1
Eimling A, Bonzheim I, Staebler A, Fend F. Detection of the BRAF V600E mutation in serous ovarian tumors: a comparative analysis of immunohistochemistry with a mutation-specific monoclonal antibody and allele-specific PCR. Hum Pathol. 2013;44(3):329?5. Ormanns S, Altendorf-Hofmann A, Jackstadt R, Horst D, Assmann G, Zhao Y, Bruns C, Kirchner T, Knosel T. Desmogleins as prognostic biomarkers in res
1
Eased DTEC and reduction in TRDEC. To prove these statements, we have tested some biophysical characteristics as indices of collagen content of the regenerated tissues at 120 DPI. Compared to the ICTs, the ITTs had a higher dry matter content. They also showed almost similar patterns of water delivery and water uptake characteristics with their normal contralateral tendons. This bio-implant was no
1
Eased DTEC and reduction in TRDEC. To prove these statements, we have tested some biophysical characteristics as indices of collagen content of the regenerated tissues at 120 DPI. Compared to the ICTs, the ITTs had a higher dry matter content. They also showed almost similar patterns of water delivery and water uptake characteristics with their normal contralateral tendons. This bio-implant was no
1
Ic cancer, there have been less than a dozen studies which correlated putative markers with survival outcome [31]. Similar to the hazard ratio (HR) estimates for death reported for CNKSR1 in this study, the majority of previously described prognostic biomarker studies reported HRs for death ranging from 1.5 to 4 [31]. Exceptions to these studies are, among others, the recently reported study of 13
1
Py, Black or Hispanic race/ethnicityQuadri et al. BMC Cancer (2017) 17:Page 10 ofFig. 7 Survival stratified by resection and CNKSR1 expression status. a Survival in limited subset of primary tumor biopsy specimens showing low CNKSR1 expression by resection status (p = 0.367). b Survival in patients with high CNKSR1 expression by resection status (p
1
Activation of ERK with induction of apoptosis by various chemopreventive and chemotherapeutic agents [39-41]. In fact, oxidants have been shown to activate ERK by taking over the growth factor receptor signaling pathways [42-46]. Moreover, ERK may get activated in response to DNA damage and can phosphorylate p53 in vitro [23,24,47-49]. We found that exposure of Capan-2 or BxPC-3 cells with apoptos
1
Ioblastoma in general. In conclusion, the orthotopic glioblastoma xenograft model recapitulates not only the invasive phenotype, but also the regional expression profile reported in human samples of glioblastoma multiforme. The value of the model (i.e., abundant tissue, high-quality RNA, andToussaint et al. Molecular Cancer 2012, 11:32 http://www.molecular-cancer.com/content/11/1/Page 10 ofFigure
1
Ed clones were compared to their GFP control counterparts. (Westerns controlled for loading by -actin IB). (D) Over-expression of galectin-1 promotes invasion. All cell counts were normalized to the parental cell line data. (Westerns controlled for loading by -actin IB).our identification of galectin-1 as a mediator of glioma invasion has been corroborated previously as detailed below. While previ

What is Kliqqi?

Kliqqi is an open source content management system that lets you easily create your own user-powered website.

Latest Comments