies have revealed the involvement of DKK-1 protein in tumorigenesis. Its exact role in tumorigenesis, Carbohydrate however, still remains unclear. Several studies reported that the expression level of DKK-1 in different tumors was different and its biological functions were different as well [4–8]. DDK-1 expression was confirmed in several cancer cell lines derived from breast and other common cancers. DDK-1 protein secretion was documented in breast, prostate and lung cancers, but was negligible in melanoma [9]. The DKK-1 concentration was significantly higher in the serum of lung cancer patients than in that of other malignant tumor patients or healthy people.

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